[{"ensembl_gene_stable_id":["ENSG00000142192"],"geneconstraints_synonymous":0.388,"description":"amyloid beta precursor protein","clinvar_pathogenic":26,"geneRIFs":["A second locus for very-late-onset Alzheimer disease: a genome scan reveals linkage to 20p and epistasis between 20p and the amyloid precursor protein region.\n","Alzheimer's disease-linked Swedish amyloid precursor protein mutation causes oxidative stress, and affects caspases and the JNK pathway\n","LXR and ABCA1-induced changes in membrane lipid organization have favorable effects on processing of APP\n","anterior pharynx defective 1B-like, anterior pharynx defective 1A, presenilin enhancer 2, and nicastrin increase amyloid beta peptide levels.\n","conformational plasticity may play a role in allowing APP to interact with a number of distinct physiological ligands\n","beta-amyloid deposition levels in brain correlate with CD36 expression independent of the occurrence of Alzheimer's disease\n","results reveal a new function for sAPP as a regulator of subventricular zone progenitor proliferation in the adult central nervous system\n","Elevated APP and PS1 gene expression is associated with dementia but not especially with Alzheimer's disease.\n","Class 1 antigens undergo extra-cellular domain cleavage mediated by alpha-secretases and the cleavage product is subsequently cleaved by PS1/gamma-secretase.\n","This study suggests a possible role for APP in normal cognitive ageing, in addition to its role in Alzheimer's disease\n","Rab5 activation via amyloid precursor protein signal pathway mediates neuronal apoptosis.\n","APP-regulated FE65 plays an important role in the early stress response of cells and that FE65 deregulated from APP induces apoptosis.\n","Study reveals that non-neurotransmitter Abeta has a binding capacity to beta(2)AR and induces PKA-dependent hyperactivity in AMPA receptors.\n","Severe neuritic abnormalities and neuron loss were found in the brains of mice transgenic for amyloid beta precursor protein and presenilin-1 (APPPS1).\n","analysis of N-terminally truncated Abeta peptides starting with pyroglutamate (AbetapE3) in human brain and mouse cells\n","Data suggest that APP variants would not contribute to the risk of developing late-onset Alzheimer's disease in the study population.\n","sortilin is implicated in APP lysosomal and lipid raft targeting via its carboxyl-terminal F/YXXXXF/Y motif.\n","Soluble APP-beta suppresses neuronal differentiation and astrocytic differentiation of U251 glioma cells.\n","Soluble amyloid Beta precusor protein alpha regulates RACK-1 gene expression.\n","The number of APP-positive cells significantly increased in denervated olfactory bulb of wild type but not APP/presenilin-1 transgenic mice.\n","I suppresses glucocorticoid receptor signaling, which has important implications for a pathogenic mechanism of Alzheimer disease.\n","these results indicate that sAPPalpha-induced gliogenesis is in part mediated by the BMP-4 signaling pathway.\n","SUCLG2 has been identified as both a determinator of CSF amyloid beta-protein (1-42) levels and as attenuator of cognitive decline in Alzheimer's disease.\n","Abeta monomer bound to the DMPC bilayer fails to perturb the bilayer structure in both leaflets\n","the mid-domain antibody used can serve as an additional tool for mapping a more complete Abeta degradation profile.\n","A cell-permeable tool for analysing APP intracellular domain function and manipulation of PIKfyve activity.\n","The Network analyses identified APP expression in temporal cortex in patient with late-onset Alzheimer's disease.\n","These results indicate that autophagosomes are key organelles to help avoid C99 accumulation preventing its deleterious effects.\n","This data demonstrates a specific function of APP or its metabolites is involved in the changes that occur during high fat diet-induced obesity.\n","RelA, RelB and c-Rel can be activated by Abeta1-40, all of which mediate pro-inflammatory cytokine transcription and retinal pigment epithelium damage.\n","This study demonstrated that Progress of Brain Amyloid Deposition in Familial Alzheimer's Disease with Taiwan D678H APP Mutation.\n","Alzheimer's disease-associated TREM2 variants bind Abeta with equivalent affinity but show loss of function in terms of signaling and Abeta internalization.\n","A novel lysosome-to-mitochondria signaling pathway disrupted by amyloid-beta oligomers.\n","FNDC5 significantly affects beta-cleavage of APP via the interaction with APP.\n","SERF(YDL085C-A) mainly affects the rate of primary nucleation in amyloid formation for the disease-related proteins Abeta40 and alpha-synuclein.\n","Abeta modulates actin cytoskeleton via SHIP2-mediated phosphoinositide metabolism.\n","The apparent mechanical effect of isolated amyloid-beta and alpha-synuclein aggregates revealed by multi-frequency MRE.\n","Computational analysis of Alzheimer-causing mutations in amyloid precursor protein and presenilin 1\n","Abeta(1-42) tetramer and octamer structures reveal edge conductivity pores as a mechanism for membrane damage.\n","Dimerization of Abeta40 inside dipalmitoylphosphatidylcholine bilayer and its effect on bilayer integrity: Atomistic simulation at three temperatures.\n","Presenilin 1 and APP Gene Mutations in Early-Onset AD Families from a Southeast Region of China.\n","Amyloid, tau, and astrocyte pathology in autosomal-dominant Alzheimer's disease variants: AbetaPParc and PSEN1DE9.\n","Oligomeric Forms of Human Amyloid-Beta(1-42) Inhibit Antigen Presentation.\n","Insights into lncRNAs in Alzheimer's disease mechanisms.\n","The Inflammasome Adaptor Protein ASC in Mild Cognitive Impairment and Alzheimer's Disease.\n","The English (H6R) Mutation of the Alzheimer's Disease Amyloid-beta Peptide Modulates Its Zinc-Induced Aggregation.\n","Accumulation of amyloid beta in human glioblastomas.\n","Phosphatidylinositol-4-phosphate 5-kinase type 1alpha attenuates Abeta production by promoting non-amyloidogenic processing of amyloid precursor protein.\n","Effect of a Cognitive Training Program on the Platelet APP Ratio in Patients with Alzheimer's Disease.\n","Segmental structural dynamics in Abeta42 globulomers.\n","Relationships Between the Deposition of Amyloid-beta and Tau Protein and Glymphatic System Activity in Alzheimer's Disease: Diffusion Tensor Image Study.\n","Germline mutations directions are different between introns of the same gene: case study of the gene coding for amyloid-beta precursor protein.\n","TNF-alpha and IL-1beta Modulate Blood-Brain Barrier Permeability and Decrease Amyloid-beta Peptide Efflux in a Human Blood-Brain Barrier Model.\n","In vitro electrochemical detection of the degradation of amyloid-beta oligomers.\n","Neurodegeneration Markers in the Cerebrospinal Fluid of 100 Patients with Schizophrenia Spectrum Disorder.\n","The associations of APP, PSEN1, and PSEN2 genes with Alzheimer's disease: A large case-control study in Chinese population.\n","Synaptogenic effect of APP-Swedish mutation in familial Alzheimer's disease.\n","The role of Abeta in Alzheimer's Disease as an Evolutionary Outcome of Optimized Innate Immune Defense.\n","Amyloid-associated increases in soluble tau relate to tau aggregation rates and cognitive decline in early Alzheimer's disease.\n","Muscular Swedish mutant APP-to-Brain axis in the development of Alzheimer's disease.\n","Amyloid Beta in Aging and Alzheimer's Disease.\n","Medin co-aggregates with vascular amyloid-beta in Alzheimer's disease.\n","Amyloid precursor protein and mitochondria.\n","Amyloid-beta and APOE genotype predict memory decline in cognitively unimpaired older individuals independently of Alzheimer's disease polygenic risk score.\n","Co-registration of MALDI-MSI and histology demonstrates gangliosides co-localize with amyloid beta plaques in Alzheimer's disease.\n","Modulation of Alzheimer's Disease Abeta40 Fibril Polymorphism by the Small Heat Shock Protein alphaB-Crystallin.\n","CryoET of beta-amyloid and tau within postmortem Alzheimer's disease brain.\n","Interplay between glypican-1, amyloid-beta and tau phosphorylation in human neural stem cells.\n","Selective suppression of oligodendrocyte-derived amyloid beta rescues neuronal dysfunction in Alzheimer's disease.\n","Mitofusin 1 and 2 overexpression reduces AbetaO-mediated ER stress and apoptosis in N2a APPswe cells.\n","Secondary Nucleation of Abeta Revealed by Single-Molecule and Computational Approaches.\n","A lowly populated, transient beta-sheet structure in monomeric Abeta(1-42) identified by multinuclear NMR of chemical denaturation.\n","Semantic intrusion errors as a function of age, amyloid, and volumetric loss: a confirmatory path analysis.\n","Age, vascular disease, and Alzheimer's disease pathologies in amyloid negative elderly adults.\n","Kunitz protease inhibitor (KPI) domain forms of APP regulate extracellular cleavage of secreted APP by inhibiting the activity of a secreted APP-degrading protease\n","Alzheimer's Amyloid-beta peptide contains catalase binding site and inhibits anti-oxidant activity\n","Mutations in APP may predispose to very-late-onset Alzheimer disease.\n","Observational study of gene-disease association. (HuGE Navigator)\n","helix-containing intermediates in amyloid beta-protein fibrillogenesis\n","Serine phosphorylation site within the Alzheimer's Amyloid-beta sequence\n","Here the technique of small angle neutron scattering has been used to determine the structure of these Abeta micelles\n","Insulin-degrading enzyme rapidly removes the beta-amyloid precursor protein intracellular domain (AICD).\n","Estrogen lowers Alzheimer beta-amyloid generation by stimulating trans-Golgi network vesicle biogenesis\n","a biomarker for Alzheimer disease\n","Tyrosine phosphorylation of the beta-amyloid precursor protein cytoplasmic tail promotes interaction with Shc.\n","mitochondrial dysfunction in Down's syndrome may lead to intracellular deposition of Abeta42, reduced levels of AbetaPPs, and a chronic state of increased neuronal vulnerability.\n","early signaling mechanisms involved in Abeta toxicity using the SH-SY5Y neuroblastoma cell line (amyloid beta protein)\n","Apolipoprotein E4 potentiates amyloid beta peptide-induced lysosomal leakage and apoptosis in neuronal cells\n","Oxidation of methionine 35 attenuates formation of amyloid beta -peptide 1-40 oligomers\n","Accelerated plaque accumulation, associative learning deficits, and up-regulation of alpha 7 nicotinic receptor protein in transgenic mice co-expressing mutant human presenilin 1 and amyloid precursor proteins\n","binds to G(M1)ganglioside and promotes the soluble amyloid beta protein polymerization\n","forms a seed of amyloid beta protein aggregation via binding to G(M1)ganglioside\n","natural oligomers of human Abeta are secreted and cerebral microinjection of cell medium containing these oligomers and abundant Abeta monomers but no amyloid fibrils markedly inhibited hippocampal long-term potentiation in rats (amyloid beta protein).\n","Activation of Cyclin-Dependent-Kinase-1 by Alzheimer's Amyloid-beta peptide\n","Munc18a acts through direct and indirect interactions with X11 proteins and powerfully regulates APP metabolism and Abeta secretion.\n","results show that the constrained decapeptide dimers rapidly form an intramolecular, antiparallel beta-sheet and polymerize into amyloid fibrils at low concentrations\n","gamma secretase cleavage of APP may contribute to Alzheimer's disease-related neurodegeneration [GAMMA SECRETASE]\n","Rac1 generates reactive oxygen species through beta-amyloid signaling\n","mutation of leucine 166 in presenilin-1 affects generation independent of effect on Abea 42 production\n","Mechanism of membrane depolarization caused by the Alzheimer Abeta1-42 peptide\n","Eliminating membrane depolarization caused by the Alzheimer peptide Abeta(1-42, aggr.).\n","REVIEW: the folding pathways of an Alzheimer's amyloid Abeta-Peptide explored by long time dynamic simulations.\n","Mutations that reduce aggregation of the Alzheimer's Abeta42 peptide: an unbiased search for the sequence determinants of Abeta amyloidogenesis.\n","[alpha]-Secretase ADAM10 as well as [alpha]APPs is reduced in platelets and CSF of Alzheimer disease patients.\n","Profile of cholesterol-related sterols in aged amyloid precursor protein transgenic mouse brain\n","Transcriptional activation and increase in expression of Alzheimer's beta-amyloid precursor protein gene is mediated by TGF-beta in normal human astrocytes\n","Transforming growth factor-beta-induced transcription of the Alzheimer beta-amyloid precursor protein gene involves interaction between the CTCF-complex and Smads\n","description of APP binding site for fibrillar Abeta and identification by alanine scanning mutagenesis\n","mutations in PSEN1 increase Abeta42 production\n","mutant proteins form annular protofibrils (similar to pore-forming bacterial toxins), suggesting that inappropriate membrane permeabilization might be the cause of cell dysfunction and even cell death in amyloid diseases, as Alzheimers and Parkinsons\n","Human APP expressed in rat cortical cell neurons in culture is processed to produce amyloid beta and soluible APP. Expression of APP triggers neuronal cell death.\n","laminin affects polymerization, depolymerization and neurotoxicity of this protein.\n","Several months after intracerebral injections of this protein into betaAPP transgenic mice, cerebral beta-amyloidosis was induced.\n","Annexin 5 and apolipoprotein E-2 protect PC12 rat cells against the cytotoxicity of this protein.\n","There is a synergetic effect of APP dysfunction, revealed by Abeta aggregation, on the neuron-to-neuron propagation of tau pathology in aging and sporadic Alzheimer's disease.\n","Differential rates of frameshift alterations in four repeat sequences of hereditary nonpolyposis colorectal cancer tumors.These repeats consisted of (A)10 in the TGF beta RII, (G)8 in the BAX, (A)8 in the CASP1, and (CCA)7 in the APP genes.\n","Coordination of copper(II) ions by the 11-20 and 11-28 fragments of human and mouse beta-amyloid peptide\n","new evidence suggests that the C-terminal cytosolic tail of beta-amyloid precursor protein may have multiple biological activities, ranging from axonal transport to nuclear signaling.\n","Amyloid subunits from chromosome 13 dementia brains are able to fully activate the complement cascade at levels comparable to those generated by Abeta1-42\n","APOE isoproteins are inefficient at complexing with synthetic Alzheimer disease amyloid beta-protein in vitro.\n","Two populations of Abeta (25-35) are detected, one in the aqueous vicinity of the membrane surface and the second inside the hydrophobic core of the lipid membrane\n","With vesicles mimicking neuronal membranes, both Abeta29-42 unprotected and Abeta29-42 N-protected peptides have similar capacity to induce membrane fusion and permeabilization; the N-terminus is not crucial for the peptide destabilizing properties.\n","Observational study of gene-disease association and gene-gene interaction. (HuGE Navigator)\n","Two genetic variants, a common +37G/C polymorphism and a rare -9G/C variant, have been identified and characterized in the core sequences of the proximal APP promoter.\n","Presenilin-1 regulation of beta APP trafficking may represent an alternative mechanism by which FAD-linked PS1 variants modulate beta APP processing.\n","Abeta accumulation in the brain is limited by endothelin-converting enzymes 1 and 2\n","These results demonstrate that late Simian virus 40 transcription factor activation is required for the neuroprotective effects of amyloid precursor protein via phosphoinositide 3-kinase/Akt signalling.\n","role of MEF2 in the anti-apoptotic signaling pathways activated by APP; model of anti-apoptotic APP signaling is proposed where APP mediates p38 MAPK-dependent phosphorylation and activation of MEF2\n","Mutation has pathogenic effects in cerebral amyloid angiopathy. (REVIEW)\n","the termini of Abeta1-40 and Abeta1-42 peptides are generated by a process involving presenilin 1\n","the effect and the mechanism of fluorinated alcohols on the amyloid beta-to-alpha conversion\n","the decapeptide region of APP is likely an active site-directed inhibitor that has high selectivity toward gelatinase A\n","APP copper binding domain (CuBD) contains a novel copper binding site that favors Cu(I) coordination\n","Abeta production in astrocytes is potentiated by TGF-beta1\n","Data indicated that variation of amyloid precursor protein (APP) gene expression in peripheral blood mononuclear cells might be a pathogenic source of Alzheimer's disease.\n","APP is cleaved by a process that involves PDGF and beta-gamma-secretase through a Src-Rac-dependent pathway\n","The transcriptional activity of the APP intracellular domain-Fe65 complex is inhibited by activation of the NF-kappaB pathway.\n","after A beta binds to raft-like membranes composed of monosialoganglioside GM1/cholesterol/sphingomyelin (1/1/1), the protein can translocate to the phosphatidylcholine membranes to which soluble A beta does not bind\n","results show that neuronal activity regulates the production and secretion of Abeta by controlling APP processing; also report that Abeta modulates synaptic strength\n","3D reconstruction of beta-amyloid in the hippocampus and entorhinal cortex of PDAPP transgenic mice\n","soluble oligomers have a unique distribution in Alzheimer disease brain that is distinct from fibrillar amyloid\n","factors that affect both nucleation and elongation in the formation of highly toxic forms of Abeta aggregates\n","Release of APP intracellular domain from the membrane takes place in a compartment downstream of the endoplasmic reticulum, is dependent on presenilin proteins, and can be inhibited by treatment with established gamma-secretase inhibitors.\n","Nornicotine covalently alters the amyloid beta peptide 1-40, leading to reduced peptide aggregation, reduced plaque formation, altered clearance, & attenuated toxicity of soluble aggregates\n","REVIEW: pathways involved in proteolytic processing of APP which could contribute to some of the age-related changes seen in Alzheimer's disease\n","Patients with high Abeta1-42 levels had more cholinergic dystrophic neurites in the plaques than cases with lower Abeta1-42.  Abeta1-42 may also trigger cholinergic dysfunction by promoting aberrant neuritic sprouting.\n","APP and Fe65 mediate transactivation with low density lipoprotein receptor-related protein\n","kinesin-I-dependent neuronal AbetaPP transport, which controls AbetaPP processing, may be regulated by JIP1\n","A beta or hydrogen peroxide (H(2)O(2)) induces oxidative stress and cell cytotoxicity. The exposure of cells to A beta results in an increased trk B expression with a concurrent reduction in truncated trk B levels\n","Unexpectedly, the frameshifted APP+1 level in the CSF of non-demented controls was much higher (1.75 ng/ml) than in the CSF of Alzheimer patients.\n","Threonine 668 within the Amyloid beta protein precursor intracellular domain is indeed phosphorylated by JNK1; JIP-1 only facilitated phosphorylation of AbetaPP but not of the two other family members APLP1 (amyloid precursor-like protein 1) and APLP2\n","ABETA in neutral aqueous solution is characterized variously as a random coil or a heterogeneous mixture.  At lower pH, a different conformation is favored. The reactivity of the monoclonal antibody 6F/3D is drastically reduced.\n","Observational study of genotype prevalence. (HuGE Navigator)\n","beta-sheet content of Abeta mutants correlates with their aggregation and role in cerebral amyloid angiopathy\n","The soluble amino-terminal ectodomain of beta-amyloid precursor protein regulates dendrite motility and melanin release in epidermal melanocytes and melanoma cells.\n","Notch1 competes with the amyloid precursor protein for gamma-secretase\n","an increase in the ratio of Abeta(WT)/Abeta(MUT(Arctic)) may result in the accumulation of potential neurotoxic protofibrils and acceleration of disease progression in familial Alzheimer's disease mutation carriers\n","expression of COX-1 and COX-2 may influence Amyloid beta peptide generation through mechanisms that involve PG-E2-mediated potentiation of gamma-secretase activity\n","CSF-Abeta1-42 showed no additional benefit in discriminating AD patients from controls but might be useful for tracking the severity of the disease.\n","endogenous A beta can be produced directly at the plasma membrane and alterations in the degree of APP endocytosis may help regulate its production\n","FE65L1 potentiates gamma-secretase processing of APP CTFs. This requires binding of FE65L1 to APP and APP CTFs. Enhanced APP CTF processing can be detected in early endosome vesicles\n","Amyloid beta peptide (Abeta42) activates PLC-delta1 promoter through the NF-kappaB binding site\n","Rho and its effector, Rho-associated kinase, preferentially regulated the amount of Abeta42 produced in vitro and only NSAIDs effective as Rho inhibitors lowered Abeta42\n","By NMR studies, supramolecular organization of beta-sheets in amyloid fibrils is determined by a sensitive balance of multiple side-chain-side-chain interactions\n","Local quinolinic acid production induced by aggregated amyloid peptide Abeta1-42 may be one of the factors involved in the pathogenesis of neuronal damage in Alzheimer's disease.\n","Patients who progressed to dementia of Alzheimer type at 2-year follow-up showed significant decrease of baseline platelet APP compared with stable mild cognitive impairment patients and patients who developed other types of dementia\n","proline scanning data are most compatible with a model for amyloid protofilament structure loosely resembling the parallel beta-helix folding motif, such that each Abeta(15-36) core region occupies a single layer of a prismatic, H-bonded stack of peptides\n","Data suggest that the insulin-degrading enzyme-mediated clearance mechanism for endoplasmic reticulum-localized amyloid beta represents an as yet unknown type of degradation which is not entirely dependent on the proteasome.\n","the internal structures are similar for beta2-microglobulin and amyloid fibril protein\n","APLP1 and APLP2 and APP are processed similarly to act via the same nuclear target and are regulated by BACE 1 in neurons\n","beta-amyloid is cross-linked by peroxidase activity of cyclooxygenase-2, which also generates toxic intracellular forms of oligomeric Abeta\n","processing of amyloid-beta precursor protein and amyloid-beta deposition are modulated by luteinizing hormone\n","Involvement of X11L in the phosphorylation of APP family proteins in cellular stress and suggest that X11L protein may be important in the physiology of APP family proteins as well as in the regulation of Abeta production.\n","spectral studies of the mode of Cu(2+) binding to Abeta in solution show that the mode of copper binding is highly pH-dependent & that histidine residues 13, 6, and 14 are involved in Cu(2+) coordination but that Tyr(10) is not.\n","Copper depletion down-regulates expression of the Alzheimer's disease amyloid-beta precursor protein gene\n","we found a change in the ratio of KPI(+)(containing a Kunitz-type serine protease inhibitor domain ) to KPI(-)(without Kunitz-type serine protease inhibitor domain) mRNA isoforms of APP.\n","Presinilin 1 Delta E9 molecules expressed in Spodoptera cells cells retain the ability to modulate amyloid beta protein levels.\n","AbetaPP and the AIDA-1 proteins interact in vitro, in living cells and, endogenously, in leukemia cell lines\n","Amyloid-beta protein accumulation induces long-term memory impairment and disturbance of the cholinergic system in APPsw transgenic mice.\n","a role of the 30-bp proximal APP promoter element in enhanced apoptotic neuronal cell death\n","Alcadein and amyloid beta-protein precursor regulates FE65-dependent gene transactivation\n","transcriptional transactivation by APP and Notch may involve distinct mechanisms; whereas the Notch intracellular domain directly functions in the nucleus, the AICD acts indirectly by activating Fe65\n","Only cells expressing RAGE at the cell surface showed hypersensitivity to Abeta.\n","glypican-1 interacts with polymerized Abeta in detergent-insoluble glycosphingolipid-enriched domains, resulting not only in amyloid deposition in senile plaques of AD brain, but also in accelerating neuronal cell death in response to stress and Abeta\n","Presenilin 1 stabilizes the C-terminal fragment(C99) of the amyloid precursor protein independently of gamma-secretase activity.\n","Abeta interacts with ABAD in the mitochondria of Alzheimer's disease patients and transgenic mice; data suggest that the ABAD-Abeta interaction may be a therapeutic target in Alzheimer's disease\n","N-acetylaspartate, glutamate and glutathione are decreased by 17%, 22% and 36%, respectively, in the cerebral cortex of APP transgenic (APPTg2576) mice at 19 months of age when Abeta deposits are widespread.\n","complexed with acetylcholinesterase, is toxic to rat brain beta-amyloid aggregation, laminin expression, reactive astrocytosis, and neuronal cell loss.\n","ADAM10 is the major alpha-secretase cleaving APP, with TACE playing a minor role\n","There was a 13-year difference in the age at onset of dementia in DS associated with the number of tetranucleotide repeat alleles in APP. APP is an important locus predicting the age at onset of dementia in people with Down syndrome.\n","memapsin 2 and APP, immunoprecipitated together from cell lysates, suggested that the interaction of these two proteins is part of the native cellular processes\n","results support the hypothesis that Abeta peptide and the oxidative state of Met-35 may be involved in the mechanisms responsible of neurodegeneration in Alzheimer's disease\n","The 5'-UTR of human APP contains several interesting control elements, such as an acute box element, a CAGA box (on a stem-loop), an IRE, and a transforming growth factor-beta-responsive element, that could control APP expression & trigger amyloid in AD.\n","Amyloid beta-protein stimulated in monocytes the gene expression for sphingosine-1-phosphate receptors 2 and 5, but not 1, 3, or 4.\n","Results suggest that the involvement of protein kinase C alpha in carbachol-induced soluble amyloid precursor protein (sAPPalpha) release is negligible, but PKC epsilon may be important in coupling cholinergic receptors with APP metabolism.\n","processing of APP by BACE1 is dependent on a mutual structural compatibility in addition to the sequence feature\n","Secretion of long Abeta-related peptides processed at epsilon-cleavage site is dependent on the alpha-secretase pre-cutting\n","Abeta peptide is secreted into cell medium upon cell death\n","Co-expression of APP695 and frame-shifted APP(+1) affects the processing of APP695 in a pro-amyloidogenic way and this could gradually contribute to Alzheimer's disease pathology, as has been implicated in Down's syndrome patients\n","The independently folded extracellular domain of amyloid-beta precursor protein (APP) constitutes the C-terminal half of the central extracellular region of APP that has been implicated in the regulation of APP cleavage.\n","Abeta engenders a dysfunctional encoding state in neurons and may initiate and/or contribute to cognitive deficit at an early stage of AD before or along with neuronal degeneration.\n","Amyloid beta-peptide (Abeta) interaction with low-density lipoprotein receptor-related protein LRP and/or Abeta-induced LRP loss at the blood-brain barrier mediate brain accumulation of neurotoxic Abeta.\n","cleavage of APP but not syntaxin 1 is independent of cell surface regulation by extracellular ligands\n","Alpha-secretase-cleaved transgenic human APP increases the expression levels of several neuroprotective genes & protects organotypic hippocampal cultures from Abeta-induced tau phosphorylation & neuronal death in mice.\n","TNFa, IL-1b and ifn-gamma stimulate gamma-secretase-mediated cleavage of amyloid precursor protein through a JNK-dependent MAPK\n","the interaction between AbetaPP and AIDA-1 is regulated by alternative splicing of the AIDA-1 protein\n","The A713T mutation may cause AD with cerebral amyloid angiopathy. The mutation is inside the A[beta] sequence & next to the gamma-secretase cleavage site. It may alter APP processing to increase fibrillogenic A[beta]42 or change its properties.\n","beta-amyloid and tau-bearing skeletal myotubes show calcium dyshomeostasis\n","Data provide functional evidence that APP can perturb intracellular calcium (Ca2+) homeostasis by emptying intracellular Ca2+ stores and triggering Ca2+ entry through store-operated channels in cultured mouse cortical neurons.\n","Hyperactivity and impaired learning abilities characterize a model of Alzheimer's disease and cerebral angiopathy in transgenic mice overexpressing the betaAPP gene with the Swedish mutation.\n","transgenic mice overexpressing both human BACE1 and APP show specific alterations in APP processing and age-dependent Abeta deposition suggesting that modulation of BACE1 activity may play a significant role in Alzheimer disease pathogenesis\n","fibrillar Abeta1-42 peptides induce neuronal apoptosis through the NADPH oxidase-superoxide-hydrogen peroxide-NS-Mase-ceramide pathway\n","the hydrophobicity of the C-terminal two residues of Abeta42 is not related to its aggregative ability and neurotoxicity, rather the C-terminal three residues adopt the beta-sheet\n","Changes in total CTFgamma levels do not correlate with either increase or decrease of any Abeta species, and inhibition of Abeta-peptide formation starting from position +1 (Abeta1-x) does not affect CTFgamma production.\n","Familial Alzheimer's disease mutations affect CTFgamma generation.\n","there is a presenilin-dependent zeta-cleavage site within the transmembrane domain of amyloid precursor protein\n","A713T in Amyloid A Precursor is implicated in the pathogenesis of Early Onset Alzheimer Disease .\n","a defect in Abeta proteolysis by IDE contributes to the accumulation of this peptide in the cortical microvasculature\n","Hmgb1 protein high mobility group 1 released from dying neurons may inhibit microglial amyloid beta42 clearance and enhance the neurotoxicity of Amyloid beta42.\n","synapse-associated amyloid-beta is prominent in regions relatively unaffected by Alzheimer Disease lesions\n","Data describe the processing of beta-secretase (BACE), implicated in Alzheimer's disease through processing of beta-amyloid precursor protein, into smaller metabolites.\n","specific role of APP isoforms containing Kunitz protease inhibitor in DLB pathogenesis\n","Targeting and functional disruption of particular synapses by Abeta oligomers may provide a molecular basis for the specific loss of memory function in early Alzheimer's disease.\n","Active gamma-secretase is present in the plasma membrane. Notch is processed at the cell surface and the majority of APP is processed by intracellular gamma-secretase\n","CLA-1 functions as an endocytic SAA receptor and is involved in SAA-mediated cell signaling events associated with the immune-related and inflammatory effects of SAA\n","Abeta, especially intracellular Abeta, counteracts the antiapoptotic function of its precursor protein and predisposes cells to p53-mediated, and possibly other, proapoptotic pathways.\n","Interaction of human and murine Abeta peptides, Abeta40 and Abeta42. Interspecies Abeta aggregates and fibers are readily formed and are more stable than homogenous human fibers.\n","beta-amyloid and APP can oxidize cholesterol to form 7beta-hydroxycholesterol\n","Data suggest an important physiological role of APP in the control of JNK/c-Jun signalling, target gene expression and cell death activation in response to cytotoxic stress.\n","beta-amyloid peptide fibrils have three distinct binding sites for thioflavin T\n","Abeta1-42 may play an important role in the negative regulation of TGF-beta1-induced MMP-2 production via Smad7 expression\n","p65FE65 may be an intracellular mediator in a signaling cascade regulating alpha-secretion of APP\n","different fibril morphologies of Abeta(1-40) have different underlying molecular structures; structure can be controlled by variations in fibril growth conditions; both morphology & molecular structure are self-propagating\n","An APP T174I mutation is associated with early-onset Alzheimer disease in an African American kindred.\n","In this mini-review, the role of the cytoplasmic domain of beta-amyloid protein precursor (APP) in APP trafficking and proteolysis is described.\n","Data describe a relationship between heparan sulfate and copper binding of amyloid precursor protein (APP) and amyloid precursor-like protein 2 (APLP2) in the modulation of nitroxyl anion-catalyzed heparan sulfate degradation in glypican-1.\n","amyloid Ass 1-42 peptide forms insoluble monolayers with high stability against lateral compression\n","Overt neuronal cell death mediated by Abeta(1-40) is critically dependent on ongoing Abeta(1-40) polymerization and is not mediated by a single stable species of neurotoxic aggregate.\n","The mechanism of Abeta-induced neuronal apoptosis sequentially involves JNK activation, Bcl-w downregulation, and release of mitochondrial Smac, followed by cell death.\n","X11alpha and X11beta have roles in beta-amyloid precursor protein processing\n","structure-activity correlation of the 1-20 and 1-16 fragments of Alzheimer's disease-related beta-amyloid peptide\n","endocytosis of LRP modulates cell surface distribution and processing of the beta-amyloid precursor protein\n","Results indicate that alleles of IDE contribute to variability in A beta deposition in the AD brain and suggest that this relationship may have relevance for the degree of cognitive dysfunction in AD patients.\n","calcium dysregulation and membrane disruption are ubiquitous neurotoxic mechanisms of soluble amyloid oligomers\n","Autoantibodies to redox-modified oligomeric Abeta are attenuated in the plasma of Alzheimer's disease patients\n","This study strongly implicates intraneuronal Abeta in the onset of cognitive dysfunction in transgenic 3xTg-AD mice, which develop both amyloid and tangle pathology.\n","Soluble oligomers of Abeta induce a profound, early inflammatory response in rat astrocyte cultures, whereas fibrillar Abeta show less increase of pro-inflammatory molecules, consistent with a more chronic form of inflammation.\n","analysis of interaction between presenilin 1 and APP (amyloid beta precursor)\n","thermodynamic analysis of the nucleation constant rate in beta amyloid fibrillogenesis\n","deletion experiments suggested that the last 50 amino acid residues of LRP-soluble tail contain the important domain for altering APP processing and Abeta production\n","Of the nine pathogenic mutations found in 12 cases, three were in APP, one in PSEN2, and five in PSEN1, including two novel Greek mutations (L113Q and N135S) in Alzheimer disease\n","activation of the G protein-coupled P2Y2 receptor (P2Y2R) subtype expressed in human 1321N1 astrocytoma cells enhanced the release of sAPP alpha in a time- and dose-dependent manner\n","mu-calpain, is a potential candidate for alpha-secretase in the regulated APP alpha-processing\n","oxidant production in the mitochondrial electron transport chain is a critical factor, acting upstream of amyloid beta peptide production in the up-regulation of Ca(2+) channels in response to chronic hypoxia\n","Aberrant accumulation of amyloid beta42 in amyotrophic lateral sclerosis (ALS) spinal cord motor neurons is associated with oxidative stress, and may play a role in the pathogenesis of neurodegeneration in ALS.\n","An HtrA1 inhibitor causes accumulation of Abeta in astrocyte cell culture supernatants and colocalizes with beta-amyloid deposits in human brain samples.\n","proposed that although CCL2 stimulates mononuclear phagocyte accumulation, it increases Abeta deposition by reducing Abeta clearance through increased apolipoprotein E expression\n","the mechanism of IL-1beta-induced-sAPP(alpha) release is dependent on MEK1/2- and JNK-activated alpha-secretase cleavage in neuroglioma U251 cells\n","Inheritance of the rs1799724-T TNF-alpha allele appears to synergistically increase the risk of Alzheimer's disease in APOEepsilon4 carriers and is associated with altered CSF Abeta42 levels\n","Based on immunoblotting studies of cerebrospinal fluid (CSF) from normals, we find that the bulk of the abetas are bound to the ER chaperones, ERp57 and calreticulin.\n","transgenic mice overexpressing wild-type human APP gene (hAPP/+) displayed a much higher expression of FAS. FAS overexpression was reduced in cortex of mice overexpressing both wild-type hAPP gene & wild-type human superoxide dismutase-1 gene.\n","glycosphingolipids are implicated in the regulation of the subcellular transport of the beta-amyloid precursor protein\n","Altogether, our results demonstrated that phosphorylated CTFs can be the substrates of the gamma-secretase and that an increase in the phosphorylation of APP-CTFs facilitates their processing by gamma-secretase.\n","PPARgamma overexpression in cultured cells dramatically reduced Abeta (amyloid-beta) secretion, affecting the expression of the APP (Abeta precursor protein) at a post-transcriptional level.\n","increased expression of wild type APP renders neuronal cells more vulnerable to oxidative stress leading to cell death\n","The strong negative correlation between net charge and oligomerization indicates that electrostatic repulsion between A beta monomers impedes their association.\n","accumulations of intramembranous Abeta peptides might affect the functions of amyloid precursor protein itself and the assembly of the PS1, Aph1, Pen 2, Nicastrin complex in Alzheimer's disease [Perspective article]\n","BRI2 gene binds the Alzheimer gene amyloid-beta precursor protein and inhibits amyloid-beta production\n","biophysical analysis of amyloid beta-protein at low pH and its protofibril formation\n","Site directed mutagenesis of the Alzheimer's Abeta (1-40) peptide to determine the effect of different side chains on the propensity of nucleation.\n","Transfected into mice, immunization ameliorates senile plaque formation, in an Alzheimer disease model.\n","Beta-amyloid (Abeta) induces a significant decrease in dynamin 1 in hippocampal neurons and in the transgenic 2576 mouse model of Alzheimer's disease\n","Study shows that there is interaction of the intracellular domain of beta-amyloid precursor protein with JKTBP2, indicating that JKTBP2 may have an important function in AD formation.\n","BRI2 had a modulatory effect on amyloid precursor protein (APP) processing, increasing levels of cellular APP and COOH-terminal fragments while decreasing COOH-terminal fragments and secretion of total APP and Abeta peptides.\n","Ultrasonication induces amyloid fibril formation of beta2-microglobulin\n","APP can induce postdevelopmental axonal arborization, which depends critically on a conserved motif in the C-terminus and requires interaction with the Abelson (Abl) tyrosine kinase.\n","We have studied the effect of alphaB-crystallin on the fibril growth of the Abeta (amyloid beta)-peptides Abeta-(1-40) and Abeta-(1-42).\n","properties of the side chains at positions 41 and 42 cause Abeta42 to aggregate more readily than Abeta40\n","parenchymal and vascular amyloid deposits in the cerebral cortex are associated with a different array of Abeta peptide species.\n","APP is internalized by a dynamin-dependent process, and alterations in the activity of proteins that mediate endocytosis might lead to significant changes in Abeta production\n","Results show the effectiveness of ectoine and hydroxyectoine on the inhibition of amyloid beta42 aggregation and toxicity to human neuroblastoma cells.\n","REVIEW: The biology, structure and physical properties of Abeta peptides are discussed, as well as existing therapeutics and future strategies for the treatment of Alzheimer's disease\n","Herpes virus infection leads to rapid loss of full length APP from neuronal cells.\n","These findings challenge the idea that tau pathology in Alzheimer's disease is merely a downstream effect of amyloid production/deposition and suggest that reciprocal interactions between beta-amyloid and tau alterations may take place in vivo.\n","Data show that amyloid beta:Cu2+ complexes oxidize cholesterol selectively at the C-3 hydroxyl group, catalytically producing 4-cholesten-3-one and therefore mimicking the activity of cholesterol oxidase.\n","Abeta but not tau is deregent-insoluble early in the pathogenesis of Alzheimer's disease\n","Abeta(1-42) globulomer is a persistent structural entity formed independently of the fibrillar aggregation pathway\n","Abeta40 evokes dose-dependent sodium and calcium ions in unicellular phosphatidylserine liposomes; a small amount of negatively charged phospholipids is sufficient to support the process of ion channel formation.\n","A novel mutation (L705V) within the Abeta sequence of AbetaPP in a family with autosomal dominant, recurrent intracerebral hemorrhages.\n","data support the presence of a turn structure at positions 22 and 23 in E22K-Abeta42 fibrils; formation of a salt bridge between Lys-22 and Asp-23 in the minor conformer might be a reason why E22K-Abeta42 is more pathogenic than wild-type Abeta42\n","Amyloid-beta induces disulfide bonding and aggregation of GAPDH in Alzheimer's disease\n","results show apoE co-localized with amyloid beta in amyloid plaques that lack immunoreactivity with antibodies to N-terminal epitopes of amyloid beta indicating that formation of apoE-amyloid beta complexes may conceal N-terminal epitopes of amyloid beta\n","in the amyloid beta-protein, the central hydrophobic cluster is particularly important in controlling Abeta40 assembly, whereas the C-terminus plays the more significant role in Abeta42 assembly\n","mitochondrial Abeta has a role in neuronal metabolic dysfunction in Alzheimer's disease\n","two protected core regions, Glu11-Gly25 and Lys28-Ala42, and that the residues in between, Ser26 and Asn27, as well as those in the N terminus, Asp1-Tyr10, are solvent-accessible, this provides a molecular explanation for the increased amyloidogenicity\n","This review describes in detail the different subdomains of APP and assigns functional significance to particular structures identified in the protein.\n","an additional hypothesis involving the amyloid-beta peptide and the role of Met-35 has been proposed to clarify the mechanisms responsible of neurodegeneration in Alzheimer's disease.\n","mutagenesis and structural analysis of Abeta-(1-40) amyloid fibrils\n","Findings show a close association between Abeta deposition and nigrostriatal pathology in transgenic mice and suggest that altered familial Alzheimer's disease-linked amyloid metabolism impairs, at least in part, the function of dopaminergic neurons.\n","Transfected into transgenic mice, involved in induction of tau pathology, making the interference of Abeta oligomerization a valid therapeutic target in Alzheimer disease.\n","apoE4 and Abeta1-42 may work in concert in neurons to increase lysosome formation while increasing the susceptibility of lysosomal membranes to disruption, release of lysosomal enzymes into the cytosol, and neuronal degeneration.\n","analysis of APP region 1-16 structural changes upon zinc binding and in vitro aging\n","the phosphorylation of APP regulates the formation of a pAPP-JIP-1 complex that accumulates in neurites independent of nonphosphorylated APP\n","age-dependent membrane modification was associated with an altered distribution of PS1 and BACE between detergent-resistant membranes (DRM) and non-DRM fractions, very likely affecting their APP processing potential\n","A decrease in presynaptic amyloid precursor protein (APP) and amyloid precursor-like protein 2 (APLP2) leads to a decrease in stimulus-driven synaptic activity.\n","Vav activity is required for fAbeta-stimulated intracellular signaling events upstream of reactive oxygen species production and phagosome formation\n","Soluble forms of amyloid beta (Abeta1-42) induce actin-containing rods in brains of transgenic Alzheimer mice; these stalled vesicles provide a site for producing Abeta(1-42), inducing more rods and expanding the degenerative zone.\n","apoE4 appears to modulate APP processing and Abeta production through both the low-density lipoprotein receptor-related protein pathway and domain interaction\n","APLP1 affects the endocytosis of APP and makes more APP available for alpha-secretase cleavage\n","Review. The most basic soluble Abeta peptides are stable dimers with hydrophobic regions. They perturb metabolic processes, cause release of harmful reactive compounds, reduce blood flow, induce mitochondrial apoptotic toxicity & inhibit angiogenesis.\n","Amyloid-beta precursor protein (APP) processing pathways are critical for cognitive, emotional, and synaptic functions\n","In cells stably overexpressing the functional PAC1 receptors, PACAP-27 & PACAP-38 strongly stimulated alpha-secretase cleavage of APP.\n","SorLA acts as a trafficking receptor that prevents beta-site APP-cleaving enzyme interactions with amyloid precursor protein & hence BACE cleavage of APP.\n","Review. Current knowledge on APP trafficking and amyloidogenic processing of APP in intracellular membrane compartments and microdomains is reviewed.\n","a cell-cell interaction occurs in the production of beta-amyloid in cell cultures\n","the neurotoxic Abeta amyloids 1-40 and 1-42, related to Alzheimer's disease, spontaneously enter the membranes of intact erythrocytes and cause their lysis but Abeta 1-38 and Abeta 1-35, which are not neurotoxic, have no observable effects on erythrocytes\n","Results show that purified human HDL and recombinant apolipoprotein A-I lipid particles bind directly to amyloid beta and apolipoprotein C-II amyloid fibrils.\n","release of Abeta- or Nbeta-like peptides is a common feature of the proteolysis during regulated intramembrane proteolysis signaling\n","Data for the two main isoforms of the soluble extracellular domain of amyloid precursor protein (APP; sAPPalpha(695) and sAPPalpha(770)) provided models of sufficiently high resolution to identify distinct structural domains of APP.\n","Lower BACE transcription is responsible for the minority of APP undergoing the amyloidogenic pathway and relatively lower Abeta production in the normal conditions, and that a slight increase in BACE1 can induce a dramatic elevation in Abeta production.\n","Abeta and hyperphosphorylated tau formation in somatostatin cells are basically independent events Decreased somatostatin only partly goes together with cytoskeletal changes in somatostatin cells in nucleus tuberalis lateralis of Alzheimer's disease.\n","first evidence that chronic stress accelerates the onset and severity of cognitive deficits and that these are highly correlated with pathological changes, as APP deposition.\n","role of APP in activation of gene transcription; findings show that antibody-bound APP induces expression of ornithine decarboxylase\n","flotillin-1 may recruit APP to lipid rafts and therefore participate in the localization and processing of APP\n","HspB8 might play important role in regulating Abeta aggregation and, therefore, development of classic senile plaques in Alzheimer's disease and cerebral amyloid angiopathy in hereditary cerebral hemorrhage with amyloidosis of Dutch type.\n","analytical ultracentrifugation of recombinant APP and sorLA fragments further narrowed down the binding domains to the cluster of complement-type repeats in sorLA that forms a 1:1 stoichiometric complex with the carbohydrate-linked domain of APP\n","analysis of involvement of NF-kappaB regulated by capacitative Ca2+ entry in muscarinic receptor-mediated sAPPalpha release enhancement\n","family with a later mean age at onset of 50 years (range 48 to 57) and mean age at death of 61 years (range 57 to 68) with a V717L APP mutation.\n","The binding of Cu2+ to the copper-binding domain (CuBD) of APP reduces the production of Abeta in cell-culture and animal studies.\n","Results suggest that intracellular domains of Notch and amyloid precursor protein are generated by gamma-secretase at the plasma membrane and/or early endosomes.\n","In an in vivo transgenic mouse model, mutant APP and Abeta localize to brain mitochondria and are associated with mitochondrial dysfunction and oxidative damage.\n","The pathological progression of plaque in Alzheimer's disease is rooted in characterizing total amyloid load in vivo and its effect on the kinetic rate constant of molecular imaging probes.\n","This suggests that distinct mechanisms are responsible for the differential deposition of Abeta in cerebral amyloid angiopathy associated with Alzheimer's disease and that associated with ischemic/cerebrovascular disease.\n","analysis of production of amyloid beta-protein and amyloid precursor protein intracellular domain from beta-carboxyl-terminal fragment by gamma-secretase\n","results show Down syndrome(DS) brains and trisomic fibroblasts in which APP is not overexpressed, compared to controls, challenging the notion that the widespread amyloid-beta deposits, found in DS individuals, result from an extra copy of APP\n","In Abeta amyloid fibrils, Met35 packs against Gly33 in the C-terminus of Abeta40 and against Gly37 in the C-terminus of Abeta42.\n","APP mediates cleavage of a receptor tyrosine phosphatase and regulation of beta catenin's trabscriptional activity.\n","The compromised activity of MnSOD, a primary antioxidant enzyme protecting mitochondria, may explain mitochondrial dysfunction and provide the missing link between Abeta-induced oxidative stress and Alzheimer's disease.\n","The constant and abundant amyloid beta x-42 deposition in sporadic dementia with Lewy bodies suggests that alpha-synucleinopathy is also promoted by amyloid precursor protein dysfunction.\n","Amyloid precursor protein (APP) processing can be regulated by caveolin-1 in neuronal cells.\n","The present study provides evidence that APP-promoter mutations that significantly increase APP expression levels are associated with AD.\n","Plasma Abeta levels representing vascular Abeta deposits years later result in impaired carbon dioxide (CO2)-induced vasomotor reactivity.\n","increased neuronal PKCepsilon activity can promote Abeta clearance and reduce AD neuropathology through increased endothelin-converting enzyme activity\n","These results suggest that the phosphorylation of APP intracellular domain (AICD) at T668 contributes to the neuronal degeneration in Alzheimer's disease (AD) by regulating its translocation into the nucleus and then affects neurodegeneration.\n","Genome-wide study of an F2 intercross between TgCRND8 on an A/J background and C57BL/6 mice, to identify genetic modulators of amyloid accumulation and deposition.\n","Studies demonstrate that the full morphological phenotype of IBM including beta-amyloid and tau protein deposits may also develop in children, and that congenital muscle defects may lead to abnormal protein aggregation in IBM-like inclusions.\n","A novel mutation (Leu705Val) within the Abeta sequence of a AbetaPP is reported in a family with autosomal dominant, recurrent intracerebral hemorrhages beginning in the sixth decade of life.\n","Our study thus provides evidence for a pathogenic mechanism for DS in which increased expression of App, in the context of trisomy, causes abnormal transport of NGF and cholinergic neurodegeneration.\n","Deleterious post-translational modifications of APP accumulate in a pathological protein fraction in Alzheimer dissease.\n","beta-amyloid peptides are released in association with exosomes\n","Amyloid precursor protein (APP) regulates neural stem cell biology in the adult brain, and that altered APP metabolism in Down syndrome or Alzheimer's disease (AD) may have implications for the pathophysiology of these diseases.\n","neuroserpin interacts with Abeta(1-42) to form off-pathway non-toxic oligomers and so protects neurons in Alzheimer disease\n","The inhibitory role of APP in innervation at the neuromuscular junction and increased expression in inclusion-body myositis suggest that presymptomatic upregulation of APP may be consistent with a potential role for APP in ALS pathology.\n","The detection of Abeta11-42 in young DS brain suggests an early role for this N-terminally truncated Abeta peptide in the pathogenesis of SPs in Alzheimer's disease and Down's syndrome.\n","Four months of continuous and diversified environmental stimulation resulted in a significant reduction of beta-amyloid (Abeta) plaques and in a lower extent of amyloid angiopathy.\n","Incorporation of two N-methyl amino acids into one beta-sheet is sufficient to disrupt that sheet while leaving the other, unmodified beta-sheet intact and able to form fibrils.\n","Accumulation of intracellular beta-amyloid protein decreases the activity of important components of the cellular energy generation system, compromises mitochondrial function, and leads to cell death.\n","This review focuses on the interactions between amyloid beta peptide (Abeta) and the pan neurotrophin receptor p75NTR and how Abeta-regulated signaling through p75NTR may explain a number of the neurodegenerative characteristics of Alzheimer's disease.\n","downstream transcription factors, heat shock factor 1, and DAF-16 regulate opposing disaggregation and aggregation activities to promote cellular survival in response to constitutive toxic Abeta(1-42) aggregation\n","APPPS1 mice are well suited for studying therapeutic strategies and the pathomechanism of amyloidosis by cross-breeding to other genetically engineered mouse models.\n","APP mRNA splicing can generate isoforms of APP containing a Kunitz protease inhibitor domain (Review)\n","quaternary structure of a mature amyloid fibril formed from the Abeta(1-40) peptide; the fibril is polar & represents a left-handed helix consisting of two or three protofilaments; these are organised in a manner so that the cross-section is S-shaped\n","measurements of the CuII binding to Abeta16 and Abeta28, models of the soluble Abeta\n","ladostigil decreased cell death via inhibition of caspase-3 activation via regulation of the Bcl-2 family proteins and decreased apoptotic-induced levels of holo-APP protein without altering APP mRNA levels, suggesting a posttranscriptional mechanism.\n","A subpopulation of dissociated muscle fibers from human betaAPP transgenic mice exhibited a 2-fold increase in resting calcium and membrane depolarization\n","Results use data from multidimensional NMR spectroscopy to elucidate the molecular interactions between Abeta peptide and alpha-synuclein which may lead to onset of Lewy body dementia.\n","biophysical analysis of conformations of the amyloid-beta (21-30) fragment\n","Overexpression of GGA1 increased the APP C-terminal fragment resulting from beta-cleavage but reduced Abeta. GGA1 confined APP to the Golgi, in which fluorescence resonance energy transfer analyses suggest that the proteins come into close proximity.\n","LRP binds and endocytoses Abeta42 both directly and via apoE but endocytosed Abeta42 is not completely degraded and accumulates in intraneuronal lysosomes\n","DNA condensation is a mechanism of Abeta toxicity: DNA conformation is altered in the presence of Abeta, and Abeta induces DNA condensation in a time-dependent manner\n","alphaB-crystallin competes efficiently for Abeta monomer-monomer interactions.\n","formation of amyloid fibrils in the plasma protein human serum albumin under different in vitro conditions\n","Thus, our present results strongly suggest that AICD triggers apoptosis through the p53-dependent mechanisms.\n","We propose that increased AbetaPP is a stressor increasing alphaBC expression in s-IBM muscle fibers. Determining the consequences of alphaBC association with Abeta oligomers could have clinical therapeutic relevance.\n","soluble Abeta and tau, but not soluble Abeta alone, have roles in cognitive decline in transgenic mice with plaques and tangle\n","These data point to a role of APP intracellular domain in developmental and injury-related cytoskeletal dynamics in the nervous system.\n","The load of Abeta aggregates in postmortem brains does not display a significant association with cerebrovascular lesions.\n","a fluid lipid monolayer develops immobile domains upon interaction with Abeta aggregates\n","The present study provides strong evidence that APP promoter polymorphisms that significantly increase APP expression levels are associated with development of SAD.\n","APP significantly modulates Ca(2+) store depletion-induced cell death in a store-operated channel- and CHOP-dependent manner, but independent of the unfolded protein response.\n","APP has the potential to activate aberrant neuronal cell cycle re-entry in Alzheimer's disease. [review]\n","In the E22Q/D23N, D23N/K28Q, and E22Q/D23N/K28Q mutants, hydration becomes much less significant because the mutated residues have neutral amide side-chains.\n","in the cortex and hippocampus of transgenic mice expressing mutant type of APP, the mRNA of some endoplasmic reticulum chaperones was up-regulated in comparison with wild-type mice\n","These data suggest mechanistic similarities in the nucleation behaviour of different amyloid-like fibrils and aggregates.\n","Amyloid-beta (Abeta) peptide fragment 1-42 increases neuronal pentraxin 1 expression before inducing apoptotic death of cortical neurons, indicating that Abeta contributes to the pathology of Alzheimer's disease.\n","Cleavage of amyloid precursor protein (APP)may play a critical role in the development of synaptic and behavioral dysfunction in APP transgenic mice.\n","alkalizing drugs induce the accumulation of amyloid precursor protein intracellular domain, a mechanism likely mediated by the endosome/lysosome pathway\n","Abeta induced integrin focal adhesion signaling pathways that mediate cell cycle activation and cell death in Alzheimer's disease [REVIEW]\n","provides comprehensive profile of non-cognitive behaviors of APP/PS1 transgenic mouse model; reveals behavior impairments that may be pertinent to behavior seen in AD patients\n","demonstrates a spatial learning deficit in 7-month-old APP(Swe) + PSEN1DeltaE9 bigenic mice using an adaptation of the Barnes maze\n","Abeta40 has anti-amyloidogenic effect in vivo.\n","beta-amyloid (Abeta) induces the proapoptotic protein Bcl-2 interacting mediator of cell death (Bim) in cultured hippocampal and cortical neurons.\n","Lipid membranes may be involved in templating the pathological misfolding of amyloid beta protein.\n","analysis of amyloid protofilaments alignment by linear dichroism\n","reduced presenilin proteolytic function leads to increased Abeta42/Abeta40 in Alzheimer disease (Review)\n","BACE1 and BACE2 may act as alternative alpha-secretase-like proteases in proteolytic processing of IL-1R2 and APP\n","Abeta peptide patterns vary between patients with tauopathies and synucleinopathies and between all diseases and the comparison group, possibly due to the influence of tau and alpha-synuclein on Abeta-processing.\n","study shows subunit mu1B of AP-1B binds to the cytoplasmic tail of APP in a Tyr653-dependent way; model proposed for polarized targeting of APP in which sorting of APP to basolateral domain depends on binding of AP-1B on Tyr653 in basolateral endosomes\n","While the N-terminal residues 1-16 may not play a major role in neurotoxicity and aggregation, a lack of N-terminal fragment Abeta peptide does not display the neurotoxicity of either full-length or 17-21, 25-35 truncated Abeta peptides\n","GxxxG motifs within the amyloid precursor protein transmembrane sequence are critical for the etiology of Abeta42.\n","APP could be acting through a semaphorin receptor as well\n","Results show significant decreases of Abeta1-42 in Alzheimer disease, and Abeta1-38 in frontotemporal dementias. A novel peptide (probably an oxidized alpha-helical form of Abeta1-40) was significantly increased in Lewy body dementia.\n","Neuronal expression of human amyloid precursor protein/Abeta is sufficient to reduce Reelin expression in a specific population of entorhinal cortical pyramidal neurons in vivo.\n","Physiological concentrations of naturally secreted Abeta dimers and trimers, but not monomers, induce progressive loss of rat hippocampal synapses in vitro.\n","Notch1 intracellular domain plays the role of a negative regulator in AICD signaling via the disruption of the AICD-Fe65-Tip60 trimeric complex.\n","altered phosphorylation state of eIF2alpha evoked by Abeta may account for the decreased efficacy of mRNA translation and de novo protein synthesis required for synaptic plasticity\n","high-density platelets undergo activation likely by increased frequency of platelet-platelet collisions, which determines the activation of APP beta-processing with consequent release of Abeta(40)\n","protein phosphorylation has a role in APP sorting under stress conditions\n","APLP2 and APP have roles in sperm function\n","APP and PS1 are closely associated in the centrosomes of the H4 cell\n","Data show that endogenous beta-amyloid precursor protein and amyloid beta peptide immunoreactivities colocalize with microtubules in interphase cells.\n","results suggest that common variation in the APP gene is not a significant risk factor for late-onset Alzheimer's disease\n","Increase in APP gene dosage is linked to a phenotype consisting of early onset dementia and CAA with frequent ICH. The phenotype does not depend on the size of the duplicated region, but may vary between families and between the genders.\n","time resolved static light scattering was applied to investigate the size and shape of growing beta-amyloid aggregates preceding plaque formation\n","findings show that the Arctic mutation favors proamyloidogenic APP processing by increased beta-secretase cleavage, as demonstrated by altered levels of N- and C-terminal APP fragments\n","multivesicular bodies are essential organelles for APP metabolism and all APP metabolites can be secreted in the extracellular space\n","Results suggest that amyloid beta40 plays a critical, protective role in Alzheimer's by inhibiting the aggregation of amyloid beta42 monomer.\n","We found that levels of mRNAs expressing mitochondrial COX subunits decreased significantly in Amyloid-beta-treated SK-N-SH cells in a dose-dependent manner\n","Abeta activates the apoptosis signal-regulating kinase 1 (ASK1)-p38MAP kinase-p53-Bax cascade to cause cerebral endothelial cell death in a protein phosphatase 2A (PP2A)-dependent manner.\n","Here, we show that long-term systemic administration of anti-APP beta-site antibodies to Tg2576 transgenic mice improved mouse cognitive functions associated with a reduction in both brain inflammation and the incidence of microhemorrhage.\n","Heparin binding domains on the proteins have been utilised to develop a one-step fast-performance-liquid-chromatography (FPLC) purification of sAPPs from the conditioned media.\n","an anti-A beta 1-11 antibody binds to different beta-amyloid species, inhibits fibril formation, and disaggregates preformed fibrils but not the most toxic oligomers\n","a specific nonfibrillar Abeta assembly Abeta*56 is a likelier determinant of functional deficits in hAPP mice than fibrillar Abeta deposits\n","aggressive presenilin-1 mutations cause insensitivity to Abeta42-lowering nonsteroidal anti-inflammatory drugs and gamma-secretase inhibitors\n","Two mutants of PrP, PG14 and A116V, that are associated with familial human prion diseases failed to inhibit the beta-secretase cleavage of APP\n","The ratio of soluble APPalpha-KPI protein levels to total APP protein increased in AD, and also correlated with GFAP protein levels in AD.\n","The data show that Abeta oligomer formation is inhibited by promoting fibril formation, which suggests that the relative pathological significance of oligomers and fibrils may be tested in vivo using methylene blue.\n","These results suggest that the neurotrophic effect of platelet-derived growth factor is mediated in part via upregulation of the expression and release of secreted amyloid precursor protein alpha.\n","Findings suggest different effects of wild-type and mutant hAPP on neuronal connectivity.\n","Distinct pathways of APP phosphorylation operate in proliferating, differentiating, stressed, and degenerating neurons.\n","Determination and assignment of the redox potentials clarify some misconceptions in the redox reactions involving Abeta and provide new insight into the possible roles of redox metal ions in the Alzheimer's disease (AD) pathogenesis.\n","Fe65 can control luciferase activity without stabilizing the labile APP intracellular domain fragment.\n","Role for the transcription factor AP-2alpha in the regulation of APP gene expression in human keratinocytes.\n","Stable insertion of ABETA peptide into the ER membrane strongly correlates with its length.\n","Decreased insulin receptor signaling promotes the autophagic degradation of beta-amyloid peptide in C. elegans.\n","HtrA2 has a role as a regulator of APP metabolism through endoplasmic reticulum-associated degradation\n","DNA prime-adenovirus boost regimen can enhance Th2-biased responses with adenovirus vector encoding 11 tandem repeats of amyloid beta 1-6 in mice.\n","In a model system of cultured mouse neurons, the deeper layer neurons are more resistant to toxic effects of Abeta than are cells from the more superficial strata, suggesting that an underlying biology drives the Alzheimer's progression pattern.\n","Soluble circulating LRP (sLRP) provides key endogenous peripheral 'sink' activity for amyloid beta in humans.\n","Data demonstrate severe amyloid deposition in mammary glands of familial amyloid polyneuropathy patients.\n","Hypericum perforatum extract and its single compounds affect amyloid-beta mediated toxicity in microglial cells\n","downregulation of myosin II-B, the major myosin isoform in neurons, is able to increase Abeta deposition, concomitantly altering the subcellular localization of APP\n","The chronic blockade of IL-1 signalling in the brain was associated with an atrophic phenotype of the brain, and with modified levels of APP and PS1.\n","results indicate that Abeta peptide increases MMP-9 secretion through integrins; MMP-9 then directly processes cell surface APP695 with an alpha-secretase like activity, substantially reducing the levels of secreted Abeta peptide\n","after addition of Abeta, platelet number, platelet mitochondrial membrane potential and ATP content were lowered while no protective effects of estradiol benzoate and genistein had been observed.\n","prostaglandin E(2) (PGE(2)), a strong inducer of inflammation, stimulates the production of Abeta in cultured human embryonic kidney (HEK) 293 or human neuroblastoma (SH-SY5Y) cells, both of which express a mutant type of APP\n","Aberrant increases in network excitability and compensatory inhibitory mechanisms in the hippocampus may contribute to Abeta-induced neurological deficits in hAPP mice and, possibly, also in humans with AD.\n","Signaling machinery activated in Abeta(1-42)-reactive T cells is differentially involved in protein kinase C (PKC)-delta and PKC-zeta expression and activity in samples from Alzheimer patients, compared to those from healthy adult or elderly subjects.\n","physiologically relevant levels of naturally secreted Abeta interfere with insulin receptor function in hippocampal neurons and prevent the rapid activation of specific kinases required for long term potentiation\n","Fe65 regulation of APP proteolysis may be integrally associated with its nuclear signaling function, as all antecedent proteolytic steps prior to release of Fe65 from the membrane are fostered by the APP-Fe65 interaction\n","Tyr687 appears to be a critical residue determining APP targeting and processing via different pathways, including endocytosis and retrograde transport\n","Abeta42 and Abeta40 act as potent opsonins for LDL, E-LDL and Ox-LDL and enhance cellular cholesterol accumulation as well as Abeta-deposition in vessel wall macrophages\n","the luminal juxtamembrane region of APP is an important regulatory domain that modulates gamma-secretase-dependent intramembrane proteolysis, particularly in differentiating gamma- and epsilon-cleavages\n","All salts examined promote aggregation strongly.In the presence of salts, fibrils are associated with smaller diameters, narrower crossover distances and lower amide I maxima\n","This structural study describes the mechanism of interaction between divalent copper ions and amyloid beta precursor protein (Abeta) that leads to a decrease in Abeta production and to alleviation of symptoms of Alzheimer disease in mouse models.\n","although the use of a specific gene influences the tissue distribution of amyloid, each light chain exhibits one or more determinants of organ-specificity, which originate from somatic mutations and post-translational modifications\n","The increasing levels of Abeta in CSF during early childhood of Down syndrome patients observed in this study are probably due to the trisomy of the Abeta precursor APP, which leads to an overproduction of Abeta.\n","HLA-B27 has a role in Beta 2-microglobulin amyloid deposit, as shown in transgenic rats\n","His6, His13, and His14 residues of Abeta1-42 control the redox activity of transition metals present in senile plaques.\n","The Alzheimer's disease-associated amino acid substitutions at Glu-22 or Asp-23 destabilized the turn and the magnitude of the destabilization is correlated with oligomerization propensity.\n","The activation of muscarinic acetylcholine receptors, PKC and MAP kinase is involved in Hup A-induced alphaAPPs secretion in neuroblastoma cells and suggest multiple pharmacological mechanisms of Hup A regarding the treatment of Alzheimer's disease (AD).\n","Data show that CSF levels of beta-amyloid(1-42) are not significantly different between the brain tumor patients and non-tumor patients.\n","These data implicate Mint3 activity as a critical determinant of post-Golgi APP traffic.\n","Abeta 1-42 induces mild endoplasmic reticulum stress in an aggregation state-dependent manner.\n","Our data indicate that different signalling pathways are involved in retinoic acid-induced up-regulation of the secretases.\n","Abeta-induced and mitochondria-dependent cytotoxic pathways might play an important role in Alzheimer's disease pathogenesis.\n","Exclusion of the native alpha-helix from the amyloid fibrils of a mixerd alpha/beta protein.\n","Data show that in AD patients, cortisol serum levels show a trend of positive correlation with Abeta 1-42 CSF levels.\n","Using transgenic mice expressing human cystatin C (encoded by CST3), study shows that cystatin C binds soluble amyloid-beta peptide and inhibits cerebral amyloid deposition in amyloid-beta precursor protein (APP) transgenic mice.\n","Study shows that overexpression of human cystatin C in brains of APP-transgenic mice reduces cerebral amyloid-beta deposition and that cystatin C binds amyloid-beta and inhibits its fibril formation.\n","Direct titrations of HSA with Abeta40 was monitored using circular dichroism spectroscopy and a dissociation constant (K(d)) of 5+/-1 microM for a HSA complex with Abeta40 was obtained.\n","analysis of protofibril assemblies of the arctic, Dutch, and Flemish mutants of the Alzheimer's Abeta1-40 peptide\n","Beta-amyloid precursor protein (APP) and CCL2 chemokine synergistically enhance aggregated APP clearance by 3 different pathways in mononuclear phagocytes derived from transgenic mouse models of Alzheimer's disease.\n","Duplication of the APP gene is not a common cause of Alzheimer's disease with cerebral angiopathy in Swedish and Finnish populations.\n","This review focuses on the highly regulated process underlying intracellular trafficking of beta-amyloid peptides (Abeta), the disturbance of which directly impacts Abeta production and its critical role in the pathogenesis of Alzheimer's disease.\n","Abeta levels measured by ELISA were comparable to those reported in mouse models, suggesting that substantially greater amounts of soluble Abeta are not required in the rat to generate Abeta deposition.\n","LRP-1/LDLR-mediated uptake of A beta results in degeneration of perivascular cells.\n","molecular-level examination of sequence-specific secondary structures and supramolecular structures of a neurotoxic amyloid intermediate of the 40-residue beta-amyloid (Abeta) peptide involved in Alzheimer's disease\n","While excessive interaction with copper and zinc may induce neocortical Abeta precipitation in AD, soluble Abeta degradation is normally promoted by physiological copper and zinc concentrations.\n","These findings suggest that secreted APP is decreased by membrane GM1 ganglioside binding to its precursor protein and provide a possible molecular mechanism to explain the involvement of GM1 in APP proteolysis and pathogenesis of Alzheimer's disease.\n","Fyn, due in part to its effects on Dab1, regulates the phosphorylation, trafficking, and processing of APP and apoEr2.\n","These results illustrate the regulatory mechanisms by which AICD transcriptional activity might be regulated via covalent conjugation with Nedd8.\n","Amyloid assembly may involve fluctuation between a fast-growing and a blocked state in which the fibril is kinetically trapped because of intrinsic structural feature\n","In fetal brain, protein expression levels of APP was comparable between DS and controls. But APP was significantly increased in adult brain.\n","Membrane fusogenic activity of the Alzheimer's peptide A beta (1-42) demonstrated by small-angle neutron scattering.\n","amyloid precursor protein (APP) ectodomain homophilic interactions are regulated by the loop region and affect beta-secretase cleavage of APP\n","Motor strength was considerably reduced in APP transgenic mice. Neurological impairments showed by APP mice had an early onset and worsened with progressive aging, in parallel to gradual accumulation of Abeta in brain.\n","The atypical clinical phenotype with long prodromal phase, autonomic failure and seizures in this new proband with the APP Thr714Ala mutation illustrates the clinical heterogeneity in families with identical pathogenic mutations.\n","Interaction of APP with toxic Abeta-species promotes toxicity in hippocampal neurons by a mechanism that involves APP-mediated Go protein activation, revealing an Abeta-receptor-like function of APP directly implicated in neuronal degeneration in AD.\n","Here, we demonstrate that deposited Abeta is SDS insoluble in tgAPP-ArcSwe, a transgenic mouse model harboring the Arctic (E693G) and Swedish (KM670/671NL) APP mutations.\n","Cellular localization of Nicastrin affects amyloid beta species production.\n","Amyloidogenic processing but not amyloid precursor protein (APP) intracellular C-terminal domain production requires a precisely oriented APP dimer assembled by transmembrane GXXXG motifs.\n","Comparing the beta2-m fragment with Abeta indicates that while both adopt similar beta-strand-turn-beta-strand motifs, the final amyloid structures can be dramatically different .\n","Synthetically prepared Abeta(1-42) specifically suppresses spontaneous synaptic activity resulting from a reduction of vesicular release at terminals of both gamma-aminobutyric acid GABAergic and glutamatergic synapses.\n","This study reiterates DL-alpha-lipoic acid as a potent free radical scavenger to combat oxidative vulnerability in the treatment for amyloid beta (25-35) toxicity.\n","The dissociation constants are correlated to both the Abeta42/Abeta40 ratio and the mean age of disease onset in AD patients.\n","analysis of the minimal copper- and zinc-binding site sequence in amyloid-beta peptides\n","Intracellular copper deficiency increases amyloid-beta secretion by diverse mechanisms.\n","wild-type or Swedish mutated betaAPP overexpression modulates BACE1 promoter transactivation and activity via an NFkappaB-dependent pathway.\n","SNX17 regulates amyloid precursor protein trafficking and processing in the early endosomes\n","The lowest values of beta amyloid were found in Alzheimer's disease subjects in moderate to severe stages of disease.\n","Findings indicate Amyloid beta protein is associated with cognitive function, body fat and physical fitness in neurologically healthy older adults\n","Results describe the effect of high cholesterol incorporated into human neuroblastoma cells in Abeta-mediated neurotoxicity and the role of reactive oxygen species (ROS) generation.\n","The effects of (1-40)betaA and (25-35)betaA peptides on human amylin (hA)-mediated cell death and [(125)I-Tyr(37)]hA precipitation, was investigated.\n","A novel amyloid protein precursor mutation (Glu693Delta)-producing variant in Japanese pedigrees has been suggested as a cause of Alzheimer's-type dementia because of enhanced formation of synaptotoxic amyloid beta oligomers rather than amyloid fibrils.\n","compare the pathogenicity of human Abeta42 mutants with differing tendencies to aggregate in the Drosophila brain\n","Promotion of amyloid beta protein misfolding and fibrillogenesis by a lipid oxidation product.\n","Abeta and tau pathology are consistent with a model in which both synaptic loss and dysfunction are linked to a synaptic amyloid cascade within the synaptic compartment.\n","overexpression of mutant (APPswe) or wild-type APP in transgenic mice is necessary and sufficient for hypertrophy of cortical neurons: suggests that the lack of neuronal loss in Alzheimer disease models may be attributed to overexpression of APP\n","The amyloid beta peptide pattern in cerebrospinal fluid is able to predict Alzheimer's disease in patients with mild cognitive impairment with a sensitivity of 91% and specificity of 64%.\n","We are the first to demonstrate the distribution of Abeta in human platelets and that Abeta activation of platelets is mediated, at least partially, by the PLCgamma2-PKC pathway, and Abeta triggers thrombus formation in vivo.\n","Data show that a presenilin-1 280Glu-->Ala mutation alters C-terminal amyloid precursor protein processing, yielding longer amyloid beta peptides, and discuss the implications for Alzheimer's disease.\n","Data show that the E280A mutation in presenilin 1 is not associated with increased production of amyloid-beta in non-neuronal peripheral tissues, which is in contrast to the expectation in a gamma-secretase gain of function.\n","Review gives further evidence for a pivotal role of intraneuronal Abeta accumulation as a main pathological trigger in transgenic mouse models of Alzheimer's disease.\n","In this review, Abeta oligomers induce a reduction of postsynaptic density protein 95 (PSD-95) and NMDA glutamate receptors in cultured rat hippocampal neurons.\n","In a model of Alzheimer's disease, mitochondrial dysfunction is exacerbated by the presence of soluble Abeta species from transgenic mice as a very early event during pathogenesis.\n","Recent studies in this review suggest that pathological alterations of APP processing in Alzheimer's disease may prevent neuronal differentiation of human neural progenitor cells.\n","Androgen regulation of Abeta involves an androgen receptor-dependent mechanism requiring up-regulation of the Abeta catabolizing enzyme neprilysin.\n","co-occurrence of pathology typical of sCJD & AD & inverse association between Abeta & PrP(Sc) in a subgroup of sCJD patients is indicative of common pathways involved in generation or clearance of Abeta & PrP(Sc) in a subgroup of sCJD patients\n","Abeta-peptide in its homogeneous globular A beta-oligomer (Abeta-globulomer) conformation is a structural entity which is independent from amyloid fibril formation.\n","identifies SNX33 as a new endocytic protein, which modulates amyloid precursor protein endocytosis and APP alpha-secretase cleavage, and demonstrates that the rate of APP endocytosis is a major control factor for APP alpha-secretase cleavage\n","The posterior cingulate is preferentially vulnerable to both effects of transgene in the PDAPP mouse, and both are independent of amyloid deposition.\n","The last 37 residues of LRP cytoplasmic tail (LRP-C37) lacking the NPxY motifs and FE65 binding mediate the core pro-amyloidogenic activity of soluble cytoplasmic tail of LRP (LRP-ST).\n","BACE and APP come into close proximity within the cell, but probably not on the cell surface.\n","The tendency for a higher prevalence of headaches held for different PSEN1 and APP mutations but was not significant unless all families were combined.\n","describe the purification and identification of six proteins that bind to the 52sce in the 3'-UTR of APP mRNA; findings suggest a novel mechanism for post-transcriptional regulation of APP mRNA\n","Transglutaminase induces protofibril-like amyloid beta-protein assemblies that are protease-resistant and inhibit long-term potentiation\n","Abeta(1-42)-induced accumulation of C-terminal fragment of the death-inducing p75(NTR) resulted from inhibition of gamma-secretase activity. (Beta-amyloid(1-42)).\n","We found that the older control group had lower Abeta1-42 and higher (p)tau compared to the younger control group. This suggests that older individuals may have Alzheimer's disease pathology, even in the absence of objective cognitive impairment.\n","the altered calcium signaling of APPswe transgenic neurons was unlikely to be due to modulation of the NMDA or nicotinic neurotransmitter systems, and did not depend on secreted APP derivates\n","TMP21 behaves as a regulator of gamma- but not epsilon-cleavages of beta-amyloid precursor protein generated by presenilin-dependent gamma-secretase complex.\n","The E22Q mutation increases aggregation rates of the 15-28 fragment by lowering the barrier for Abeta monomer deposition onto a fibril.\n","the catalytic domain of insulin-degrading enzyme forms a denaturant-resistant complex with amyloid beta peptide\n","Affected and nonaffected carriers of the Arctic APP mutation from the Swedish and American families were investigated clinically.\n","Positron emission tomography with 11C-PiB and magnetic resonance imaging were performed for 2 patients, 49-year-old and 60-year-old siblings with APP locus duplication, with hereditary Alzheimer disease and cerebral amyloid angiopathy.\n","These results suggest that HS codeposits with Abeta40 in neuritic plaques and is mainly derived from glial cells.\n","beta-sheet architecture underlies in vitro and in vivo beta2-microglobulin amyloid fibrils\n","Abeta42 and Abeta38 species can be independently generated by gamma-secretase and there is probably not a precursor-product relationship between these peptides\n","ER stress-induced homocysteine toxicity may play an important physiological role in enhancing the pathogenesis of Abeta-induced neuronal degeneration\n","I213T mutant presenilin-1/gamma-secretase in cell models and knock-in mouse brains: familial Alzheimer disease-linked mutation impairs gamma-site cleavage of amyloid precursor protein C-terminal fragment beta\n","GM-CSF operates downstream of CD40/CD40L interaction and that GM-CSF modulates Abeta production by influencing APP trafficking\n","PSEN1 and APP gene mutations may not be uncommon in Korean patients with early-onset Alzheimer's disease\n","the expressions of Swedish double mutation of amyloid precursor protein (Swe-APP)increased mRNA and protein levels of cyclin D1 and cyclin B1\n","the alpha-helical membrane-bound human islet amyloid polypeptide has a role in membrane-mediated misfolding\n","CD147 expression influences Abeta levels by an indirect mechanism involving MMPs that can degrade extracellular Abeta.\n","results suggest that in cognitively healthy elderly subjects, biochemical changes in CSF tau and Abeta42 have an effect on cerebral function; CSF biomarkers and EEG theta activity might indicate early abnormal degenerative changes in the brain\n","rodent and human Abeta are effective in modulating K currents\n","AIP-1 mutant lacking the predicted farnesylation site failed to protect against Abeta toxicity.\n","Thyroid cancers are characterized by APP upregulation, increased membrane targeting of the APP ectodomain and significantly increased mRNA levels of the APP scaffold proteins JIP1, ShcA and Fe65.\n","A three-dimensional structure of a mature amyloid fibril formed by Abeta(1-40) peptide, determined by electron cryomicroscopy at approximately 8-A resolution, was presented.\n","Data suggest a possible role for APP and/or amyloid-beta in the development of obesity-related insulin resistance and adipose tissue inflammation.\n","The results of this study demonstrate that the D664A mutation either completely precludes, or markedly delays (beyond 13 mo) the appearance of AD-like deficits in this mouse model of AD.\n","results show that CSF biomarkers are better predictors of progression to Alzheimer's disease than plasma Abeta isoforms\n","Abeta pathology is regulated by beclin 1 through a pathway that involves autophagy\n","beclin 1 deficiency disrupts neuronal autophagy, modulates APP metabolism, and promotes neurodegeneration\n","Beta-amyloid peptide stimulates endozepine release from rat astrocytes through an N-formyl peptide receptor positively coupled to protein kinase A and protein kinase C.\n","This is the first report, evidencing the presence of changes in eating and drinking behavior in a single transgenic Alzheimer mouse model.\n","Our findings indicate that hippocampal and DLS dendritic spines in hAPPswe mutants undergo a different pattern of morphological changes over time and point to minor alterations in the microanatomy of DLS spines.\n","These studies suggest that glioma and glioblastoma exhibit robust upregulation of proinflammatory and neurodegenerative genetic markers beta-amyloid precursor protein.\n","familial Alzheimer's disease mutations in the polypeptide backbone of APP can affect processing of the attached N-glycans; however, whether these changes in N-glycosylation affect Abeta production remains to be established\n","combinations of the cube copying test with MMSE, rCBF and CSF A beta (42) measurements can identify subgroups of MCI subjects with either substantially reduced or increased risk for future development of Alzheimer's disease\n","In patients with Alzheimer disease, low plasma levels of Abeta40 and Abeta42 are associated with a significantly more rapid cognitive decline than are high levels in patients with Alzheimer disease, using the Blessed Dementia Scale.\n","Data show that Alzheimer's disease patients have ower Abeta1-42 levels.\n","An increase in APP intracellular domain generation does not directly promote gene activation of previously proposed target genes.\n","Amyloid-beta protein dimers impair synaptic plasticity and memory\n","APPs-alpha regulates the function of APP in neurite outgrowth via the novel mechanism of competing with the binding of APP to Itgbeta1\n","amyloid-beta rise and gamma-secretase inhibitor potency depend on the level of substrate expression\n","Abeta was found to be associated with plasma lipoproteins, especially those enriched with triglyceride; Abeta may be increased in normolipidaemic Alzheimer's disease subjects, commensurate with possible disturbances in postprandial lipoprotein homeostasis\n","Study determined that the CALHM1 P86L polymorphism is associated with Alzheimer's disease, further found that the P86L polymorphism increases abeta levels by interfering with CALHM1-mediated Ca(2+) permeability.\n","Data show that increased Abeta42 levels and an elevated Abeta42/Abeta40 ratio in neurons from sporadic as well as from familial cases of Alzheimer's disease, whereas Abeta40 levels remain unchanged between the cases and controls.\n","the 24-28 bend motif is retained in all E22 mutants, suggesting that mutations involving residue E22 may not affect the structure of the folding nucleation site of Abeta\n","Numb endocytic adapter proteins regulate the transport and processing of the amyloid precursor protein in an isoform-dependent manner and have roles in Alzheimer disease pathogenesis\n","structure of the high-affinity Cu(2+) binding site is consistent with the hypothesis that the redox activity of the metal ion bound to Abeta can lead to the formation of dityrosine-linked dimers found in AD\n","Hence, the experimental model demonstrates that a prion infection of the CNS promotes selectively formation of FA-extractable Abeta(1-42) in Tg2576 mice.\n","Lysines 587 and 595 of APP, which are immediately adjacent to the site of beta-secretase cleavage, are covalently modified by SUMO proteins in vivo.\n","simultaneous presence of human mutated Tau(VLW) and plaque-amyloid (and/or APP(SW)) potentiates and anticipates tau phosphorylation at the 12E8 epitope, intensifying pyramidal neuron immunostaining and tau filament formation in this alzheimer's model\n","APP may serve as a cellular cholesterol sensor that is linked to mechanisms for suppressing cellular cholesterol uptake.\n","The intracellular domain of amyloid precursor protein can induce neuron-specific apoptosis.\n","study found strong positive correlation between changes in brain interstitial fluid Abeta concentrations & neurological status of acute brain injury patients, with Abeta increasing as neurological status improved & falling as neurological status declined\n","The central core sequence of Abeta peptide associated with Alzheimer's disease, Abeta(16-22), is developed as an experimental system in order to evaluate amino acid cross-strand pairing interactions in protein beta-structural assembly and stability.\n","The age-related elevation of oxidative damage was observed in human mutant APP mice brain compared to that of wild-type mice brain.\n","Pathological accumulation of amyloid-beta protein and hyperphosphorylation of tau develop concomitantly within synaptic terminals of Swedish mutant transgenic mice.\n","Intracellular Ass accumulation is an early pathological alteration contributing to cell death in Alzheimer's disease.\n","High calcineurin (CaN) activity, and consequently CaN-dependent memory deficits, could be a downstream effect of the presence of prefibrillar Abeta species in the central nervous system of APP transgenic mice.\n","APPrearranges to form a micelle-bound structure with alpha-helical segments with additions of SDS or lithium dodecyl sulfate\n","Accumulation of beta-amyloid and episodic memory deficits which increase with age are not accompanied by an alteration in synaptic transmission or sustained long term potentiation in APPswe/presenilin-1deltaE9-deleted transgenic mice.\n","Beta-amyloid may contribute selectively to cognitive impairment of Lewy body disease and may contribute to timing of dementia relative to motor signs of parkinsonism.\n","Alzheimer's-associated single nucleotide polymorphisms show a change in secreted amyloid beta consistent with the CSF phenotype and known Alzheimer's disease variants.\n","polyphenols have an effect on amyloid beta-protein self-assembly and cytotoxicity\n","Physiological concentrations of Ass peptides can regulate the release of glutamate by acting on glutamatergic terminals in adult rat brain slices.\n","analysis of how sulfated polysaccharides promote the assembly of amyloid beta(1-42) peptide into stable fibrils of reduced cytotoxicity\n","Study determined the crystal structure of the carboxy-terminal APP intracellular domain in complex with the C-terminal phosphotyrosine-binding (PTB) domain of Fe65; The unique interface involves the NPxY PTB-binding motif and two alpha helices.\n","study demonstrated that Abeta(1-40), levels of sCD40 and sCD40L are increased in Alzheimer's disease and declining MMSE scores correlated with increasing sCD40L, which in turn, correlated positively with Abeta(1-42)\n","the association between intraneuronal Abeta and reduced brain volumes\n","Data show that the pathological deposits with antibodies against amyloid-beta protein has involved in the neuropathogenesis of the amyotrophic lateral sclerosis/parkinsonism-dementia complex of Guam.\n","thioflavin T and its neutral analog BTA-1 bind to protofibrils of the Alzheimer's disease Abeta(16-22) peptide\n","These results suggest that phosphorylation of APP at Tyr687 regulates APP processing by alpha- and gamma-secretases, determining the expression level of APP intracellular domain.\n","Dexras1 functions as a suppressor of FE65-APP-mediated transcription, and FE65 tyrosine 547 phosphorylation enhances FE65-APP-mediated transcription, at least in part, by modulating the interaction between FE65 and Dexras1\n","Microdomain switching is a mechanism of cholesterol- and activity-dependent regulation of APP processing in neurons.\n","rapid LRP1-dependent internalization of A beta occurs under the blood-brain barrier-specific cellular context\n","Data show that valproic acid decreased amyloid beta production by inhibiting GSK-3beta-mediated gamma-secretase cleavage of amyloid protein precursor both in vitro and in vivo.\n","Data show a significant positive correlation between beta-amyloid burden and progranulin in the medial temporal lobe in dementia with Lewy bodies.\n","analysis of amyloid beta peptide hydrolyzing activity of nonphysiological immunoglobulin variable domain scaffolds\n","Data show that transient intraneuronal A beta correlates with neuron loss in the frontal cortex of APP/PS1KI mice.\n","p120 catenin is a unique positive regulator of the gamma-secretase processing of cadherins and a negative regulator of the amyloid precursor protein processing\n","study describes a full structural model for amyloid fibrils formed by the 40-residue beta-amyloid peptide associated with Alzheimer's disease (Abeta(1-40)), based on numerous constraints from solid state NMR and electron microscopy\n","S-palmitoylation plays a role in stability and raft localization of nicastrin and APH-1, but does not directly modulate gamma-secretase processing of APP and other substrates.\n","intralysosomal content affects the rate of apoptosis in mutant cell lines\n","APP, through amyloid beta production, causes an imbalance of mitochondrial fission/fusion that results in mitochondrial fragmentation and abnormal distribution, which contributes to mitochondrial and neuronal dysfunction\n","Our results suggest that impaired cell adhesion and migration induced by abnormal cleavage of APP could contribute to the pathological effects in FAD brain.\n","chromatin immunoprecipitation analysis also reveals AICD binding to the neprilysin promoter in rat primary neurons but not in HUVEC cells\n","Data support the hypothesis that APP is involved in mediating increased vascular adhesion and extravasation of immune cells but also may mediate a phenotypic change in endothelial cells leading to vascular dysfunction.\n","findings show that primary astrocytes derived from different sources can bind and internalize A beta1-42, and fetal astrocytes were more efficient in A beta1-42 uptake than adult astrocytes\n","post-translational S-palmitoylation of BACE1 is not required for APP processing, and that BACE1 can efficiently cleave APP in both raft and non-raft microdomains.\n","Abeta induces the formation of cross-linked AT2 oligomers that contribute to the dysfunction of Galphaq/11 in an animal model of Alzheimer disease.\n","Data describe the identification of three specific O-glycosylation sites of the human secreted amyloid precursor protein APP695, using a combination of high-performance liquid chromatography and electrospray-tandem mass spectrometry.\n","The amyloid-beta protein precursor/ nitric oxide synthase 2 inducible bigenic mice progress from production and amyloid deposition to hyperphosphorylated normal mouse tau at Alzheimer's disease associated epitopes--REVIEW\n","APP gene polymorphisms at codon 718 (I>L), 720 (L>S), and 710 (V>G) can be found in certain Chinese/Taiwanese patients with Alzheimer's disease.\n","These data demonstrate that a specific oligomeric Abeta(1-42) aggregation species can potently initiate the THP-1 monocyte maturation process.\n","in mice overexpressing wild-type human APP we found an early memory impairment, particularly in the water maze and to a lesser extent in the object recognition task, but beta-amyloid peptide was barely detectable in the hippocampus\n","The increased prevalence of alpha-synuclein and beta-amyloid in the brains of older HIV-infected individuals may predict an increased risk of developing neurodegenerative disease.\n","These data suggest that DNM2 expression is reduced in late-onset Alzheimer's disease , which results in the accumulation of APP in lipid raft-rich plasma membranes.\n","Coexpression of APP with APLP1 or APLP2 leads to diminished generation of Abeta42\n","in conclusion, in patients with Alzheimer disease, macrophages appear to shuttle Abeta from neurons to vessels where their apoptosis may release fibrillar Abeta, contributing to cerebral amyloid angiopathy\n","Beta-amyloid specifically interrupts the PDK-dependent activation of Akt.\n","DIF-1 decreases the ratio of Abeta42 to Abeta40 & diminishes APP phosphorylation at Thr668. It affects G0/G1-associated amyloidogenic processing of APP by a gamma-secretase-, proteasome- & calpain-insensitive pathway, requiring residue Thr668. T668.\n","Sequence deletion and Abeta oligomers produced exhibit toxicity in the extracellular space and within the cells themselves\n","study concludes that Abeta can modulate the cellular expression of agrin and glypican-1, which may contribute to the accumulation of these heparan sulfate proteoglycans in Alzheimer's disease lesions\n","findings show JNK plays a key role in phosphorylation of APP-T668 in a model of Alzheimer's disease; results suggest important link between APP metabolism & the JNK pathway & contribute to shed light on the molecular signalling pathway of this disease\n","These results suggest that IGF-1 promotes Abeta production through a secretase-independent mechanism involving APP phosphorylation.\n","Mutant human APP expression exacerbated degenerative changes of deprived barrel neurons. Degradation of apical arbors was pronounced, demonstrating opposite effects of wild-type and mutated human APP on deprivation-induced dendritic restructuring.\n","O-mannosylation is required for the solubilization of exogenously expressed human APP.\n","Data show rating the regional distribution of amyloid-beta protein, i.e. the phase of Abeta as a diagnostic tool while analyzing subjects with suspected Alzheimer's disease.\n","data demonstrate the role amyloid precursor protein (APP) has in glial differentiation of NT2 cells through MCP-1(MCP-1)/MCP-1-induced protein (MCPIP) signaling\n","An oAbeta-specific ELISA reveals a tight link between oAbeta and Abeta(42) monomer levels in plasma and brain. Both forms can decline over time in plasma, presumably reflecting their increasing insolubility in the brain.\n","The NMR data indicate that these soluble forms have a mixed parallel and antiparallel beta-sheet structure that is different from fibrils which contain only parallel beta-sheets.\n","Amino acid substitution in ABPP inhibits parenchymal amyloidosis but exacerbates vascular amyloid, explaining the destribution of amyloid in amyloidosis.\n","Amyloid-beta and Tau affected aging-prone astrocyte cell death, metabolism and cytoskeleton.\n","These data show that senile plaques are a potential reservoir of oligomeric Abeta, which colocalizes with the postsynaptic density and is associated with spine collapse.\n","human APP gene plays role in synaptogenesis in transgenic lines of Drosophila melanogaster whose nerve cells express the human APP695 isoform, truncated APPs, and the presynaptic marker synaptotagmin driving the sequence of the green fluorescent protein.\n","the cellular prion protein (PrP(C)) is an amyloid-beta-oligomer receptor\n","Overexpression of RanBP9 resulted in the enhancement of APP interactions with LRP and BACE1 and increased lipid raft association of APP.\n","The C terminus of Abeta forms the inside wall of the hollow core, which is supported by partial proteolysis analysis.\n","The pervasive, age-related structural changes between wild and transgenic mice (and mouse and human) suggest subtle but fundamental species differences and Alzheimer transgene effects\n","Data show that in sporadic inclusion-body myositis muscle fibers, Abeta42 is accumulated more than Abeta40.\n","Data show that I716F and V717I APP mutations increase the proportion of interacting molecules earlier in the secretory pathway, resulting in an increase in amyloid beta generation.\n","Dysmorphic findings in two cases involving ABETA are reported.\n","study found an APP mutation (A673V)] that causes disease only in the homozygous state; heterozygous carriers were unaffected; A673V mutation affected APP processing, resulting in enhanced beta-amyloid production & formation of amyloid fibrils in vitro\n","Fibrillar Abeta protein is identified as a pathogenic entity powerfully altering neuronal membrane properties such that hyperexcitability of pyramidal cells culminates in epileptiform activity.\n","signaling effectors, other than the NMDA receptor, may be responsible for resistance of theta burst-induced long term potential to amyloid beta 42 dependent inhibition\n","c-Abl modulates APP intracellular domain dependent cellular responses: transcriptional induction and apoptosis.\n","Cu(2+) reduction activity of APP facilitates copper uptake and may represent an early step in cellular copper homeostasis.\n","it is not the Abeta(40)-Cu(I)/Fe(II) complex per se that is responsible for the oxidative damage in Alzheimer's disease\n","This study demonstrated that the Arctic APP mutation is sufficient to cause amyloid deposition and cognitive dysfunction.\n","Cu(2+) affinity for Abeta of 10(11) M(-1) supports a modified amyloid cascade hypothesis in which Cu(2+) is central to Abeta neurotoxicity\n","study found nitric oxide produced in response to beta-amyloid protein triggered mitochondrial fission & neuronal damage, in part by S-nitrosylation of drp1; SNO-Drp1 is increased in Alzheimer disease patients brains\n","findings suggest that fibrillar Abeta burden in cognitively normal older people is associated with APOE epsilon4 gene dose, the major genetic risk factor for Alzheimer's disease\n","Novel beta-sheet stuctures are reported for fibrils formed from D23N-Abeta40 peptides (Iowa mutation).\n","The results of the present study indicate that intracellular Abeta and C99 aggregates induce mitochondria-dependent apoptotic cell death via elevation of Bax levels as a result of proteasome inhibition in a cell type-specific manner.\n","This study identified three affected subjects with the AbetaPP A713T mutation in southern Italy.\n","BRI3 inhibits the various processing of amyloid protein precursor by blocking the access of alpha- and beta-secretases.\n","Reduction of endogenous amyloid precursor protein expression increases the frequency and reduces the amplitude of calcium oscillations in a cortical neuronal network.\n","REVIEW: role of APP in neuronal trafficking associated with Alzheimer disease\n","APP functions as a novel regulator of osteoblast activity\n","Amyloid beta protein up-regulates CC-type chemokine receptor 5 (CCR5) expression and promotes T cell transendothelial migration via receptor for advanced glycation end products (RAGE) on brain endothelial cells.\n","S655 phosphorylation is a signal that positively modulates APP secretory traffic\n","using the APP/PS1KI mouse model for Alzheimer's disease, we provide evidence that a variety of different Abeta peptides accumulate intra- and extracellularly in the critical period between 2 and 6 months of age\n","dysfunctions of brain insulin and IGF-1 receptors contribute to Abeta aggregation and subsequent synaptic loss\n","The charge group of the carboxy terminus makes a large contribution to the interactions and thus appears to have a critical role in determining the registry.\n","Using an ELISA assay detecting Abeta-IgM complexes, we observed that high levels of Abeta-IgMs were detectable in HC and MCI patients; however, there was no significant difference to the AD group.\n","characterization of disordered and ordered aggregates populated during the process of amyloid fibril formation\n","Data suggest that CD40/CD40L interaction modulates amyloid protein precursor processing independently of TRAF signaling.\n","beta-sheets were the most abundant structures in amyloid beta-peptide.\n","JNK and p38MAPK inhibition prevented both Abeta 1-40-mediated down-regulation of occludin and the increase in paracellular permeability in hCMEC/D3 cells.\n","RNA interference-mediated knockdown of AP180 reduces the generation of Abeta1-40 and Abeta1-42, whereas CALM knockdown has no effect on Abeta generation.\n","study demonstrates familial Alzheimer disease mutation of APP is associated with loss of its synaptotrophic activity; suggests not only \"too much Abeta\" but also \"too less functional intact APP\" may be relevant for synaptic pathology & degeneration in AD\n","Abeta peptide (1-43) is a longer peptide than Abeta40, therefore Abeta43 polymerizes rapidly; the Abeta43 variant may be of importance for Alheimer's disease.\n","Our results suggest that mild membrane cholesterol reduction impacts the cleavage of APP upstream of gamma-secretase and appears to be mediated by changes in APP trafficking and partitioning into lipid rafts.\n","While the exact role of the patient-specific miRNA variants within the 3' UTR region of APP and BACE1 demands further analyses, this study does not support a major contribution of miRNA genetic variability to AD pathogenesis\n","Intracellular amyloid beta directly interacts with SOD1, and that this interaction decreases the enzymatic activity of the enzyme.\n","Parkin promotes ubiquitination and proteasomal degradation of intracellular Abeta42.\n","Data suggest that Tfam overexpression protects mitochondria against Abeta-induced oxidative damage in SH-SY5Y cells.\n","a functional role of GSK-3beta in amyloid-beta precursor protein processing, further implicating this kinase in the amyloid-beta-dependent pathogenesis\n","Amyloid beta peptides trigger CD47-dependent mast cell secretory and phagocytic responses.\n","These findings demonstrate that Reelin interacts with APP, potentially having important effects on neurite development.\n","REVIEW: intracellular pathways triggered by Abeta, which involve membrane receptors such as nicotinic-R, NMDA-R, integrins, TNF-R1, RAGE, FPRL and p75NTR and their intracellular mediators such as GSK3, PKC, PI3K, Akt, FAK, MAPK family, Src family and cdk5\n","The increased Abeta42 oligomer ratio for Alzheimer's disease and mild cognitive impairment indicates the presence of oligomers in CSF and that the lowering of natively measured Abeta42 is caused by oligomerization.\n","copper modulates flotillin-2 association with cholesterol-rich lipid raft domains, and consequently Abeta synthesis is attenuated via copper-mediated inhibition of APP endocytosis\n","somatostatin decreases in Alzheimer's disease and its expression may be linked with Abeta deposition\n","Tyr(1)-substituted homologues of Abeta40 and Abeta42 assembled the slowest and yielded unusual patterns of oligomer.\n","we biophysically characterized different variants of the Abeta12-28 fragment to determine the relevance for aggregation and toxicity of residue 22 of the Abet peptide, which suggests that it is crucial for the aggregation profile of the peptide\n","The investigated AbetaPP as well as PS mutations were associated with an overall reduction of Abeta species, except for Abeta(10-40).\n","The data demonstrate that VEGF may affect APP processing, at least in vitro, suggesting a role of VEGF in the pathogenesis of Alzheimer's disease.\n","APP dimerization can directly affect gamma-secretase processing and dimerization is not required for Abeta production\n","Amyloid beta protein (Abeta) possesses multiple binding sites toward iron. Abeta is capable of binding ferric iron [Fe(III)] in the presence of nitrilotriacetic acid, forming a ternary complex with a 1:1:1 stoichiometry.\n","Studies indicate that a mutated variant protein or precursor protein including amyloid beta peptide, cystatin C, prion protein, transthyretin and gelsolin is abnormally metabolized and accumulates as amyloid.\n","Amyloid-beta-peptide binding to mitochondrial Abeta-binding alcohol dehydrogenase (ABAD) enzyme triggers a series of events leading to mitochondrial dysfunction characteristic of Alzheimer's disease.\n","study shows synaptic activity reduces intraneuronal beta-amyloid (Abeta), protects against Abeta-related synaptic alterations, & promotes transport of the APP to synapses, & that the protease neprilysin is involved in reduction of intraneuronal Abeta\n","Multiple assembly forms of Abeta are present throughout the life of the J20 transgenic mouse line and highlight the difficulty in attributing synaptotoxicity to a single Abeta species.\n","Data show that knock down of APP in zebrafish results in fish with reduced body length and a short, curly tail, and that wild-type human APP rescues the morphant phenotype, but the Swedish mutant APP, which causes familial AD (fAD), does not.\n","the repeat domain of the melanosome fibril protein Pmel17 forms the amyloid core promoting melanin synthesis\n","The results of this pilot study suggest that increased circulating plasma levels of Abeta peptides in obesity may be due to increased adipocyte APP gene expression.\n","Studies indicate that RAGE is subject to ectodomain shedding by ADAM10 and MMP9 and the derived sRAGE can sequester Abeta for systemic clearance and antagonize Abeta binding to cell surface RAGE.\n","These findings suggest both that DMT1 plays a critical role in ion-mediated neuropathogenesis in Alzheimer's disease (AD) and that pharmacological blockage of DMT1 may provide novel therapeutic strategies against AD.\n","amyloid beta protein is degraded by purified myelin basic protein\n","Plasma beta-amyloid(1-40) levels are independently associated with the diffuse-SVD subtype. These results are consistent with the pathophysiological role of fraction Abeta(1-40) in disrupting endothelial vascular function.\n","MPL histograms extracted from TB-TEM images show Ab40 fibrils, fit to four peaks at 8.2, 20.1, 27.7, and 34.9 kDa/nm, with 6.4, 6.3, 6.4, and 5.8 kDa/nm FWHM, respectively.\n","the TMP21 transmembrane domain promotes its association with the presenilin complex that results in decreased gamma-cleavage activity\n","A molecular mechanism for the formation of a DOR/secretase complex that regulates the specificity of secretase for Abeta production.\n","This study suggested that overexpression of hAPP suppresses the phenotypic shift toward neuronal differentiation under conditions of enriched environment. In summary, the results reveal a dual effect of APP on adult hippocampal neurogenesis.\n","Our findings provide new insight into the mechanisms of gamma-secretase-mediated APP processing and may contribute to the development of methods of prevention and treatment of Alzheimer's disease aimed at modulating gamma-secretase activity.\n","the level of insoluble Abeta, but neither oligomeric nor soluble Abeta, was associated with Braak stage, CAA severity and APOEepsilon4 frequency, raising questions as to the role of soluble and oligomeric Abeta in the progression of Alzheimer's disease\n","The consequences of amyloid precursor protein and amyloid-beta peptide accumulation in mitochondria and their involvement in Alzheimer disease pathogenesis, is discussed.\n","The expression of amyloid precursor protein in human HEK293 cells potently promotes synaptogenesis in contacting axons.\n","A fragment of the scaffolding protein RanBP9 is increased in Alzheimer's disease brains and strongly potentiates amyloid-beta peptide generation.\n","Abeta derived diffusible ligands are able to contribute to in vivo plaque formation in a peptide-specific manner\n","X11beta-mediated reduction in cerebral Abeta is associated with cognition and long-term potentiation in Alzheimer's disease APPswe transgenic mice.\n","Abeta42 was a stronger predictor of progression to Alzheimer's disease in APOE epsilon4 non-carriers than in carriers.\n","this study provides an additional possible mechanism of neurotoxicity in Alzheimer's disease, the induction of p17(FAM72B), through which Abeta acts to induce apoptosis and exhibit other Alzheimer's disease characteristics.\n","characterization of patient-derived, toxic, high mass amyloid beta-protein (Abeta) assembly from Alzheimer disease brains\n","Hsp90 modulates intermediate steps of amyloid assembly of the Parkinson-related protein alpha-synuclein.\n","APP is expressed at high levels in advanced-stage melanomas, and that the cells cleave APP and secrete sAPP\n","Structural analyses of variant Abeta peptides showed that apoptosis preceded fibril formation, correlating with the presence of oligomers and/or protofibrils in brain microvascular endothelial and smooth muscle cells in cerebral amyloid angiopathy.\n","Amyloidogenic cleavage, despite representing the minor cleavage pathway of APP, is predominantly responsible for APP intracellular domain-mediated nuclear signaling.\n","upregulation of GnT-III in AD brains may represent an adaptive response to protect them from additional beta-amyloid production\n","brain interstitial fluid Abeta correlated with wakefulness; Abeta increased during sleep deprivation & orexin infusion but decreased with orexin receptor antagonist infusion; sleep-wake cycle & orexin may play a role in pathogenesis of Alzheimer's disease\n","analysed opposing model structures and examined the necessary structural elements within the amyloid core structure, as well as producing idealised models to test the limits of the core conformation\n","It is therefore possible to speculate that the mechanism by which Abeta(42) interacts with tau in the pathogenesis of Alzheimer's disease is by down-regulating endogenous wnt signalling\n","amyloid precursor protein, but not tau, has a role in neuronal accumulation of amyloid peptides\n","Fibril fragmentation enhances amyloid cytotoxicity\n","These results indicate that naturally secreted Abeta induces neuronal injury/death by activating an apoptotic pathway involving impaired mitochondria function and cellular homeostasis.\n","This study suggested that the partial or total deficit of parkin triggers the compensatory overexpression of multiple mechanisms of cell protection, which reduce the pathology in human mutant APPswe mice\n","Beta-amyloid peptide acts as an antagonist of vascular endothelial growth factor receptor 2 (VEGFR-2) signaling, by a mechanism that explains the anti-angiogenic activity of Abeta peptides.\n","data suggests that peptides starting with position 1 of Abeta are N-truncated as Alzheimer's disease progresses and that Abeta(pE3) positive plaques are resistant to age-dependent degradation likely due to their high stability and propensity to aggregate\n","Findings reveal that RAP is a novel Abeta-binding protein that promotes cellular internalization of Abeta.\n","Alterations in the levels of amyloid protein precursor intracellular domain contribute to network dysfunction in Alzheimer's disease and transgenic model mice.\n","APP-presenilin 1 mutations enhance Abeta and disrupt basal excitability via divalent calcium (Ca2+)-dependent enhancement of afterhyperdepolarization, suggesting disruption of a learning-related Alzheimer's disease model of intrinsic excitability.\n","find APP intracellular domain levels to be elevated in brains from Alzheimer's disease patients.\n","possibility that amyloid-beta is secreted by enterocytes as an apolipoprotein component of chylomicrons. However, secretion of amyloid-beta appears to be independent of chylomicron biogenesis\n","Results indicate that for the discrimination of AD from ND control subjects, measurement of a set of markers including Abeta1-42, ApoA1 and HPX improved diagnostic performance over that obtained by measurement of Abeta1-42 alone.\n","Human serum albumin inhibits Abeta fibrillization through a \"monomer-competitor\" mechanism\n","Estrogen stimulates degradation of beta-amyloid peptide by up-regulating neprilysin.\n","Data indicate that RAGE contributes to mechanisms involved in the translocation of amyloid beta from the extracellular to the intracellular space, thereby enhancing Abeta cytotoxicity.\n","analysis of aptamers that did not recognize Abeta40 oligomers but reacted with fibrils of Abeta40, Abeta42, and several other amyloidogenic protein\n","CuII coordination to ABETA in the presence of equilibria between different ligands observed at pH 6.6\n","We review studies of Abeta deposition imaging in Alzheimer's Disease, Mild Cognitive Impairment, and normal adults, its cognitive consequences, and the role of genetic risk and cognitive reserve.\n","similar to other pore-forming neurotoxins, A beta induced a rapid increase in intracellular calcium and miniature currents, indicating an enhancement in vesicular transmitter release\n","Cross-linking efficiency varies with the amyloid beta(1-42) species and the cross-linking agent, each of which is highly specific to certain residues and prescribes a well-defined set of potential cross-links in Abeta(1-42) fibrils.\n","Data indicate a low complement expression in mice from the C3 component onwards, and show that starting at C5 the mRNAs did not increase in response to amyloid deposition, which is in contrast to human brain.\n","MPEP reduces seizure severity in Fmr-1 KO mice over expressing human Abeta.\n","Processing by mesotrypsin may ablate the protease inhibitory function of APP/protease nexin 2 in vivo and may also modulate other activities of APP/protease nexin 2 that involve the Kunitz domain.\n","Abeta alone does not cause neurodegeneration but induces toxicity through phosphorylation of wild-type tau in an NMDA receptor-dependent pathway.\n","Endothelial APP regulates immune cell adhesion and stimulates a tyrosine kinase-dependent response driving acquisition of a reactive endothelial phenotype.\n","allosteric changes in PS1 conformation underlie changes in the Abeta(42/40) ratio\n","Data indicate that oxidants, such as hydrogen peroxide, are not necessary for oxidation of beta-amyloid copper ion complexes, and understanding these processes could be pivotal for the development of therapeutic treatments.\n","These data provide mechanistic insight into how disruptions in lipid metabolism can determine neuronal response to accumulating oligomeric amyloid-beta(42).\n","pathologic features of Alzheimer's disease are exaggerated in the brain of APP transgenic mice that have concurrent insulin-deficient diabetes, and underscore a possible mechanism of brain dysfunction common to AD and diabetes\n","Only after extensive Abeta deposition has been present for longer periods of time does Abeta become the driving force for decreased metabolism in clinical AD and, only in more vulnerable brain regions such as parietal and precuneus cortices.\n","Results describe the temporal profile for amyloid precursor protein, amyloid-beta and tau expression in primary cortical cultures from 3x transgenic mice-Alzheimer disease mice.\n","Further evidence is given for existence of a protracted, purely amnestic phenotype related to valineAPP717glycine mutations in autosomal dominant familial Alzheimer disease over a period of 14 years.\n","oligomers of stefin B and amyloid-beta interact in vitro and in cells\n","The current study demonstrates that APP overexpression in mice results in better motoneuron survival after peripheral nerve injury.\n","we found no evidence that CALHM1 P86L is associated with altered CSF levels of the investigated Alzheimer's disease biomarkers A beta 42, tau and phospho-tau\n","In 135 people without clinically detectable cognitive impairment, the mean cortical binding potential of Abeta peptide was skewed.\n","Mutations of the genes for amyloid precursor protein (APP), presenilin 1 (PSEN1), and presenilin 2 (PSEN2) are responsible for development of the disease in 50 percent of patients with FAD.\n","the amyloid precursor protein I716F mutation is associated with the youngest age of onset for this locus and strengthen the inverse association between amyloid-beta42/40 ratio and age of onset\n","Regulation of amyloid precursor protein processing identified by target-assisted iterative screening modulates the activities of Mint3/TAZ and Mint3/YAP complexes.\n","These results demonstrate that mislocalization of mitochondria underlies the pathogenic effects of Abeta42 in vivo.\n","Report pathology associated memory deficits in Swedish mutant genome-based amyloid precursor protein transgenic mice.\n","screened a library of semi-randomized amphipathic helical sequences, each expressed as a fusion protein with an Abeta42-yellow fluorescent protein sequence serving as a reporter for folding and solubilization\n","Data show that oxidative stress can be inhibited in the presence of tBHQ, an inducer of nuclear factor-erythroid 2 related factor 2 (Nrf2) in NT2N neurons and can be used to show the relationship between oxidative stress, amyloid beta formation and Nrf2.\n","Results indicate that amyloid beta-induced microtubule and Tau-dependent microtubule transport dysfunction leads to aneuploid neurons and may thereby contribute to the pathogenesis of Alzheimer disease.\n","The present data suggest that apoE produced by pericytes, rather than astrocyte-produced apoE, modulates Abeta cytotoxicity and Abeta removal near the vasculature in the brain.\n","These data suggest a model for how the processing of Bri2 and APP are interrelated.\n","Studies characterized the aggregation properties of Abeta with CD spectrum and transmission electron microscopy.\n","Full length protein Abeta(1-42) alters hippocampal network activity at concentrations commonly observed in Alzheimer's disease patients, a potent effect of Abeta(1-42) that increases with age.\n","Comparative measurement of cerebrospinal fluid Abeta42/Abeta40 ratio may improve differential diagnosis between Alzheimer's and other dementia syndromes such as vascular dementia, dementia with Lewy bodies, and frontotemporal dementia.\n","Although the biophysical properties of Abeta42 carboxy-terminal fragments are length-dependent, the correlation between peptide length, peptide conformation, solubility, aggregation tendency, and inhibitory activity is complex.\n","Abeta(1-42) cerebrospinal fluid (CSF) levels correlate with brain atrophy and ventricular expansion in a subgroup of cognitively normal elderly individuals. Reductions independent of CSF levels of Abeta(1-42) is common.\n","disulfide bond does not play a significant role in islet amyloid polypeptide-membrane interactions\n","In mice overexpressing amyloid-beta protein precursor, RhoA decreases in synaptic terminals and increases in dystrophic neurites.\n","Marked heterogeneity documents the extent of Abeta deposition in Alzheimer brains at final stages of disease that cannot be completely explained by a simple regular build up of pathologic protein in the cerebral cortex during the course of the disease.\n","Neither intraneuronal Abeta nor phospho-tau has obligatory effects on reducing the expression of genes important for memory and cognition in hippocampus of Alzheimer brains.\n","Reduced expression of the enzyme that converts desmosterol into cholesterol, Alzheimer indicator 1 gene (seladin-1/dhcr24), in cortex and cerebellum may underlie increased desmosterol levels in 21 month-old amyloid-beta mutant mice.\n","This review suggests that pathologic Abeta is polymorphic, producing conformational form(s) or speci fi c pool(s) of Abeta that are disease-relevant while others are less so.\n","The authors show that APP possesses a substrate inhibitory domain (ASID) that negatively modulates gamma-secretase activity for Agamma production by binding to an allosteric site within the gamma-secretase complex.\n","APP is involved in protective adaptive responses against oxidants\n","The nuclear magnetic resonance data suggest a binding mechanism in which one or a few Congo red molecules bind to Abeta and induce a slightly more compact (folded) conformation in the peptide.\n","NMR data revealed that the sugar-lipid interface is primarily perturbed upon binding of Abeta to the micelles.\n","show that morphological and functional endocytic abnormalities in fibroblasts from individuals with down syndrome are reversed by lowering the expression of APP or beta-APP-cleaving enzyme 1 (BACE-1) using short hairpin RNA constructs.\n","AMP-activated protein kinase signaling activation by resveratrol modulates amyloid-beta peptide metabolism\n","the data of this study demonstrated that the mutant C100 fragment is an effector of biochemical and both cognitive and non-cognitive behaviours. These transgenic mice may be a model for the psychotic features associated with early Alzheimer's disease.\n","Abeta oligomers target specific temporal facets of consolidation-associated synaptic remodelling in rat brain whereby loss of functional synapses results in impaired consolidation.\n","ATXN1 functions as a genetic risk modifier that contributes to AD pathogenesis through a loss-of-function mechanism by regulating beta-secretase cleavage of APP and Abeta levels\n","polymerization kinetics of 2.5, 5, 10 and 20 microM Abeta in the presence or absence of air-water interface using fluorescence spectroscopy and fluorescence microscopy with the amyloid specific dye, thioflavin T.\n","the large hydrophilic loop of PS1 appears to differentially regulate the relative production of different Abeta peptides without affecting Notch processing\n","Ganglioside binding is the initial and common step in the development of a part of human misfolding-type amyloidoses, including Alzheimer's disease.\n","The intracellular domain of APP is needed to inhibit neuronal calcium oscillations, because phosphorylation of Thr-668 controls APP trafficking at the plasma membrane.\n","Data show that the interaction of amyloid precursor protein and beta -site amyloid cleavage enzyme 1 is enhanced during the aging process, and the APP-BACE1 complex accumulates in the endosome.\n","Abeta deposits exhibit complex sinusoidal fluctuations in density in the temporal lobe in Alzheimer's disease, which may reflect the formation of Abeta deposits in relation to the modular and vascular structure of the cortex\n","Both amyloid-beta precursor protein and adapter protein Fe65 are co-localized in model Hirano bodies associated with Alzheimer's disease.\n","Up-regulation of the alzheimer amyloid precursor protein is associated with colon and pancreatic neoplasms.\n","Aph-1 associates directly with full-length and C-terminal fragments of gamma-secretase substrates\n","We propose, based on the findings here, a novel, apolipoprotein-like function for Abeta that is involved in maintenance of cellular and cerebral cholesterol homeostasis.\n","Studies indicate that intracellular Abeta is able to interact with the mitochondrial proteins ABAD and CypD resulting in disruption of cell homoeostasis and ultimately cell death.\n","show that both A beta and human amylin (HA) deregulate identical proteins, a quarter of which are mitochondrial, supporting the notion that mitochondrial dysfunction is a common target in these two amyloidoses.\n","To understand the initial stage of amyloid-beta peptide aggregation, conformational characteristics of monomers of wild-type Abeta(28-35) and mutant peptides A30G and A30I were investigated using density functional theory analysis and experimental studies\n","REVIEW: the current understanding on the conformations and biological activity of Abeta(25-35) exploring aggregation, cytotoxic and neurodegenerative properties of this fundamental Abeta fragment\n","Alzheimer's disease-associated amyloid beta-protein peptides display antimicrobial activity against C. albicans, E. coli, S. epidermidis, S. pneumoniae, S. aureus, L. monocytogenes, E. faecalis, and S. agalactiae.\n","there are reciprocal interactions between Ca(2+) pathways and amyloid pathology; altered Ca(2+) signaling accelerates Abeta formation\n","crystal structure of the entire N-terminal APP-E1 domain consisting of the growth factor like and the copper binding domains at 2.7-A resolution\n","APP and AP-4 engage in a distinct type of signal-adaptor interaction that mediates transport of APP from the trans-Golgi network (TGN) to endosomes, thereby reducing amyloidogenic processing of the protein.\n","Children of parents with late-onset Alzheimer's disease, particularly those with affected mothers, have increased fibrillar Abeta load in AD-vulnerable regions compared with controls, perhaps accounting for the known increased risk for AD.\n","In the cerebral cortex of Alzheimer's disease patients, amyloid protein precursor colocalizes with significantly decreased levels of HRD1 protein.\n","APP may have a broad role in not only mediating cell-matrix adhesion but also in the function of peripheral immune cells\n","Cell biology of APP, beta- and gamma-secretases and the data on their association with lipid rafts.\n","the high-density lipoprotein receptor SR-B1 has a role in synovial inflammation via serum amyloid-A\n","findings demonstrated that the metabolism of the APP-PS1 transgenic mouse was associated with early-stage Alzheimer's disease\n","The alpha-cleaved ectodomain of APP stimulates the interleukin (IL)-6/glycoprotgein (gp)130 signaling pathway for induction of gliogenesis within neural progenitor cells.\n","analysis of parallel, in-register beta-strands of beta2-microglobulin in amyloid fibrils\n","our calculations revealed that the small wild-type Abeta17-42 oligomers at neutral pH and the Dutch mutants with the pronounced beta-sheet structure have positive association free energy\n","Beta-amyloid precursor protein mutants respond to gamma-secretase modulators\n","Abeta42 stimulates PI3K, which in turn causes memory loss in association with an increase in accumulation of Abeta42 aggregates\n","Morin destabilizing Abeta(42) by binding to the ends of the fibrils to block the attachment of an incoming peptide.\n","Identical products were obtained when Abeta25-35 and Abeta1-42 were treated with a hypochlorous acid generating system.  Conversion of Met35 to Met35 sulphoxide in Abeta abolished the aggregation of Abeta25-35.\n","Clinical trial of gene-disease association and gene-environment interaction. (HuGE Navigator)\n","In comparison to Abeta40, Abeta42 is more flexible and interacts through a smaller number (17-22) of hydrogen bonds in the catalytic chamber of IDE.\n","Transgenic mouse TgCRND8 encodes a mutant form of the amyloid precursor protein APP 695 with both the Swedish and Indiana mutations and develops extracellular amyloid beta-peptide deposits as early as 2-3 months.\n","The findings of this study reveal that analysis of cellular changes induced by spatial training facilitates detection of hippocampal synaptic abnormalities in APP23 mutants.\n","Data suggest that changes in cholesterol levels per se and not isoprenoid levels account for the observed modifications in amyloid beta production in Alzheimer's disease.\n","analysis of the destruction of amyloid fibrils of beta(2)-microglobulin K3 fragments by laser irradiation coupled with the binding of amyloid-specific thioflavin T\n","results and conclusions depended strongly on the chosen antibody and the pretreatment strategy and thus multiple antibodies must be used when assessing the intracellular accumulation of APP\n","spherulites of amyloid beta and senile plaques in Alzheimer's disease tissue are one and the same structures\n","an incremental number of CaV1.2 expressing reactive astrocytes was found with increasing age of animals and number of amyloid-beta plaques\n","The objective of this study was to determine the significance of plasma Abeta as an Alzheimer's disease biomarker and its relationship with Abeta load\n","beta-amyloid 1-40 induces HIPK2 degradation and alters HIPK2 binding activity to DNA, in turn regulating the p53 conformational state and vulnerability to a noxious stimulus.\n","These results showed that Tg2576(APP) mice display severe degeneration of motor neurons in the spinal cord and associated motor function deficits.\n","Positive feedback mediates Abeta-induced over-activation of N-methyl D-aspartate (NMDA) 2A receptors and is involved in neuronal impairment in an Alzheimer disease model.\n","Evidence in this review of Abeta's multifunctional activities includes protection against metal-induced reactive oxidizing species, modification of cholesterol transport, and novel role as a potential transcription factor.\n","Aberrant amyloid precursor protein (APP) processing in hereditary forms of Alzheimer disease caused by APP familial Alzheimer disease mutations can be rescued by mutations in the APP GxxxG motif\n","These results indicate that PERK-eIF2alpha pathway is a potential target for therapeutic applications in neurodegenerative diseases including Alzheimer's disease.\n","Tau phosphorylation at Ser262 is crucial for Abeta42-induced tau toxicity in vivo.\n","sAPPalpha was able to protect PC12 cells from apoptosis triggered by epoxomicin, as well as by genotoxic stress (UV irradiation)\n","FMRP represses translation by recruiting APP mRNA to processing bodies, whereas hnRNP C promotes APP translation by displacing FMRP, thereby relieving the translational block.\n","Abeta, PrP and tau all play a role in the neurodegenerative process via their connection to the cell cycle and cell death.\n","The effect of mevalonate pathway blockade on neurite outgrowth is strikingly enhanced by over-expression of human amyloid precursor protein in cultured neuroblastoma cells.\n","Elevated levels of APP intracellular domain peptides (AICD) render neurons hypersensitive to stress and induce hippocampal circuit reorganization, which can further exacerbate hyperexcitability.\n","Murine NPC1 mRNA levels were increased in the hippocampus of 12-month-old transgenic mice expressing a familial AD form of human amyloid-beta precursor protein (APP) and presenilin-1 (APP/PS1tg) compared to 12-month-old wild type mice.\n","These findings confirm increased Abeta accumulation as a key pathogenic determinant linking lens and brain pathology in both Down syndrome and Alzheimer's disease.\n","In 2 Italian families showing the London missense mutation in exon 17 of the amyloid precursor protein gene, all Alzheimer subjects showed a cognitive profile consisting of early impairment in long-term memory, shifting abilities and affective symptoms.\n","The significance of the time course of A(beta) peptide biomarker abnormalities in Alzheimer disease correlates with hippocampal volume and radial distance when compared with apolipoprotein E4 carriers and noncarriers.\n","During progression of Alzheimer's disease stages, the dynamics of Abeta 1-42 biomarker follows a steep curve, stabilizing early in the disease course.\n","cultured primary human astrocytes preferably take up Ab1-42 oligomers over fibrils, without evidence of pro-inflammatory activation\n","X-ray results and modeling imply that in the assembly of A beta 16-22 the F19 side chain is localized within the intersheet space and is involved in hydrophobic contact with amino acids across the intersheet space.\n","An important contribution of Abeta to Alzheimer's disease is via its effects on fibrin clots in transgenic mice, implicating fibrin(ogen) as a potential critical factor in this disease.\n","A mechanism is revealed whereby Abeta oligomers induce abnormal accumulation and overstabilization of a glutamate receptor, thus providing a mechanistic and molecular basis for Abeta oligomer-induced early synaptic failure.\n","Study shows that prefibrillar aggregates of E22G (arctic) variant of the Abeta(1-42) peptide bind strongly to 1-anilinonaphthalene 8-sulfonate and that changes in this property correlate significantly with changes in its cytotoxicity.\n","role of ApoE isoforms on the peripheral clearance of Abeta from blood may impact on clearance from the brain\n","Different amyloid beta peptide fragments appear to alter specific neuronal network activities instead of having the same generalized inhibitory effect on neuronal network function.\n","Selective translational control of the Alzheimer amyloid precursor protein transcript by iron regulatory protein-1.\n","Fe65 and Dab1 compete for binding to APP.  Dab1 significantly decreased the amount of APP bound to LRP and the level of secreted APP and APP-CTF in LRP expressing cells\n","Abeta1-42-induced reactive oxygen species accumulation might trigger the onset of autophagy and subsequent autophagic cell death\n","The presence of a subpopulation of amyloid-beta oligomers in the brains of patients with Alzheimer's disease might be related to alterations in selected synaptic proteins and cognitive impairment.\n","MMP-2 release and activation differentially degrades Abeta species, delaying their toxicity for endothelial cells.\n","characterized the interaction between synthetic Abeta42 oligomers and the recombinant human prion protein; this binding is highly specific for a particular conformation adopted by the peptide in soluble oligomeric species\n","Macroautophagy may be a crucial mediator between inflammation and beta-amyloid-associated degeneration within skeletal muscle.\n","Cholesterol increase in Alzheimer's disease could be responsible for the enhanced internalization of clathrin-, dynamin2-, Eps15- and Rab5-dependent endocytosis of APP and the ensuing overproduction of Abeta.\n","[review] The amyloid precursor protein gene (APP, OMIM 104,760, chromosome 21q21) encodes a ubiquitously expressed, integral type I membrane glycoprotein that causes early onset Alzheimer's disease.\n","Calpain activation plays an important role in Aamyloid precuresor protein processing and plaque formation, probably by regulating the expression of BACE1.\n","Abeta9-induced antibodies exhibit stronger abilities not only to inhibit Abeta9-induced aggregation and to disassemble Abeta42 aggregation, but also to inhibit and neutralize Abeta42-induced cytotoxicity in vitro.\n","Low amyloid beta(1-42) cerebrospinal fluid levels are found in Alzheimer's disease patients in North India compared to those of controls.\n","five structurally distinct fibrillar aggregates of the Alzheimer's plaque peptide Abeta(1-40), as well as a non-fibrillar aggregate induced by Zn(2+)\n","Vascular beta-amyloid deposits contribute to hypoperfusion and neurological deficits observed in Alzheimer's and other transgenic cerebral amyloid angiopathies.\n","Data show that the amyloid-beta (25-35) peptide induced membrane alteration even at only 3mol% might be involved in the pathology of Alzheimer's disease as well as be a clue in early diagnosis and therapy.\n","Results compare the effect of secretase inhibitors and modulators on Abeta formation in primary chicken telencephalic neurons and in a human neuroglioma cell line (H4) ectopically expressing human APP with the Swedish double mutation.\n","Using brain tissue from Alzheimer's disease and normal subjects, a negative correlation was found between the expressed levels of HRD1 and of amyloid-beta; this suggests the possibility that generation of amyloid-beta involves HRD1.\n","Increased level and processing of amyloid protein precursor is associated with the development of pathology and/or degenerative events observed in the brains of Niemann-Pick type C (Npc1) protein-deficient mice.\n","Amyloid-beta peptide alteration of tau exon-10 splicing is related to its activation of GSK-3beta which in turn phosphorylates SC35.\n","APP protein levels significantly increase in the hippocampus of aged senescence-accelerated mouse prone (SAMP)8 Alzheimer's disease model mice.\n","Ventricular enlargement as a biomarker of Alzheimer's disease correlates strongly with lower levels of cerebrospinal fluid (CSF) Abeta(1-42) peptide but not with CSF Tau protein, after adjusting for age, gender, and educational level.\n","curcumin potently lowers Abeta levels by attenuating the maturation of APP in the secretory pathway.\n","Observational study of gene-disease association, gene-environment interaction, and pharmacogenomic / toxicogenomic. (HuGE Navigator)\n","These data show that a prolonged, substantially elevated level of Abeta are not sufficient to cause deficits in the induction or expression of long-term potentiation in the CA1 hippocampal region.\n","Data report that retro-inversion of two peptides, RGKLVFFGR (OR1) and RGKLVFFGR-NH(2) (OR2) containing the sequence KLVFF, which is the central region (residues 16-20) of Abeta, increases their efficacy in inhibiting aggregation and toxicity of beta-amyloid.\n","Data show that the ligand-Abeta fibril interactions cannot explain differences in the binding affinities of naproxen and ibuprofen.\n","Cerebral oligomeric Abeta-derived assemblies generated in brain in situ from human APP transgenes may be associated with cognitive impairment.\n","PN2KPI is a highly specific inhibitor of FXIa among coagulation enzymes, but the flexibility of trypsin renders it susceptible to inhibition by both wild-type and mutant forms of PN2KPI and BPTI.\n","Retroposition of Rps23 mRNA occurred multiple times in different species but only generated another functionally expressed Rps23rg1-homologous gene, Rps23rg2, in mice.\n","The data obtained indicate that VEGF-driven mechanisms may affect APP processing, suggesting a link of angiogenesis and pathogenesis of Alzheimer's disease.\n","the tubular Abeta(42) fibril models exist at both acidic and physiological pH; however, the relative populations of the polymorphic models shift with pH\n","This study results reveal a novel and unexpected relationship between APP and male sexual behavior. We speculate that declining APP during normal aging in males may contribute to the loss of sexual function.\n","HSV-1 causes functional changes in cortical neurons that promote APP processing and amyloidbeta production compatible with the co-factorial role for HSV-1 in the pathogenesis of Alzheimer's disease.\n","In this review, APP is a major Alzheimer's disease susceptibility gene that interacts with the herpes simplex virus and might be able to modify the virus life cycle in a therapeutic strategy.\n","Results reveal an unforeseen role for alpha-secretase in generating an endogenous gamma-secretase inhibitor that down-regulates the production of Abeta.\n","Soluble Abeta42 peptide can invoke non-pathological and anti-viral effects through inactivation of an HSV-1 challenge to human brain cells by simple viral sequestration, viral destruction, or by complex neurogenetic mechanisms.\n","Findings further establish that APP intracellular domain (AICD), in addition to Abeta, contributes to AD pathology and that neuroinflammation plays a much broader role in AD pathogenesis than previously thought.\n","an essential function of the conserved APP intracellular domain in developmental regulation, and this activity can be genetically uncoupled from APP processing and Abeta pathogenesis.\n","Study shows that an increase in pH is responsible for amyloid beta peptide fibril fragmentation, while increased ionic strength is responsible for the aggregation of fibril fragments.\n","This study indicated that APP mutations linked to hereditary cerebral hemorrhage with amyloidosis, reinforcing the link between this phenotype and codon 693 of Amyloid Protein Precursor.\n","Dictyostelium requires PS for phagocytosis and cell-fate specification in a cell-autonomous manner, and show that regulation of phagocytosis requires an active gamma-secretase.\n","mutated APP associated with FAD has no direct effect on intracellular calcium homeostasis\n","Abeta40 and Abeta42 self-assemble via different pathways and provide a candidate in the Abeta42 dodecamer for the primary toxic species in Alzheimer's disease.\n","Monte Carlo simulations using an atomistic force field and implicit solvent model indicate that at physiological temperatures, both alloforms of amyloid beta assume a largely collapsed globular structure.\n","Transgenic mice expressing familial Alzheimer-associated amyloid precursor protein and presenilin transgenes show increased brain amyloid beta (Abeta) levels and Abeta plaques from the age of 3 months.\n","Amyloid beta-induced dysfunction of gap junctional communication in cultured astrocytes does not reflect the maintenance of dye transfer through astrocytic syncytial networks in transgenic mice.\n","Mutations alter the geometry and mechanical properties of Alzheimer's Abeta(1-40) amyloid fibrils.\n","The structural and mechanistic observations based on these simulations agree with the recent NMR experiments and provide the driving force and structural origin for the Abeta42 aggregation process to cause Alzheimer's disease.\n","An Abeta(25-35) fragment, which contains the cytotoxic sequence of the amyloid peptide, activates the intrinsic apoptotic pathway in human neuroblastoma cells expressing the HFE allelic variant H63D to a greater extent than in cells with wild-type HFE.\n","The deleterious effects of beta-amyloid on cognition may be delayed in those subjects with larger brain (temporal) volume. APOE epsilon4 carriers are more likely to have higher Abeta load than non-carriers.\n","APP/presenilin-1 transgenic mice have significantly decreased hippocampal N-acetyl aspartate/total creatine at 16 months of age, associated with degeneration and intracellular deposition of thioflavine S-positive materials in CA3 pyramidal neurons\n","Data show that MBP purified from either brain or a bacterial recombinant expression system comparably bound to Abeta and inhibited Abeta fibril assembly indicating that post-translational modifications are not required for this activity.\n","Study found that the Alzheimer's Disease beta-amyloid protein precursor (APP) possesses ferroxidase activity mediated by a conserved H-ferritin-like active site.\n","Neurotoxicity of Alzheimer's disease Abeta peptides is induced by small changes in the Abeta42 to Abeta40 ratio.\n","The observations demonstrate that both mature APP as well as total APP and tau protein levels are greatly reduced in human cerebellum\n","MEGF10 is involved in the uptake of amyloid-beta peptide (Abeta42) in the brain.\n","findings show Abeta requires tau to impair axonal transport, and tau reduction protects against Abeta-induced axonal transport defects\n","[review] While Abeta is often abundant in the brains of cognitively normal elderly people, the brains of Alzheimer's disease patients are highly enriched for N-terminally truncated Abeta bearing the pyroglutamate modification.\n","A primate model of Alzheimer's disease (AD)is generated in rhesus monkeys by combined infusion of amyloidbeta42 and thiorphan, which duplicates a subset of neuropathological changes in AD brains, thereby having implications in the elucidation of AD.\n","Ass-associated increases in bone morphogenetic protein 6 (BMP6) expression in a transgenic mouse model of Alzheimer's disease may have deleterious effects on neurogenesis in the hippocampus.\n","This review analyzes the critical nature of the caspase cleavage site of amyloid-beta protein precursor for cell death induction, synaptic loss, hippocampal atrophy, long-term potentiation, memory loss and other aspects of the Alzheimer's phenotype.\n","This review examines the functional impact of Abeta on synaptic plasticity.\n","Upregulation of presenilin (PS)1 leads to Abeta overproduction and accumulation in sporadic Alzheimer's disease.\n","The temporal appearance of APP on the cell surface preceded that of C99 in the recycling compartment, further supporting the cleavage of APP in recycling endosomes.\n","subtle lipid-peptide interactions suffice in controlling the overall aggregation properties and drastically accelerate, or delay, the fibrillation kinetics of Abeta peptide in near-physiological buffer solutions\n","Electroencephalography readings, locomotor activity and sleep architecture are abnormal in transgenic amyloid-beta protein precursor mice.\n","Our current data show that the generation ratio of AICDepsilon51 and Abeta42 do not always change in parallel.\n","Data demonstrate that loss of neuron-microglial fractalkine signaling leads to reduced beta-amyloid deposition in mouse models of AD that is potentially mediated by altered activation and phagocytic capability of CX3CR1-deficient microglia.\n","Infusion of an at-risk subpathogenic dose of amyloidbeta in chronically stressed rats causes significant impairment of cognitive functions and late-phase long-term potentiation, which may play a critical role in the etiology of Alzheimer's disease.\n","Studies indicate that the misfolding and aggregation of the prion protein are akin to the genesis of amyloid fibrils.\n","The present review summarizes the signaling pathways pertinent to the regulation of APP beta cleavage.\n","Data provide substantial evidence that APP and cystatin C are target secreted proteins of EGFR in NPC, and upregulation of secretory APP by EGFR may be involved in the pathogenesis of NPC.\n","the monomers probe different binding modes during their search for the fibril conformation\n","None of the assayed APP gene sites showed any sign of methylation in either of the investigated brain regions in any of the analyzed Alzheimer disease patients\n","trehalose affects the interaction of Alzheimer's Abeta-peptide and anionic lipid monolayers\n","catalase-amyloid interactions have a role in Abeta-induced oxidative stress\n","Inhibition of eIF4A reduced the synthesis of APP and tau.\n","analysis of teh structure of amyloid {beta} protein fibrils\n","Findings suggest that fibril formation by Abeta(1-42) as the process primarily responsible for the fatal neuropathological manifestation of AD.\n","Striatal amyloid beta pathology is common in both Parkinson's disease with dementia and Lewy body dementia and may reflect the development of dementia in these conditions.\n","Genetic association of rs242557 tau gene variant in Parkinson disease patients is only observed in individuals with low cerebrospinal fluid amyloid-beta protein levels.\n","unique soluble APP770beta has the potential to serve as a marker for cortical dementias such as AD and vascular dementia.\n","Abeta and functional AICD appear to be preferentially synthesized through beta-secretase action on APP(695)\n","Proteolysis of calcineurin is increased in human hippocampus during mild cognitive impairment and is stimulated by oligomeric Abeta in primary cell culture.\n","Although the Abeta barrels adopt the right-handed beta-sheet twist, the barrels still break into heterogeneous, loosely attached subunits, in good agreement with atomic force microscopy images and previous modeling.\n","KCa3.1 activity and excessive NO release are required for AbetaO-induced microglial neurotoxicity; AbetaO, generally considered a neurotoxin, may more potently cause neuronal damage indirectly by activating microglia in AD\n","Structural insight into the differential effects of omega-3 and omega-6 fatty acids on the production of Abeta peptides and amyloid plaques.\n","Cu2+ ions accelerate the kinetics of fiber formation and promote cell toxicity of amyloid-{beta} from Alzheimer disease\n","Data indicate that PG46 binds to beta-amyloid oligomers and displayed an increase in FlAsH fluorescence upon binding.\n","The expression of APP-swe modulates global gene expression directed to Alzheimer's disease pathogenesis.\n","Abeta accumulation in neuronal cells correlated with neuronal iron homeostasis disruption and probably contributed to the pathogenesis of Alzheimer disease.\n","liposomal DHA is able to restore or maintain physiological membrane properties, which are required for neuroprotective sAPPalpha secretion and autocrine modulation of neuronal survival\n","Review discusses the phosphorylation of APP and the relevance of its proteolytic products carboxy terminal fragment, the APP intracellular C-terminal domain (AICD) its interactions with other proteins and how it functions.\n","Immobilization stress does not increase soluble or insoluble amyloid beta levels in transgenic mice; increased cortisol levels lower the threshold for a neuroinflammatory response, independently from amyloid beta.\n","Study of the interaction between the amyloid beta peptide (1-40) and antioxidant compounds by nuclear magnetic resonance spectroscopy.\n","APP can coimmunoprecipitate NEEP21 from nontransgenic mouse brain and from mammalian cells stably coexpressing both proteins.\n","Findings demonstrate that HSV-1 infection of neuronal cells can generate multiple APP fragments with well-documented neurotoxic potentials.\n","Data show that no cerebral amyloid angiopathy (CAA) patient harbored a known or novel APP mutation or gene duplication.\n","Data provide a simple and general mechanism for targeting of amyloid-beta oligomers without the requirement of conformational-dependent epitopes.\n","Data suggest that the interaction between Abeta and fibrinogen may be an important contributor to the vascular abnormalities found in Alzheimer's disease.\n","selective activation of D1/D5 receptors could protect synapses from the deleterious action of Abeta oligomers; a selective D1/D5 receptor agonist, prevented the reduction in surface levels of AMPA and NMDA receptors induced by AbetaOs in hippocampal neurons\n","Plasma Abeta can help predict cognitive function in adults with Down syndrome independently of the presence or absence of dementia.\n","This review examines recent studies on the thermodynamics of copper association with amyloid-beta, alpha-synuclein and prion protein. [Review]\n","Results suggest that immunization with non-toxic Abeta derivative may offer a safer therapeutic approach to AD.\n","endothelial NO plays an important role in modulating APP expression and processing within the brain and cerebrovasculature\n","cerebrospinal fluid Abeta(1-38) was reduced in frontotemporal dementia as compared to each of the other diagnostic groups, including primary progressive aphasia\n","The interruption of the Wnt signaling pathway by oligomeric amyloid beta(1-42) peptide may have clinical implications for the treatment of impaired neurogenesis in Alzheimer disease.\n","iron delays the formation of well ordered aggregates of Abeta and so promotes its toxicity in Alzheimer disease.\n","LR11 is phosphorylated in vivo and indicate that ROCK2 phosphorylation of LR11 may enhance LR11 mediated processing of APP and amyloid production.\n","study shows the common late-onset form of Alzheimer's disease is characterized by an overall impairment in CNS beta-amyloid clearance\n","The development of transgenic mouse models engineered with overexpression of APP carrying familial Alzheimer's disease mutations has been extremely useful and supports the amyloid hypothesis.\n","Abeta42 neurotoxicity is mediated by ongoing nucleated polymerization process rather than by discrete Abeta42 species.\n","Data show that HeLa cells stimulated with EGF or PDGF or overexpressing EGFR exhibit increased APP proteolysis in a Ras-dependent way.\n","This work reports a novel mechanism regulating non-amyloidogenic processing of APP, which involves calmodulin dissociation and activation of the alpha-secretase activity of an ADAM family metalloproteinase.\n","Data suggest that the clinical benefit by certain antihypertensive DHPs against AD is unrelated to their antihypertensive activity, but rely on their ability to lower brain Abeta accumulation by affecting both Abeta production and Abeta clearance acr [...]","endogenous miR-101 regulates expression of APP in human cells via a specific site located within its 3'-UTR.\n","Copper promotes the trafficking of the amyloid precursor protein.\n","Beta-amyloid 1-42 oligomers impair function of human embryonic stem cell-derived forebrain cholinergic neurons\n","Abeta-induced cellular redistribution and inactivation of neuronal HKI play important roles in oxidative stress and neurodegeneration in Alzheimer's disease\n","O-GlcNAcase and O-GlcNAc transferase regulate the level of O-GlcNAcylated APP.\n","The amyloid precursor protein C-terminal fragment occurs in monomeric and dimeric conformations and binds to gamma-secretase.\n","The Abeta oligomers are recognized by albumin through sites that are evenly partitioned across the three albumin domains and that bind the Abeta oligomers with similar dissociation constants.\n","A range of imaging, neuropsychological, cerebrospinal fluid, and pathological findings are reported that extend the known phenotype. APP but not PRNP duplication is a significant cause of early onset dementia in the UK. T\n","Amyloid-beta inhibits No-cGMP signaling in a CD36- and CD47-dependent manner\n","unfolding of Abeta conformation leads to reduced formation of mature fibrils, but an increase in nonfibrillar, amorphous type of aggregates\n","analysis of Alzheimer's Abeta peptides with disease-associated N-terminal modifications\n","analysis of the presence of Abeta40 oligomers in Alzheimer's disease and its potential use as a diagnostic biomarker\n","These results suggest that L17 and F19 are the critical residues responsible for conformational changes which may trigger neurotoxic cascade of Abeta(40).\n","In neuronal cells, bet-amyloid precursor protein metabolism is physiologically modulated by cyclic AMP.\n","Zn(2+), Cu(2+), Fe(3+), and Al(3+) adopt distinct folding and aggregation mechanisms to affect Abeta, where Abeta destabilization promotes annular protofibril formation\n","The objective of this study was to elucidate an association between Apo- Eepsilon4 allele and CSF biomarkers Abeta42 and tau for the diagnosis of Alzheimer's Disease (AD) patients\n","These data have thus established an important role for protein dynamics in the mechanism of Abeta aggregation.\n","Protein interacting with NIMA (PIN1) changes are a constant feature of Alzheimer's disease pathology and could serve as a biomarker of the onset or spread of Alzheimer's disease neuropathology independent of tau or amyloid beta(Abeta) proteins.\n","[review] Recent studies of synthetic Abeta precursor protein transgenic mice models suggest that pre-fibrillar forms of Abeta are more deleterious than extracellular fibril forms.\n","lower plasma beta-amyloid 42/40 is associated with greater cognitive decline among elderly persons without dementia over 9 years, and this association is stronger among those with low measures of cognitive reserve\n","Data show that indicate that PAP(248-286) is unfolded to an unusual degree for an amyloidogenic peptide but adopts significantly helical structures in TFE solutions.\n","Bioluminescence imaging of Abeta deposition in bigenic mouse models of Alzheimer's disease\n","neural precursor cell Ptch1 overexpression is due to the amyloid precursor protein fragment AICD\n","Observations suggest that apoE4 strongly stabilizes Abeta oligomers, the pathological species responsible for Alzheimer's disease.\n","The results suggest that enhanced levels of wild-type human amyloid precursor protein do not result in degenerative changes of neuronal morphology, but rather promote dendritic growth.\n","Two distinct amyloid beta-protein (Abeta) assembly pathways leading to oligomers and fibrils identified by combined fluorescence correlation spectroscopy, morphology, and toxicity analyses.\n","findings show the APP intracellular domain (AICD) activates transcription by targeting MED12; the AICD binds to MED12/Mediator in vitro and in vivo; results identify the MED12 interface in Mediator as a crucial transducer of AICD transactivation\n","Abeta is toxic to brain endothelial cells via binding to RAGE and induction of ROS production, which ultimately leads to disruption of TJs and loss of BBB integrity.\n","a pathway by which isoform specific conformational differences increase the level of cleavage at the hinge region of ApoE4, leading to a loss of ApoE function to mediate clearance of Abeta and increase the risk of AD for carriers of the APOEepsilon4 allele.\n","aluminum, beta(1-42)-amyloid or the beta(1-42)-amyloid aluminum complex seems critical in modulating key AD-related pathways such as glutamatergic transmission, Ca(2+) homeostasis, oxidative stress, inflammation, and neuronal apoptosis\n","Extracellular amyloidbeta(1-42) peptide targets neuronal mitochondria to exert its toxic effects.\n","Suggest that lead acetate causes both the overexpression of beta-amyloid precursor protein and repression of neprilysin resulting in the buildup of amyloid beta.\n","Data show that there was agreement between in vivo amyloid imaging and CERAD NP scores in participants with either high or negligible Abeta levels in vivo, only limited agreement was observed among those with intermediate levels of Abeta.\n","DHA directs amyloidogenic processing of APP toward nonamyloidogenic processing, effectively reducing Abeta release\n","Study show that there is a 4-fold accumulation of 27OHC in different regions of the cortexes of patients carrying the Swedish amyloid precursor protein (APPswe) 670/671 mutation.\n","The model is used to provide a satisfying structural and energetic interpretation of death cell receptor 6-growth factor-like domain of APP binding and to suggest the possibility of and a mechanism for spontaneous apoptosis.\n","REVIEW on the core AD biomarkers, Abeta and phosphor-tau (p-tau), on different methods and modalities of assessing them [eg, cerebrospinal fluid analysis and PET imaging], and on their diagnostic and predictive value in preclinical and clinical stages of AD\n","environmental enrichment efficiently ameliorates early hippocampal-dependent spatial learning and memory deficits in APP(Sw,Ind) transgenic mice\n","analysis of the amyloid-beta monomer and the monomer-oligomer equilibrium\n","results indicated that all key components involved in APP processing were expressed in prostate cancer cell lines\n","Overexpression of wild-type or mutant APP causes Casp6-dependent but Abeta-independent neuritic degeneration in human neurons.\n","Expression of Abeta(1-42) in rat motor cortex leads to an increase in Tar DNA-binding protein (TDP)-43 pathology identical to the pathological changes seen in Alzheimer's disease.\n","Aluminum, copper, iron and zinc differentially alter amyloid-Abeta(1-42) aggregation and toxicity\n","The pattern of reduced APP is consistent with heightened vulnerability of episodic memory-related brain regions in Alzheimer's disease, whereas the observed increases in funcitonal connectivity may reflect a compensatory response.\n","insoluble prion protein is the major prion protein species that interacts with insoluble Abeta42 in vivo.\n","The E22Delta mutation strongly accelerated fibril formation of Abeta1-42 E22Delta compared to Abeta1-42 wild type. Fibrils of Abeta1-40 E22Delta formed a unique quaternary structure characterized by a strong tendency to form fibrillar bundles.\n","The results from this study demonstrated that the mThy1-hA PP751 Tg mouse modelincorporates robust and progressive cognitive impair-ments related to hA PP overexpression\n","[review] Extracellular deposition of beta-amyloid peptide fibrils represents the body's pathological adaptation mechanism, aimed at preservation of autonomic functioning; cognitive decline may be severe, yet the other organ systems continue to function.\n","Findings extend understanding of ApoE/Abeta interaction and may guide the discovery of inhibitors that treat AD by antagonizing ApoE/Abeta interaction.\n","REVIEW: progress in understanding Alzheimer's beta-amyloid structures\n","Microglial cells from transgenic mice in the preplaque stage display intermediately activated morphology and appear to be recruited toward intracellular amyloid-beta peptide (Abeta)-oligomer burdened neurons.\n","Epitope-dependent effects of Beta-amyloid antibodies on Beta-amyloid clearance in an in vitro model of the blood-brain barrier\n","High-molecular weight amyloid-beta aggregates, particularly A-beta(42) species, are most prevalent in the soluble fraction of the AD brain and may play an important role in the pathogenesis of AD\n","Subcellular fractionation of Alzheimer's disease cortex with low levels of Golgi-localized GGA proteins shows an alteration of beta-secretase distribution and extensive co-localization with amyloid beta precursor protein APP.\n","Specific dimerization-affecting mutations located mostly at the N-terminus of the transmembrane domain dimer of APP-betacarboxy-terminal fragment were identified.\n","The ratio of Abeta42 to Abeta40 rather than absolute levels of the peptides can aid in the identification of incipient Alzheimer's disease among patients with mild cognitive impairment.\n","Considering the ubiquitous expression modus of APP, beta- and gamma-secretases and type-1 VDAC/eukaryotic porin a basic model of apoptosis might be given.\n","These results demonstrate that TgCRND8 mice show significant deficits in spatial and nonspatial behavioral tasks at advanced stages of amyloid pathology.\n","Asp421-cleaved tau and Abeta cooperate to impair mitochondria, which likely contributes to neuronal dysfunction in Alzheimer disease.\n","Neuronal damage occurs by activation of neuronal hemichannels induced by adenosine triphosphate (ATP) and glutamate released from Abeta(25-35) peptide-activated glia.\n","thyroid hormone receptors actively facilitate T3 thyroid hormone-dependent silencing of amyloid precursor protein gene expression via the recruitment of distinct histone modifying enzymes associated with transcriptional repression\n","Data show that Abeta binding to RBC appeared to cause RBC aggregation and hemolysis.\n","[review] The self-association of the amyloid precursor peptide and the dimerization and oligomerization of its homologues are key factors under native and pathogenic conditions.\n","in patients with AD, increased production of Abeta and the interaction of Abeta with Drp1 are crucial factors in mitochondrial fragmentation, abnormal mitochondrial dynamics and synaptic damage.\n","Age-dependent accumulation of soluble amyloid beta oligomers reverses the neuroprotective effect of soluble amyloid precursor protein-alpha by modulating phosphatidylinositol 3-kinase/Akt-GSK-3beta pathway in Alzheimer mouse model.\n","APP genetic variants, point mutations and locus duplication are not a common cause of cerebral amyloid angiopathy-related intracerebral hemorrhage in the Spanish population.\n","data suggest that an increased constitutive internalization and/or concurrent signaling of the delta-opioid receptor-Cys27 variant affects APP processing through altered endocytic trafficking of APP\n","amyloid pathology in aged Tg2576 mice may specifically disrupt context-outcome associations supported by the hippocampus and/or its interaction with the amygdala.\n","Abeta-mediated neuronal cell death involves the loss of full-length Tau and/or the generation of toxic fragments but does not involve or require hyperphosphorylation of full-length Tau.\n","The amyloid hypothesis for Alzheimer's disease needs to be reformulated to explain the lack of efficiency of targeting Abeta.\n","an inverse change in amyloid beta (A4) C-terminal and N-terminal epitope accessibility provides the basis of a sensitive method for assessing early steps in amyloid beta (A4) oligomerization\n","These results provide a biological function for Abeta peptides and may help to define the pathogenic relationship between cholesterol metabolism in brain and Alzheimer's disease\n","Intraneuronal Abeta oligomers cause cell death by inducing endoplasmic reticulum stress, endosomal/lysosomal leakage, and mitochondrial dysfunction in vivo.\n","Functional analysis revealed that this E682K mutation in APP blocked the beta'-site and shifted cleavage of APP by BACE1 to the beta-site, causing increased Abeta production.\n","The level of amyloid-beta peptide in cerebrospinal fluid significantly decreases after heart surgery, clearly demonstrating post-surgical cognitive impairment associated with changes in biomarkers similar to that seen in Alzheimer's disease.\n","[review] Amyloid-beta peptide (Abeta) appears to play a pivotal role in the development of Alzheimer's disease (AD); clearance of Abeta from the brain represents an important therapeutic strategy for prevention and treatment of AD.\n","Abeta(1-42) plasma levels are associated with the rate of cognitive decline in Alzheimer's disease patients and may be influenced by atherosclerotic vasculopathies such as stroke and myocardial infarction.\n","The spatial learning and memory abilities of injected amyloid-beta peptide(1-40) rats are improved in each group with grafted neural stem cells that survive and differentiate with high yield into neurons of diverse neurotransmitter subtypes.\n","Patients with mild cognitive impairment and low Abeta42 peptide fragment, plus high tau levels in the cerebrospinal fluid, have a substantially increased risk of developing Alzheimer's disease, even after adjustment.\n","It is not likely that incubation with docosahexaenoic acid (DHA) reduces Abeta(1-42) secretion through prostaglandin E2-related pathways, but rather is a more direct consequence of increased membrane content of DHA and altered membrane ratio in PUFAs.\n","Evidence of cognitive impairment is found in AbetaPP23 transgenic mice, indicated by deficits in the delayed-non-matching-to-place task.\n","In Alzheimer's disease, aromatic amino acid pi-stacking interactions are not critical for Abeta aggregation or for the inhibition of Abeta aggregation; steric packing of hydrophobic residues--rather than aromatic pi-stacking interactions--promotes Ab [...]","Knockdown of retromer activity produces no change in the quantity or cellular distribution of total cellular APP and has no affect on internalization of cell-surface APP.\n","Cell viability studies of SH-SY5Y cells and rat primary hippocampal neurons showed that exogenous heme can protect the cells by reducing cytotoxicity in the presence of Cu(2+) and/or amyloid beta (1-40).\n","mice overexpressing mutations in the human amyloid precursor protein gene (APP) showed preserved spontaneous respiration up to 12mo, but starting at 14mo showed significant differences from WT.\n","Phosphorylation of Abeta at serine residue 8 could represent an important molecular mechanism in the pathogenesis of the most common sporadic form of Alzheimer's disease.\n","These results suggest an unexpected function of APPswe/Abeta, reveal a mechanism underlying altered bone remodeling in Alzheimer's disease (AD) patients, and implicate APP/Abeta and RAGE as common denominators for both AD and osteoporosis.\n","malfunction of neprilysin in infected macrophages may contribute to acceleration of beta amyloidosis in HIV-inflicted brains\n","[review] The impact of SorLA on the cellular processing of amyloid precursor protein (APP) is an important component in Alzheimer's disease.\n","The ratios of total tau to amyloidbeta1-42 and p-tau181 to Abeta1-42 outperforms any single analyte, including Abeta1-42, in discriminating individuals with vs without cortical amyloid in a large cohort of research participants.\n","Collectively, our results demonstrate that APP intracellular domain functions as a negative regulator in Notch1 signaling through the promotion of Notch1 and RBP-Jk protein degradation\n","Abeta impairs the assembly and maintenance of the mitotic spindle.\n","Comparison with an earlier APP structure, which was determined in a different space group, shows that the E2 domains share a conserved and antiparallel mode of dimerization. Heparin binding induces E2 dimerization.\n","Knock-in mice with familial Danish dementia, a mouse model congruous to human disease since they carry one mutant and one wild-type Bri2 allele, show that the Danish mutation causes loss of Bri2 protein, synaptic plasticity and memory impairment.\n","Data suggest that APP/SOD1 overexpressing mice are less sensitive for neuropathic pain associated with neuroma.\n","These novel APP-hESC lines represent a valuable tool to investigate the potential role of APP in development and neurodegeneration and allow for insights into physiological functions of this protein.\n","Monte Carlo study of Abeta42 finds the probability of turns centered in the 25-30 region of Abeta42, where there is a loop in Abeta fibrils, to increase upon dimerization and to correlate with experimental rates of fibril formation for the different  [...]","The Abeta42-induced presenilin-1 (PS1) increase is abolished by small interfering RNA acetylcholinesterase (AChE) pretreatment, demonstrating its participation in the pathological feedback loop between PS1 and Abeta.\n","Mechanistic insights into processes involved in Abeta1-42 assembly in the presence of Abeta C- terminal fragments (CTFs) provide an explanation of the putative mechanism(s) by which these CTFs inhibit Abeta toxicity.\n","Our mild cognitive impairment patients with lower APP levels and an increased P-tau(181p) /APP ratio progressed quickly to Alzheimers disease\n","a possible involvement of CD36 and SR-B1 in microglial interaction with amyloidogenic fragments of beta-amyloid and prion proteins\n","Data show that interaction of IAPP-GI with Abeta resulted in a concentration-dependent co-aggregation of Abeta and IAPP-GI that was enhanced for the more aggregation prone Abeta42 peptide.\n","Neuronal-glial, astroglial and microglial cell types from Alzheimer brain each respond differently to Abeta42-peptide+tumor necrosis factoralpha-triggered stress.\n","elevation in Abeta secretion by BACE1-GPI is mainly attributed to preferential cleavage at the beta-site and failure to detect +11 Abeta species secreted by cells expressing WTBACE1\n","Cu(II) mediates kinetically distinct, non-amyloidogenic aggregation of amyloid-beta peptides\n","Aluminum lactate did not alter the recognition memory and beta-amyloid plaque loads of Tg2576 mice overexpressing the human amyloid precursor protein.\n","Low-density lipoprotein receptor-related LRP-carboxy terminal domain and APP compete for binding to Fe65 protein interaction domain 2.\n","Promoter mutations or common allelic variation in the AbetaPP gene do not have a major contribution to cortical or cerebrovascular Abeta deposition, or very late-onset Alzheimer disease.\n","Platelet APP could be considered a potential reliable peripheral marker for studying Alzheimer's disease.\n","Consistent with neuropathological findings from postmortem studies, positron emission tomography shows high binding levels of amyloid-beta protein in Down syndrome comparable to Alzheimer disease and greater levels than in members of a control group.\n","5-HT4 receptor binding was a positively correlated to amyloid beta (A4) burden and negatively to MMSE score of the Alzheimer disease patients\n","Performance on a demanding test of face-name associative memory was related to Abeta burden in brain regions associated with memory systems. Associative memory for faces and names may be a sensitive marker of early Abeta-related impairment.\n","NCAM-140 interacts with APP, potentially playing a role in neurite outgrowth and neural development.\n","we reviewed homology and structures of AbetaPP family members in organisms and further discussed potential biological function in normal and Alzheimer's disease brains--{REVIEW}\n","This method can be used to enhance our understanding of the biological processes dependent upon AbetaPP-AbetaPP interactions\n","we found out in frontotemporal dementia a significant decrease of cerebrospinal fluid sAbetaPPbeta\n","the high-resolution structure of Abeta1-40 at 15C at pH 7.3 with 50 mM NaCl was soled. Under this condition Abeta1-40 adopts a folded conformation notably different from that seen in most previous NMR experiments.\n","Isolation of proteins that are oxidatively modified in APP/PS1 mice compared to age-matched controls.\n","sAPPalpha levels are generally elevated in severe autism.\n","A modified formulation of Chinese traditional medicine SuHeXiang Wan improves memory impairment and reduces Abeta level in the Tg-APPswe/PS1dE9 mouse model of Alzheimer's disease.\n","examined the crystal structure of the complex between the catalytic domain of FXIa and the Kunitz protease inhibitor domain of protease nexin 2; Six FXIa catalytic domain residues were subjected to mutational analysis to examine molecular interactions\n","S100B and APP levels are simultaneously increased within Down syndrome neural progenitors, their secretions are synergistically enhanced in a paracrine fashion, and their overexpressions disrupt mitochondrial membrane potentials and redox states.\n","The PACT/protein kinase PKR pathway represents a potential link between Abeta accumulation, PKR activation and tau phosphorylation.\n","Although PrP(C) exerts no control on cleavage of APP(Swe) by BACE1, it has a profound influence on the cleavage of APP(WT), suggesting that PrP(C) may be a key protective player against sporadic Alzheimer disease.\n","Beta-amyloid peptide variants in brains and cerebrospinal fluid from amyloid precursor protein (APP) transgenic mice: comparison with human Alzheimer amyloid.\n","Observations of molecular dynamics simulations characterize the tertiary structure ensemble of Abeta42 and Abeta21-30 fragments from the perspective of their classification as intrinsically disordered peptides\n","APP intracellular domain (AICD) is stabilized and the AICD mediated transcriptional activity is promoted by canonical Wnt/beta-catenin signaling independent of Fe65.\n","Positional effects of phosphorylation on the stability and morphology of tau-related amyloid fibrils\n","NMR is used to evidence Fe(II) coordination to full-length amyloid beta 40 and truncated amyloid beta 16 peptides at physiological pH and to show that the Fe(II) binding site is located in the first 16 amino-acid residues.\n","eye-specific expression of human ABETA42 in Drosophila results in a degeneration of eye structures that progresses with age.\n","Plasma Abeta(1-42) shows mild correlation with other biomarkers of Abeta pathology and is associated with infarctions in magnetic resonance imaging.\n","Experimental multinutrient protection of rat cholinergic system against Abeta42-induced toxicity suggests a role for nutrition in management of Alzheimer's disease.\n","These results demonstrate a spatial separation between APP and BACE1 during surface-to-endosome transport, suggesting subcellular trafficking as a regulatory mechanism for this proteolytic processing step.\n","Within each Alzheimer clinical group the cerebrospinal fluid (CSF) Abeta42 marker level is abnormal more often than is the CSF total tau level or the adjusted hippocampal volume.\n","we utilized an ex vivo assay to demonstrate that adult astrocytes respond to human Abeta by upregulating neprilysin expression\n","Interactions of pathological hallmark proteins: tubulin polymerization promoting protein/p25, beta-amyloid, and alpha-synuclein.\n","Polymorphic triple beta-sheet structures contribute to amide hydrogen/deuterium (H/D) exchange protection in the Alzheimer amyloid beta42 peptide.\n","ursolic acid inhibits amyloid beta protein interactions with its receptor CD36\n","Amyloid beta-peptide binds to the extracellular domain of neuroligin-1 with a K(d) in the nanomolar range.\n","Neurological effects of the Danish form of BRI2 dementia caused by toxic amyloid Abeta protein precursor metabolites suggest that familial Danish and Alzheimer's dementias share common pathogenic mechanisms.\n","The concentration of N-acetylaspartate marker is coupled with neuronal mitochondrial function and correlates with cerebrospinal fluid amyloid Abeta42 peptide fragment deposition in the brain.\n","The tryptophan substitutions at amyloid beta (1-40) positions F19 and F20 revealed clear environmental differences between the two residues after fibril formation.\n","Familial Alzheimer disease patients with Osaka mutation of APP show severe dementia, cerebellar ataxia, and gait disturbances\n","APP, specifically tyrosine residue 682, regulates activation of the nerve growth factor NGF/TrkA receptor signaling pathway in vivo, the subcellular distribution of TrkA and the sensitivity of neurons to the trophic action of NGF.\n","Abeta1-42-, but not Abeta42-1-, induces inflammatory responses characterized by increases in markers for rat microglia and astrocytes and increases in rat mRNA for inflammatory cytokines and chemokines.\n","ubiquilin-1 chaperone activity is necessary to regulate the production of APP and its fragments and that diminished ubiquilin-1 levels may contribute to AD pathogenesis.\n","Data suggest that a deficiency of cellular neuroprotective mechanisms (decrease of sAPP) is linked to progressive neuro-axonal damage (increase of NfH(SMI35)) and to progression of disease.\n","End-stage Abeta and tau pathologies in triple transgenic Alzheimer's disease (AD) model mice are similar to those observed in sporadic AD, but the pathophysiological mechanisms leading to these lesions are quite different.\n","Abeta1-16 peptide fragment aggregates and forms oligomers and fi brils mainly possessing regular non-amyloid -sheet and -turn structures that are toxic to cells and can contribute to Alzheimer's disease pathogenesis.\n","In cognitively normal older adults, higher choline/creatinine is associated with worse performance on domain-specific cognitive tests independent of Abeta load and magnetic resonance spectroscopy metabolite changes.\n","e 624 of the amyloid precursor protein (APP) is a critical determinant of amyloid beta peptide length: support for a sequential model of gamma-secretase intramembrane proteolysis and regulation by the amyloid beta precursor protein (APP) juxtamembrane region\n","the GXXXG motif within APP appeared to be critical to GSM activity\n","Data report that annular protofibrils (APFs) are in human Alzheimer's disease brain samples and that amyloid-beta APFs are associated with activated astrocytes.\n","BRI2 protein regulates beta-amyloid degradation by increasing levels of secreted insulin-degrading enzyme (IDE).\n","Human mesenchymal stromal cells and their neuronally differentiated counterparts are susceptible to the aggregated toxicity of Abeta42 oligomers.\n","sAPPalpha is a proliferation factor of adult progetitor cells\n","Comprehensive solid-state NMR studies on well-ordered fibril samples of ABETA(40) with an additional N-terminal methionine provide high-resolution spectra which lead to an accurate structural model.\n","Striatal-enriched protein tyrosine phosphatase (STEP) of 61 kDa is required for Abeta transgene-mediated internalization of GluA1/GluA2 glutamate receptors in an in vitro mouse model.\n","An abnormal cerebrospinal fluid (CSF) Abeta level is associated with greater hippocampal volume loss over 1 year in patients with mild cognitive impairment.\n","The transmembrane (TM) domain of APP, APPTM was studied.  Using the pETM41 vector, an MBP-APPTM fusion protein was successfully expressed.\n","Study of combined cerebrospinal fluid biomarkers beta-amyloid(42), tau, and phosphorylated tau (ptau181) with education and normalized whole-brain volume predicts incident cognitive impairment.\n","Data show that ABETA-heme peroxidase activity is independent of the aggregation state of ABETA, suggesting an important role of soluble ABETA in addition to ABETA aggregates and oligomers in Alzheimer's disease pathogenesis.\n","Factors that control initial proteolysis of APP at the epsilon-cutting site of proteolytic activity apparently differ significantly from factors affecting subsequent trimming and distribution of APP beta-peptides.\n","These results indicate that a helical intermediate precedes the aggregation of the amino-terminal fragment of the beta amyloid peptide (Abeta(1-28); however, starting the simulations from helical conformations does not speed up the process.\n","[review] The physiological function of APP cannot be explained by the focus on APP protein alone but rather in combination with various direct or indirect interaction partners within the cellular environment.\n","Beta-Amyloid protein and amylin regulated apoptotic genes through the amylin receptor.\n","The heterogeneity of Abeta-specific CD4+ T cell responses in mice is related to qualitative and quantitative differences in Abeta-derived epitopes restricted to various histocompatibility type II alleles.\n","To elucidate Abeta polymorphism in atomic detail, we determined microcrystal structures of fiber-forming segments. These structures, all of short, self-complementing pairs of beta-sheets termed steric zippers, reveal a variety of modes of self-association.\n","Autophagosomes accumulate within thalamic cells after cerebral cortical infarction, which is associated with thalamic APP deposition and secondary neuronal degeneration via elevated levels of beta-site APP-cleaving enzyme 1 BACE1).\n","administration of freshly prepared Abeta42 oligomers to a neuroblastoma (SH-SY5Y) cell line results in a reduction in survival, and that Abeta42 enters the cells prior to cell death.\n","ADAM10 activity is regulated by inhibition of ADAM9, and this regulation may be used to control shedding of amyloid precursor protein by enhancing alpha-secretase activity, a key regulatory step in the etiology of Alzheimer disease\n","Overexpression of APP causing widespread neurodegeneration could be rapidly rescued by reducing APP expression levels in immature neurons.\n","the PSEN1, PSEN2, and APP genes exhibited no pathogenic mutations in our cohort of early-onset Alzheimer disease and frontotemporal lobar degeneration patients\n","[review] Understanding neuron-specific mechanisms of APP processing helps to illuminate the physiological roles of APP-derived proteolytic fragments, providing novel insights on Alzheimer's disease pathogenesis.\n","simulation study of coherent two-dimensional chiral signals of three NMR structures of Abeta protein fibrils associated with Alzheimer's disease, two models for Abeta(8-40) peptide wild-type (WT) and one for the Iowa (D23N) Abeta(15-40) mutant\n","Pyroglutamate amyloid-beta (Abeta): a hatchet man in Alzheimer disease.\n","beta-sitosterol effectively inhibited high cholesterol-driven platelet Abeta release. In addition, beta-sitosterol prevented high cholesterol-induced increase of activities of beta- and gamma-secretase\n","Disordered binding of small molecules to Abeta(12-28).\n","Cerebrospinal fluid soluble amyloid-beta protein precursor concentrations may be considered as an extension of already available neurochemical dementia diagnostics tools in Alzheimer's disease patients.\n","independent relationship between amyloid-beta and tau in controlled cortical impact model (CCI) of traumatic brain injury\n","report an EPR, CD and NMR study of Cu(II) binding to the Abeta peptide and to ten mutants; describe the pH dependent Cu(II) binding to this series of peptides from pH 4 to 12\n","ERalpha and metabotropic (mGlu1) receptors interact in neurons to produce neuroprotection against beta-amyloid toxicity.\n","the oligomerization of Abeta42 in the context of a fusion protein containing GroES and ubiquitin fused to the N-terminus of Abeta sequence was investigated.\n","gamma-Secretase modulators did mot exert their modulatory effect by directly targeting a site located in the Abeta42 domain of free C99.\n","A specific fragment of Abeta serves as a generating site for senile plaque formation in this study of Alzheimer's disease cerebral cortex.\n","the effect of the APP-sw mutation on alteration of DNA methylation and subsequent gene expression was demonstrated.This epigenetic regulatory mechanism may contribute to the pathogenesis of Alzheimer's disease.\n","Data indicate that Abeta-associated volume loss occurs only in the presence of phospho-tau in humans at risk for dementia.\n","Induction of c-Myc by amyloid-beta peptide or other disease factors may be key to mediation of cell cycle activation and consequent cell death that is a feature of neurodegenerative diseases.\n","Inoculation of Abeta3-10 fragment induces a predominant humoral response and production of interleukin (IL)-4 and IL-10 in splenocytes in vitro, indicating a T helper cell type 2-polarized immune response.\n","Soluble and insoluble amyloid beta peptide (Abeta) and oligomers increase as a function of age in DS frontal cortex.\n","Very early expression of noncognitive Alzheimer-like symptoms (i.e., deficits in social interest, interaction and communication) is demonstrated in APP and APP-presenilin 1 transgenic mice.\n","hUCB-MSC-derived sICAM-1 decreases Abeta plaques by inducing NEP expression in microglia through the sICAM-1/LFA-1 signaling pathway.\n","The results of this study demonistrated that common variants at AbetaPP, PSEN1, and PSEN2 and MAPT are unlikely to make strong contributions to susceptibility for late onset Alzheimer's disease.\n","study found links between Abeta, endocytosis, and human Alzheimer's disease risk factors can be ascertained with yeast as a model system\n","Alteration of glycosaminoglycans in hippocampus of aged subjects could participate in tissue impairment during aging.\n","Data suggest that HEs-1/Hey-1 transcriptional modulation of insulin degrading enzyme may impact amyloid beta metabolism by providing a functional link between Notch signaling and the amyloidogenic pathway.\n","The results of this study demonstrated that upregulation of APP upregulation of BACE1 is an ancient, conserved, and thus selectively advantageous response to hypoxia/oxidative stress.\n","The results of this study do not support a pathogenic role of AbetaPP overexpression in sporadic AD although a small subset of patients displays AbetaPP overexpression in the same range as Down syndrome patients.\n","Within a spectrum of normal aging cardiovascular disease and Abeta aggregation appear to be independent processes with cardiovascular disease primarily affecting cognition.\n","Regulation of the amyloidbeta-induced formation of autophagic vacuoles by the RAGE-calcium-CaMKKbeta-AMPK pathway.\n","The results of thia study illuminated the in vivo dynamics of soluble Abeta during the development of AD-type neuropathology and after gamma-secretase inhibition and help explain the apparent paradox that CSF Abeta(42) levels fall as humans develop AD.\n","Phase diagram of polypeptide chains of amyloid fibrils was studied.\n","SOD1 (copper/zinc superoxide dismutase) deficiency drives amyloid beta protein oligomerization and memory loss in mouse model of Alzheimer disease.\n","the PS1 complex is only marginally less active than the PS2 complex in Abeta production.\n","Data show that transgenic sAPP-alpha-overexpressing (TgsAPP-alpha) mice displayed increased proportions of CD8(+) T cells, while effector memory T cells were decreased in the thymus.\n","Studied dimerization of APP isoforms and mutants. APP751 formed more homodimers than APP695. Mutation of dimerization motifs in the TM domain did not affect fluorescence complementation, but native folding is critical for APP751 homodimerization.\n","Abeta42 globulomers have an antiparallel beta-sheet arrangement\n","This review proposes that a reduction of APP processing along the non-amyloidogenic pathway during brain aging may result in an enhanced susceptibility of neurons to cellular stress and could contribute to neurodegeneration in Alzheimer's disease.\n","Down-regulation of the ATP-binding cassette transporter 2 (Abca2) reduces amyloid-beta production by altering Nicastrin maturation and intracellular localization.\n","A molecular understanding of the interactions of apoE4 with Abeta, NO and IL-1beta on the regulation of the COX-2/prostaglandin pathway may open new avenues in understanding the mechanism of development of neurodegenerative disease.\n","The study provides first evidence that a fraction of APP can associate via intermolecular disulfide bonds, likely generated between cysteines located in the extracellular E1 domain.\n","upregulation of macroautophagy and resulting Lysosomal Abeta accumulation are essential for oxidant-induced apoptosis in cultured neuroblastoma cells.\n","This work supports that cholesterol acts as a promoter for Abeta-membrane interactions, which would facilitate Abeta aggregation and membrane insertion.\n","In triple transgenic Alzheimer's disease mice accumulate amyloid-beta protein precursor instead of amyloid-Beta within neurons.\n","MOCA is a key molecule of the Alzheimer disease-relevant neuronal death signals that links the presenilin-mediated death signal with the APP-mediated death signal at a point between Rac1 or Cdc42 and ASK1.\n","APP contributes to changes in brain microvessel tight junction and matrix metalloproteases expression, which compromises blood-brain barrier integrity\n","Amyloid-beta is differentially implicated in Alzheimer's disease with microbleeds and vascular dementia.\n","Abeta wild-type and Abeta Arctic peptides of amyloid protein precursor codeposited; Alzheimer brain parenchymal deposits are highly enriched in both N- and C-terminally truncated Abeta.\n","A novel pathway that regulates ATP-binding cassette sub-family A protein (ABCA)1 expression may provide new strategy for regulating cholesterol metabolism and Abeta levels via miR-106b.\n","[review] Normal brain function is highly sensitive to any changes in APP metabolism and microRNAs function at several steps to ensure that the correct APP end product is produced and in the right form and abundance.\n","This review discusses current understanding about endogenous oligomeric Abeta production and relative toxicity in vivo and in vitro, and potential future directions needed for Alzheimer research.\n","This review explores the role of heavy metal ions in Alzheimer disease, in brain tissue, blood, and cerebral spinal fluid and how iron, copper, and zinc may be involved through their interactions with APP.\n","This review suggests that amyloid beta-induced impairment in synaptic plasticity that is accompanied by cognitive decline and dementia represent key pathogenic steps of Alzheimer's disease.\n","This review describes the mechanisms involved in APP metabolism and the likely functions of its various proteolytic products to give a better understanding of the pathologic and physiological functions of APP.\n","The structural properties of the Asp1-Lys16 and Asp1-Lys28 regions of the full-length amyloid beta peptide 42 cannot be captured fully by studying the smaller amyloid beta 16 and amyloid beta 28 fragments.\n","The carboxyl-terminal fragment Abeta(39-42) inhibits full-length amyloidbeta-induced toxicity by a unique mechanism, modulating early assembly into nontoxic hetero-oligomers, without preventing fibril formation.\n","Simple benzoic acid derivatives distinguished by the number and position of hydroxyls on the aromatic ring display different abilities to dissociate preformed biotinyl-Abeta(1-42) oligomers.\n","Dynamics of amyloid beta fibrils revealed by solid-state NMR.\n","apoE-induced intracellular Abeta degradation is mediated by the cholesterol efflux function of apoE, which lowers cellular cholesterol levels and subsequently facilitates the intracellular trafficking of Abeta to lysosomes for degradation.\n","Lacmoid binds Abeta(1-40) in a surfactant-like manner and counteracts the formation of all types of Abeta(1-40) and Abeta(1-42) aggregates.\n","the N-terminal region containing the leucine-rich repeats along with the transmembrane and cytoplasmic domains of LINGO-1 are not required for self-interaction or interaction with APP\n","This study provides a mechanistic insight into the kinetic evolution of cell-toxic assemblies in mixtures of ABETA with the highly amyloidogenic IAPP under cellular membrane-like conditions.\n","ApoE-containing astrocyte lipoproteins exhibit the most robust interactions with Abeta.\n","Abeta mediates inhibition of the DNA-PK-dependent nonhomologous end joining pathway contributing to the accumulation of DSBs that, if not efficiently repaired, may lead to the neuronal loss observed in AD.\n","Structural and aggregation data indicate that Zn(II) binding induces the formation of the dimeric Zn(II)(1)(ABETA 11-28)(2) species, which is the building block of fibrillar aggregates and explains why Zn(II) binding accelerates ABETA 11-28 aggregation.\n","This review suggests that the properties of Abeta monomers and the neurotrophic capacity of soluble APPbeta to stimulate axonal outgrowth suggest that Abeta production is not deleterious per se.\n","findings suggest that Abeta metabolism may be affected in depression.\n","Butyrylcholinesterase-positive plaques are Abeta positive, and butyrylcholinesterase may play a role in Alzheimer's disease maturation. plaque maturation.\n","Cerebrospinal fluid amyloid beta42 protein, total tau, and phosphorylated tau are useful biomarkers in differential dementia diagnosis.\n","disposition of Abeta and tau is likely important in both LRRK2-related and sporadic Parkinson disease, even during early phases of the disease\n","APP.V7171 mice are trained and cognitively capable of learning normally when co-housed with their wild-type littermates, in contrast with clearly impaired learning observed when the transgenic mice are housed alone.\n","The gas-phase basicity of the peptide charge state and ligand drive the type of complexes amyloid beta 1-40 peptide forms with various amino sugars, irrespective of their structural differences.\n","[review] Abeta as well as other APP cleavage products play an essential role in regulating lipid homeostasis, arguing for complex regulatory cycles in which lipids control APP processing and vice versa.\n","influence both the aggregation and disaggregation of amyloid-beta(1-40) peptide by sequestration of the amyloid beta oligomers.\n","Rare coding variants in APP, PSEN1 and PSEN2, increase risk for or cause late onset Alzheimer's disease\n","Below the bilayer melting temperature, Abeta(1-40) monomers adsorb to, and assemble on, the surface of dipalmitoyllecithin bilayers to form layers that grow laterally and normal to the bilayer plane.\n","Amyloid beta production/accumulation in the retina is common to different degenerative retinal pathologies.\n","a novel role of Pin1 in inhibiting GSK3beta kinase activity to reduce APP protein levels, providing a previously unrecognized mechanism by which Pin1 protects against Alzheimer disease.\n","alpha-Secretase-derived fragment of cellular prion, N1, protects against monomeric and oligomeric amyloid beta (Abeta)-associated cell death.\n","APOE isoforms modulate the harmful effects of amyloid beta on cognitive function\n","our results reveal that, APP may be one of the physiological proteolytic targets of matrix metalloproteinase 9\n","These data provide the first direct evidence in living humans that ischemia acutely increases Abeta levels in blood.\n","Bone marrow stromal cell transplantation retards Alzheimer's disease-like pathology and upregulates deltaNp73 expression in hippocampuses of amyloid peptide precursorAPP/PS1 transgenic mice\n","Dietary fat markedly deteriorates memory impairment and increases beta-amyloid oligomers as well as Abeta deposition in amyloid precursor protein (APP) transgenic mice, which is reversed by exposure to an enriched environment.\n","Ths amyloid precursor protein transgenic J20 mice perform normally in tasks for fear conditioning, short-term object recognition and short-term memory of context familiarity but exhibit a robust spatial reference memory impairment.\n","The homocysteinylation of lysine residues increase the neurotoxicity of the Abeta peptide by stabilizing soluble oligomeric intermediates.\n","A link is demonstrated between hippocampal amyloid beta deposits and the dysfunction of a specific pathway involved in memory processes of Alzheimer's disease.\n","In vivo calpain inhibition mediated by calpastatin transgene expression reduces Abeta pathology in APP23 mice.\n","Pathologically low cerebrospinal fluid levels of beta-amyloid 1-42 (1-42) in clinic patients with mild cognitive impairment (MCI) predict conversion from MCI to Alzheimer dementia\n","This study showed down regulation of PS1 and amyloidbeta42 in IMR32 cells transfected with siRNA against presenilin1. The results provide the rationale for therapeutic strategies aimed at influencing amyloidbeta42 production.\n","The study shows a direct structural evidence of the pore-like morphology of the natural l-ABETA 1-42 peptide and its mirror image, the d-ABETA 1-42 isomer.\n","Abeta42 may increase the BACE1 level independently of either Cdk5 or caspase 3 and that Cdk5 inhibition for AD may cause BACE1 elevation, a potentially negative therapeutic outcome.\n","Using in vivo electrophysiological methods, early Abeta-related functional deficits can be robustly detected in the brainstem-hippocampus multisynaptic network with age.\n","analysis of plaque formation in a mouse model of Alzheimier's disease transgenic for human APP and PS1 mutations with reduced serum IGF-I levels\n","Amyloid-beta protein precursor, in addition to amyloid formation, modulates the phosphorylation of tau and its subcellular compartmentalization.\n","It can be concluded that Abeta1-42 and phosphorylated-tau reliably predict conversion to Alzheimer's disease in mild cognitive impairment patients.\n","Amyloid-beta oligomers induce differential gene expression in adult human brain slices.\n","Lower concentrations of Abeta (1-42) and Abeta (1-40) were attributed to loss of Abeta equilibrium between the brain and blood\n","Study of non-natural Abeta1-42 amino acid substitutions is useful for results of their Abeta channel membrane toxicity in bilayers to gain information about structural requirements for optimizing the models.\n","The novel high-affinity binding site for copper and zinc in the amyloid precursor protein E2 domain was characterized. Metal-specific coordination spheres induced large conformational changes and enforced distinct structural states.\n","The effect of Abeta (at different concentrations) on the neurotransmitter release stimulated by the activation of pre-synaptic cholinergic nicotinic receptors (nAChRs, alpha4beta2 and alpha7 subtypes), is reported.\n","Measures of platelet APP and immunoglobulin merit further study as potential peripheral biomarkers for Alzheimer's disease.\n","A neuroproprotective function of APP and fly APPL (amyloid precursor protein-like) is achieved in vivo in several Drosophila mutants with progressive neurodegeneration.\n","Phosphorylation of amyloid-beta peptide at serine 8 attenuates its clearance via insulin-degrading and angiotensin-converting enzymes.\n","Biochemical inhibition of the acetyltransferases ATase1 and ATase2 reduces beta-secretase (BACE1) levels and Abeta generation.\n","analysis of how Abeta toxicity and tau are physiologically connected, and how membrane trafficking may play an important role in the pathogenesis of Alzheimer's disease [review]\n","Data suggest that KLC1 is required for normal neural differentiation, ensuring proper metabolism of AD-associated molecules APP and Tau and for proliferation of neural precursors (NPs).\n","The structured state of Abeta40 monomer has three more ordered segments at 14-18, 29-30, and 38-40.\n","While intracellular membrane expression of Abeta1-42 in transgenic mice does not lead to lesions typical of Alzheimer's disease, Abeta aggregates develop within cells accompanied by considerable neurodegeneration.\n","As a major driving force, the authors identify the electrostatic interactions between Abeta charged side chains, including E22, D23, and K28, and lipid headgroups of lipid membranes.\n","A nucleation-dependent polymerization model of Abeta peptide is indicated by the presence of a nucleation phase followed by an exponential growth phase during the early stages of amyloid formation at the nanometer level.\n","The conformational ensemble of ABETA 17-42 trimer can be described by 14 clusters with each peptide essentially adopting turn/random coil configurations; the most populated cluster is characterized by one peptide with a beta-hairpin at Phe19-Leu31.\n","This study measured levels of alpha-cleaved soluble APP (alpha sAPP) and beta-amyloid 42 (Abeta42) in the cerebrospinal fluid (CSF) of 42 multiple sclerosis, 10 neuromyelitis optica and 25 clinically isolated syndrome patients and 21 healthy controls.\n","Detailed Abeta structural changes upon loss of helicity in the presence of the ligands are also revealed, which gives further insight into which ligand may lead to which path subsequent to unwinding of the Abeta central helix.\n","A unique mechanism of interleukin (IL)-4/IL-13-induced clearance of amyloidbeta may provide an additional strategy to prevent and/or cure Alzheimer's disease in young transgenic mice.\n","H component of CUTA as a novel BACE1-interacting protein that mediates the intracellular trafficking of BACE1 and the processing of APP to Abeta\n","an autoinhibitory mechanism in Mint1 is important for regulating APP processing and may provide novel therapies for Alzheimer's disease\n","This study aimed to clarify the role of APP intracellular domain in regulating PrP(C).\n","Abeta-induced release of gliotransmitter ATP plays a protective role against Abeta(1-42)-mediated disruption of synaptic plasticity.\n","thioflavin T binds to amyloid fibrils, which can be assessed through the equilibrium microdialysis-based technique\n","Tacrine-6-ferulic acid, a novel multifunctional dimer, inhibits amyloid-beta-mediated Alzheimer's disease-associated pathogenesis in vitro and in vivo\n","Myr and RA may play key roles in blocking the toxicity and early assembly processes associated with Abeta through different binding.\n","metabolomic signatures of PS1, APP, and APP/PS1 indicate individual differences and common metabolic traits in disease development and progression\n","F-box and leucine rich repeat protein (FBL)2 binds APP specifically at its C-terminal fragment (CTF), which promotes APP/CTF ubiquitination.\n","the antiparallel D23N-Abeta(1-40) fibril model represents a specific \"toxic intermediate\" in the aggregation process of a disease-associated Abeta mutant\n","If this stable device can be developed, it would be highly interesting to monitor Ab40/42 concentrations in real time at different sites in the brain\n","t aberrant Abeta production might be a mechanistic link underlying the pathology of insulin resistance and type 2 diabetes mellitus and Alzheimer's disease\n","[review] The amyloid hypothesis of Alzheimer's disease recognizes the Abeta peptide as principal player in the pathological process and highlights the soluble Abeta oligomer accumulation, rather than insoluble Abeta fibrils and disease progression.\n","effect of APP gene on synaptotagmin 1 mRNA level\n","findings show that calsyntenin-1 is reduced in Alzheimer's disease brains and that the extent of this reduction correlates with increased amyloid-beta\n","A chemical analog of curcumin as an improved inhibitor of amyloid Abeta oligomerization.\n","the formation of extended beta-strands by monomeric Abeta proteins suggests a plausible mechanism whereby the formation of amyloid fibrils may be nucleated in the human brain\n","The structural properties of dimers from molecular dynamics studies\n","Our data suggest a correlation between the role of APP intracellular C-terminal domain in gene regulation and its removal operated by proteasome activity.\n","The Abeta domain directly mediates a central step in APP trafficking, driving its own conversion into neurotoxic peptides.\n","new mouse line based on the presence of 2 copies of the human genomic region encoding the wild-type AbetaPP and the L166P presenilin 1 mutation; neither mutations in AbetaPP nor overexpression of an AbetaPP isoform are a prerequisite for Abeta pathology\n","Small amphipathic molecules modulate secondary structure and amyloid fibril-forming kinetics of Alzheimer disease peptide Abeta(1-42).\n","APP secretion from the calpain overexpressing cells was robustly increased under both resting and stimulated conditions over wild-type cells.\n","Small soluble Abeta oligomers possess a much greater neurotoxicity than mature amyloid fibrils and are highly dynamic and polymorphic, as characterized by circular dichroism, size exclusion chromatography and top-down hydrogen exchange mass spectrometry.\n","A cerebrospinal fluid model transforms values for tau and amyloid beta(1-42) detected by the xMAP platform, showing that patients with autopsy-confirmed Alzheimer's and frontotemporal lobar degeneration are differentiated with high sensitivity.\n","occurrence and generation of APP N-terminal fragments in cell culture (SH-SY5Y) in order to delineate the cellular pathways implicated in their generation\n","Soluble amyloid precursor protein-alpha modulates BACE1 activity and amyloid-beta generation.\n","study shows that APP mutations and locus duplications are a very rare cause of EOFAD and that the contribution of common APP variants to AD susceptibility is insignificant.\n","The association between low plasma Abeta42/Abeta40 and increased risk of incident depression among those with one or more apolipoprotein E e4 allele implies a synergistic relationship similar to that found with dementia.\n","This review describes the identification of regulatory RNA binding proteins, where and under what conditions they interact with APP mRNA and how those interactions control AbetaPP and Abeta synthesis.\n","The expression of APP mRNA fell by 31 +/- 9%, and that of protein fell by 36 +/- 14% after gastric bypass surgery.\n","Levels of miR-153 are significantly decreased at early- and late-stage of Alzheimer's disease in a APPswe/PSDeltaE9 murine model.\n","Due to the K16N mutation APP secretion is affected and a higher amount of Abeta peptides is being produced.\n","studies clarify the function of the neuronal retromer, and suggest specific mechanisms for how retromer dysfunction observed in Alzheimer's disease affects APP transport and processing.\n","The present study uses high-resolution NMR spectroscopy to monitor the residue-specific interactions of Cu(II) and Zn(II) with (15)N- and (13)C,(15)N-labeled Abeta(1-40) peptides at varying pH levels.\n","Cerebrospinal fluid (CSF)Abeta42, total tau, and phosphorylated tau levels differentiate between Alzheimer's disease and depression in a Brazilian sample.\n","Increased cerebrovascular fluid (CSF) concen-trations of amyloidbeta(1-15/16) peptide measured by high-throughput immunoassay is useful as a biomarker for secretase inhibition in Alzheimer disease.\n","an effective modulation of gamma-secretase activity by membrane thickness, which may provide an approach to lower the generation of the pathogenic Abeta(42/43) species.\n","PICALM, an adaptor protein involved in clathrin-mediated endocytosis, regulates APP internalization and subsequent Abeta generation. PICALM contributes to amyloid plaque load in brain likely via its effect on Abeta metabolism.\n","Specific soluble oligomers of amyloid-beta peptide undergo replication and form non-fibrillar aggregates in interfacial environments.\n","APOE differentially regulates multiple aspects of Abeta accumulation.\n","Wild-type human APP rescues the defective phenotype caused by knockdown of amyloid precursor protein in zebrafish but APPswe mutation, which causes familial Alzheimer's disease, does not.\n","the weakened neuronal binding follows the mutation order of H13G < H14G < H13,14G in amyloid beta-protein, this suggests that there are multiple pathways of binding/internalization for the different Abeta proteins\n","findings show that decreased plasmalogen levels are not only a consequence of AD but that plasmalogens also decrease APP processing by directly affecting gamma-secretase activity\n","Higher dietary intake of omega-3 PUFA is associated with lower plasma levels of Abeta42, a profile linked with reduced risk of incident Alzheimer's disease and slower cognitive decline in a healthy elderly cohort.\n","Data show that cleavage of amyloid precursor protein (APP) by beta-site amyloid precursor protein (APP)-cleaving enzyme 1 (BACE1) occurs in post-endoplasmic reticulum (ER) compartments.\n","Transmission electron microscopy shows that the regular fibrillar aggregates formed by Abeta(1-40) alone are replaced by a major fraction of amorphous aggregates in the presence of the beta-cyclodextrin dimer.\n","Alterations in the circuitry of the cerebellar cortex permit better understanding of the amyloid-beta deposition resulting in impaired cerebellar function in AbetaPP/presenilin-1 transgenic mice and the implications in familial Alzheimer's disease.\n","Frontal and temporal amyloid-reduced activation/suppression was associated with poorer processing speed, verbal fluency, and fluid reasoning in a subgroup with elevated amyloid, suggesting it is detrimental, rather than compensatory in nature.\n","Cholesterol sequestration in Abeta-treated neurons results from impairment of intracellular cholesterol trafficking secondary to inhibition of protein prenylation.\n","NDM29-dependent cell maturation induces amyloid precursor protein (APP) synthesis, leading to the increase of amyloid beta peptide (Abeta) secretion.\n","The dimerization mechanism of APP transmembrane domain is described at atomic resolution for the first time.\n","Although intraresidue contacts between Glu-22 and Ile-31 were found in Abeta protofibrils, these contacts were completely absent in mature Abeta fibrils.\n","Data show that that soluble amyloid-beta (Abeta) is crucial for hippocampal hyperactivity.\n","Cererospinal fluid marker APP of Alzheimer pathology is associated with voxel-based morphometry-measures of brain atrophy in Parkinson-related (PD) dementia and within the PD cognitive continuum.\n","Cultured human migroglia-like THP-1 macrophages are pathogenically challenged with Abeta1-42 peptide to initiate an inflammatory response.\n","Following Abeta1-42 treatment at sub apoptotic concentrations, both intra- and extra-cellular alpha-synuclein levels are significantly increased.\n","Data show that a chronic vascular insult can activate brain vascular receptor for advanced glycation end products (RAGE), favoring parenchymal amyloid beta protein deposition and the onset of cognitive deterioration.\n","On basis of these results, propose that GGA1 facilitates LR11 endocytic traffic and that LR11 modulates A-beta levels by promoting amyloid-beta precursor protein traffic to the endocytic recycling compartment\n","APPxPS1 transgenic mice are generated to humanize the mouse amyloid Abeta sequence and create a presenilin (PS)-1 mutation identified in patients with familial early-onset Alzheimer's disease.\n","Aggregation of Abeta42 appears the most likely cause for the decreased CSF Abeta42 concentration in AD: the aggregated state inhibits Abeta42 from being transported from the ISF to the CSF. Review.\n","C99 structure determination and observation that it forms a complex with cholesterol provide insight into amyloidogenesis; flexibly curved TMD of C99 offers insight into how it is recognized and proteolyzed by gamma-secretase and discovery that its G [...]","A fraction of APP, including its amino-terminal portion, may be localized in the nucleus as well as in the nucleolus, suggesting an important role of APP in RNA metabolism and other intra-nucleolus functions.\n","Abeta(3(pE)-42) confers tau-dependent neuronal death and causes template-induced misfolding of Abeta(1-42) into structurally distinct low-n oligomers that propagate by a prion-like mechanism; results raise the possibility that Abeta(3(pE)-42) acts si [...]","In cell-based assays, the peptide strongly suppressed APP shedding, demonstrating that it exerts the inhibitory effect already upstream of gamma-secretase, most likely through steric hindrance\n","Strong binding of beta-amyloid peptide to TIAALLSPYSYS (residues 106-117) was detected, corresponding to strand G on the inner beta-sheet of TTR.\n","The results show that the template consisting of ABETA peptides with cross-beta structure can induce the formation of beta-rich conformations for the monomeric ABETA, which is the key feature of the aggregation-prone conformers.\n","results show that sAPPalpha is a suitable biomarker for the diagnosis and prognosis of idiopathic normal pressure hydrocephalus\n","the specific interaction of oligomeric Abeta with DR4 and DR5 whereas apoptosis protection achieved through RNA silencing of both receptors\n","Diagnosis of dementia might be predicted by a combination of amyloid-beta pathology and a ratio of the brain burden of copper to the brain burden of aluminum, when compared with the burden of amyloid-beta.\n","We conclude that the clinical features of Alzheimer's disease can be different even when caused by the same mutation in the APP gene.\n","plasma Abeta oligomers level is an useful biomarker for Alzheimer's disease diagnosis.\n","data suggest that exposure to transgenic APP during maturation influences the development of neuronal circuits controlling motor activity\n","Overexpression of SNX12 does not affect the steady-state levels of APP, BACE1 or gamma-secretase components, but dramatically reduces the levels of Abeta, soluble APPbeta and APP beta-carboxyl terminal fragments.\n","Heme-ABETA is catalytically more competent than Cu-ABETA in reducing O2.\n","Abeta levels in primary cortical neurons are similar between genotypes, indicating that leucine-rich repeat transmembrane 3 (LRRTM3) is not required for Abeta generation in developing mice.\n","Abeta aggregates are capable of self-propagation and hence might be prions.\n","Amyloid precursor protein (APP) traffics from the cell surface via endosomes for amyloid beta production in the trans-Golgi network.\n","These data provide evidence that neuronal activity regulates endogenous APP-PS1 interactions.\n","The low amount of Abeta oligomers detected in native cerebrospinal fluid of Alzheimer disease may be inversely related to their levels in the brain, as occurs for Abeta monomers, representing a biomarker for the amyloid pathogenic cascade.\n","a significant role for HSA regulating Abeta fibril growth in the brain interstitium.\n","By reducing the BACE1 protein level, miR-195 downregulates Abeta formation.\n","low miR-153 levels may drive increased APP expression in a subset of AD patients.\n","Mutations of key motifs responsible for the recycling of LDLR-related protein 10 (LRP10)to the trans-Golgi Network results in the aberrant redistribution of APP with LRP10 to early endosomes and a concomitant increase in APP beta-cleavage into Abeta.\n","NRG1 attenuated the neurotoxicities induced by the expression of APP-CTs in neuronal cells.\n","MFG-E8 significantly attenuates oligomeric human amyloid beta-induced neuronal cell death in a primary neuron-microglia coculture system.\n","Conserved features of intermediates in amyloid assembly determine their benign or toxic states\n","Systemic inflammation causes deficits in both Abeta transport and bulk flow resembling those observed in Alzheimer's disease.\n","Aggregation kinetics and morphology of the amyloid fibrils formed by Alzheimer's amyloid beta protein and the variant Arctic mutation.\n","protein-conjugated acrolein and Abeta40/42 ratio in plasma for 120 mild cognitive impairment and Alzheimer's disease patients were significantly higher than those for 101\n","a novel interaction between APP and HSP60, which accounts for its translocation to the mitochondria.\n","Current findings established the involvement of APP, PS1, and PS2 in familial case of Alzheimer disease, while APO polymorphism suggests the existence of other unknown genetic factors or risk factors in the cause of this disease.\n","Amyloid beta was increased in Alzheimer disease patients.\n","Cell surface expression of the major amyloid-beta peptide (Abeta)-degrading enzyme, neprilysin, depends on phosphorylation by mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (MEK) and dephosphorylation by protein phosphatase 1a.\n","Our results imply that Abeta fibril formation arises from a sequence of events in a highly predictable manner\n","our novel approach facilitates drug screening, increases the probability of success of antibody therapeutics, and improves antibody-based detection and identification of different conformations of Abeta\n","baseline Abeta+ scans were associated with greater clinical worsening on the Alzheimer's Disease Assessment Scale-Cognitive subscale\n","BRICHOS domains efficiently delay fibrillation of amyloid beta-peptide.\n","coding mutation (A673T) in the APP gene that protects against Alzheimer's disease and cognitive decline in the elderly without Alzheimer's disease\n","This review has focused on the biological and biophysical properties of the beta-amyloid peptide and its role in Alzheimer's disease. [review]\n","Molecular basis of beta-amyloid oligomer recognition with a conformational antibody fragment.\n","propose that the strength of inter-strand side-chain interactions determines the degree of beta-sheet twist, which then leads to the different association patterns between different cross beta-units and thus distinct fibril morphologies\n","the high-resolution crystal structures of two AICD-derived phospho-peptides: (QNGPYENPTY and its E-->V modification QNGPYVNPTY) in complex with the SH2 domain of Grb2 (Grb2-SH2) and complimentary spectroscopic studies to reveal their functional impli [...]","the molecule curcumin is a potential Abeta toxicity inhibitor as a beta-sheet breaker by having a high propensity to interact with certain Abeta residues without binding to them.\n","High cerebrospinal fluid concentrations of cholesterol and its metabolites are associated with increased production of soluble amyloid precursor protein in Alzheimer's disease.\n","Second generation gamma-secretase modulators exhibit different modulation of Notch beta and Abeta production.\n","The study shows how a surface can facilitate fibrillation: the surface serves to locally concentrate peptide molecules and the confinement of the two-dimensional environment promotes inter-peptide interaction, leading to fibrillation at ABETA peptide.\n","our results reveal that overexpression of APP in Npc1-deficient mice can negatively influence longevity and a wide spectrum of behavioral/neuropathological abnormalities.\n","For the Abeta40 region on chromosome 1, association of several SNPs was observed at the presenilin 2 gene (PSEN2) in 125 subjects with severe hypertension.\n","S-nitrosylation pathway wherein Cdk5/NOS1 interaction enhances S-nitrosylation of Cdk5, mediates mitochondrial dysfunction and synaptic loss during the ABETA etiology of Alzheimer's disease.\n","The study presents a novel murine model of amyloid deposition in mice expressing human wild-type ABPP Gene.\n","Molecular dynamics simulations of ABETA 9-40 fibrillar oligomers modeled as protofilament segments, probe the first steps in the mechanism of ABETA-membrane interactions.\n","Pathologic effects of ABETA can be mediated by binding to PrPc.\n","Higher cortical amyloid burden is associated with lower memory performance among clinically normal older subjects.\n","metalloprotease meprin beta generates amino terminal-truncated amyloid beta peptide species\n","Differential gene expression of BACE1 and PSEN1 in the knockdown cells, which is possibly a consequence of MAT2A deregulation and may indicate a self regulatory mechanism.\n","A detailed immunochemical and mass spectrometry study of primary structures of Abeta peptides stably transfected and secreted by Chinese hamster ovary cells is presented; abundant anti-Abeta immunoreactive bands in molecular weight range 4-20 kDa are found.\n","Preservation of nitric oxide/cyclic/GMP signaling is an important modulator of expression and processing of AbetaPP in a transgenic mouse model of Alzheimer's disease.\n","In APP transgenic mice loss of nitric oxide and increased oxidative stress are the major causes of endothelial dysfunction. PPAR-gamma activation mediates vascular protection.\n","model system to study the effects of intracellular Abeta in fusion with green fluorescent protein. We sent this fusion protein into the secretory pathway and showed that intracellular traffic pathways are necessary for the generation of toxic species.\n","apoE isoform-specific formation of soluble apoE/Abeta modulates oAbeta levels, suggesting a basis for APOE4-induced AD risk and a mechanistic approach to AD biomarkers\n","Lower plasma Abeta1-42/1-40 and brain amyloid was observed in those reporting higher levels of physical activity, consistent with the hypothesis that physical activity may be involved in the modulation of pathogenic changes associated with Alzheimer disease\n","Ezrin/radixin/moesin are required for the purinergic P2X7 receptor (P2X7R)-dependent processing of the amyloid precursor protein.\n","This study supports the hypothesis that extracellular human IAPP contributes to human IAPP-induced beta cell cytotoxicity.\n","A ternary complex consisting of AICD, FE65, and TIP60 down-regulates Stathmin1.\n","Fiber diffraction patterns from the 40-residue form Abeta(1-40) confirm a number of features of a 3-fold symmetric Abeta model from solid-state NMR but suggest that the fibrils have a hollow core; refinement of a hollow-core model against ssNMR data  [...]","The connectivity of the peripheral olfactory neural circuit is perturbed in mice overexpressing human APP.\n","An unusual enhancement for the amide II' VCD intensities of Abeta(25-35:(13)C-29/30) and Abeta(25-35:(13)C-33/34) peptide fibrils, considered to originate from inter-strand coupling\n","Hyperphosphorylation of Tau induced by naturally secreted amyloid-beta at nanomolar concentrations is modulated by insulin-dependent Akt-GSK3beta signaling pathway.\n","Soluble prion protein inhibits amyloid-beta (Abeta) fibrillization and toxicity\n","REVIEW: synaptic synthesis, processing and function of APP and amyloid-beta (Abeta), as well as discusses how these proteins could contribute to the altered synaptic plasticity and pathology of the aforementioned disorders\n","[review] Based on the apparent common pathogenic role of amyloid precursor protein in both Down's syndrome and Alzheimer's disease (AD), the idea that the dementia associated with Down's syndrome is in fact AD is supported on many levels.\n","We conclude that Niemann-Pick C patients have altered Abeta metabolism which may cause subtle but different effects on APP degradation pathways\n","Study shows an association between amyloid-beta deposition in the brain and subjective cognitive complaints in cognitively normal older adults.\n","Results show that the inverse coupling of APP cleavage by ADAM10 and BACE1 depends on the cellular model\n","The effect of fulvic acid on pre- and postaggregation state of Abeta(17-42): molecular dynamics simulation studies\n","Stability of early-stage amyloid-beta(1-42) aggregation species.\n","late onset AD-susceptibility genes do not specifically alter the Abeta42/40 ratios and suggest that these genes probably contribute to AD through distinct mechanisms\n","In the absence of a functional nerve growth factor (NGF)/TrKA-mediated signaling pathway in AbetaPP-null mice, exogenous application of NGF can rescue long-term potentiation de fi cit.\n","Parkin co-localizes with intraneuronal Abeta1-42 in the hippocampus and cortex in Alzheimer's disease.\n","analysis of the interaction between amyloid-beta peptide and membranes\n","\"Lipid raft aging,\" a metaphenomenon, is considerably exacerbated by the induced amyloid burden in APP/presenilin-1 genotype of this familial Alzheimer disease model.\n","A higher level of baseline plasma Abeta was associated with worse cognitive status two years prior to incident dementia diagnosis.\n","Reviewed a series of studies showing that ABETA oligomer binding to PrPc mediates deleterious effects on neurons. [review]\n","Data suggest that, in vivo, the outcome of amyloidogenesis may be affected by both macromolecular crowding and spatial heterogeneity.\n","The complex in vivo amyloid-beta peptide array and variations thereof is critical in Alzheimer disease.\n","The finding of a non-coding (nc) RNA (hereafter referred to as 51A) that maps in antisense configuration to intron 1 of the SORL1 gene, is reported.\n","Compared with Alzheimer's disease, elevated tau or reduced amyloid-beta1-42 are usually not found in other forms of neurodegenerative dementia.\n","The results confirm that size and hydrophobicity are key for the aggregation and stability of the hydrophobic core region of ABETA(16-22).\n","Avagacestat was safe, well tolerated, and resulted in a notable decrease in CSF Abeta concentrations, suggestive of gamma-secretase inhibition.\n","analysis of biological aspects of BACE1, and the effects of several natural products that modulate BACE1-processing of APP [review]\n","Amyloid-beta oligomer detection by ELISA in cerebrospinal fluid and brain tissue.\n","Report binding of Alzheimer's Abeta1-42 to nicotinic alpha-7 acetylcholine receptors.\n","A 'power-law' model fits the size distributions of primitive APP deposits in Alzheimer's disease (AD), Down syndrome, dementia with Lewy bodies, corticobasal degeneration, and the diffuse deposits in AD.\n","enhancing CatB activity could lower Abeta, especially Abeta42, in AD patients with or without familial mutations.\n","The study presents a kinetic and thermodynamic characterization of the isomer-specific interaction between Pin1-WW domain and the APP cytoplasmic tail phosphorylated at Thr668.\n","tau deletion had a protective effect against amyloid induced toxicity even in the presence of mutant PS1 and reduced the production of Abeta.\n","Soluble amyloid precursor protein 770 is released from inflamed endothelial cells and activated platelets.\n","Lysophosphatidic acid,the most bioactive component of oxLDL induces increased production of Abeta and BACE1 expression.\n","Our results indicate that rs3851179 may not be an AD susceptibility locus in the Chinese population and the APOEepsilon4-negative subgroup.\n","Overview of the role of amyloid-beta in Alzheimer disease pathogenesis. [Review Article]\n","RER1 modulates amyloid-beta production by altering trafficking of gamma-secretase and amyloid precursor protein.\n","The fibrillar form of ABETA suppresses Cu redox cycling and reactive oxygen species production.\n","Animal behavior, amyloid plaque deposition, and transgenic AbetaPP processing are sensitive to genetic differences between mouse strains.\n","Both electrophysiological and behavioral results show an effect of Abeta peptide on cholinergic synaptic transmission via a possible mechanism by which Abeta peptides cause cholinergic neuron degeneration and consequent memory loss.\n","Data show that amyloid beta peptide forms NMR invisible non-toxic co-aggregates together with lacmoid as well as Congo red, and suggest that even such weak binders might be effective as therapeutics against pathogenic protein aggregation.\n","Microvascular impairment is directly correlated with transgenic APP accumulation and highlights the importance of targeting cerebrovascular amyloid angiopathy clearance for diagnosis, monitoring of disease progression and treatment of Alzheimer's disease.\n","CSF sAPP and Abeta peptide levels were reduced in MS patients; but they increased again towards normal, after natalizumab treatment. A multivariate model of Abeta species separated the SPMS patients from controls, with RRMS patients having intermedia [...]","high cerebral Abeta load was associated with greater decline in episodic and working memory over 18 months\n","A living mouse model of Alzheimer's disease using Fourier domain optical coherence microscopy provides high-resolution images of individual beta-amyloid plaques in brain parenchyma and vasculature and requires no staining of the Alzheimeric sample.\n","study identified 20 novel amyloid precursor protein intracellular domain (AICD)-interacting proteins; several of these novel interactors might be useful in understanding the protein interaction network in Alzheimer's disease pathogenesis\n","In APP transgenic mice models showed Neurologic and motor dysfunctions.\n","Alterations in the hippocampal nerve growth factor (NGF) signaling pathway in mild cognitive disease and Alzheimer disease favor proNGF-mediated proapoptotic pathways, and that this is independent of Abeta accumulation during progression.\n","A rare variant A673T reportedly protects against alzheimer's disease )AD) and age-related cognitive impairment and might functionally inhibit proteolytic cleavage at the beta-secretase site of APP.\n","observations indicate that the immobilized Abeta undergoes a conformational change upon exposure to the metal ions. A difference in metal binding affinity between Abeta(1-28) and Abeta(1-42) was also detected.\n","The heat shock response is modulated by and interferes with toxic effects of scrapie prion protein and amyloid beta.\n","disturbed Abeta metabolism has an effect on Parkinson's disease beyond cognition and may contribute to the variable rate of motor and functional decline in Parkinson's disease\n","Synoviolin up-regulates amyloid beta production by targeting a negative regulator of gamma-secretase, Rer1, for degradation.\n","These data indicate that the levels of full-length (fl) APP and APP C-terminal fragments (CTFs] associated with exosomes mirror the cellular levels of flAPP and APP CTFs.\n","ApoE3 more efficiently facilitates Abeta trafficking and degradation than apoE4.\n","analysis of conformations of islet amyloid polypeptide monomers in a membrane environment\n","The results suggest that APP mutations in the Abeta coding region favour Abeta38 accumulation in the brain.\n","our work identifies C99 as the earliest betaAPP catabolite and main contributor to the intracellular betaAPP-related immunoreactivity\n","Amyloidbeta-DNA interaction needs to be considered as a significant cause of toxicity in the pathogenesis of Alzheimer's disease.\n","Adults with amnestic mild cognitive impairment and high amyloid-beta levels show greater decline in working memory and in verbal and visual episodic memory at 18 months.\n","Abeta can stimulate microglial cells and be phagocytosed through a mechanism that is distinct from that of Abeta removal, thus contributing to the clearance of Abeta, even by defective microglial cells.\n","Overexpression of amyloid precursor protein in acute myeloid leukemia enhances extramedullary infiltration by MMP-2.\n","transgenic Abeta1-40 protein acts on distinct luminal and abluminal vascular targets, the deleterious cerebrovascular effects of which are additive.\n","analysis of how anti-Abeta IgGs can target conformational epitopes on synthetic dimer assemblies and the AD brain-derived peptide\n","physiopathological events underlying the chronic Abeta production/clearance imbalance in sporadic and Autosomal-dominant Alzheimer disease are different\n","In vitro oligomerization and fibrillogenesis of amyloid-beta peptides.\n","Experimental inhibition of fibrillogenesis and neurotoxicity by amyloid-beta (Abeta) and other disease-related peptides/proteins by plant extracts and herbal compounds.\n","amyloid deposition is associated with Alzheimer's disease-like atrophy in dementia with Lewy bodies Parkinson disease patients\n","Linkage between plaques and oligomers may be a key pathophysiological event underlying dementia of the Alzheimer type; therefore, the amyloidbeta oligomer assay may be useful for many tests of the oligomer hypothesis.\n","Microglial activation induced by amyloid beta peptide is possibly mediated by NADPH oxidase, which could be a potential target to prevent oligomeric Abeta-induced neurodegeneration.\n","Data suggest that amyloid-beta (1-42) aggregates, unlike their monomeric form, can seize copper from serum albumin; these studies provide insight into how and why senile plaques accumulate copper in vivo.\n","The role of AbetaPP in calcium homeostasis is linked to enhanced calcium content in the endoplasmic reticulum.\n","There is no evidence for notable changes in the number of functional CB1 cannabinoid receptors in the common APPswe/PS1dE9 mouse model of Alzheimer's disease.\n","We demonstrate that extending the transmembrane domain of the amyloid precursor protein-derived C99 substrate in proximity to the cytosolic face strongly influences gamma-secretase cleavage specificity.\n","Regulation of AbetaPP metabolism/processing by mild oxidative stress requires ubiquitin/proteasome activity with a simultaneous reduction in that of the autophagy/lysosome system.\n","Increased expression of AbetaPP and AbetaPP metabolites in neurons is sufficient to drive early endosomal abnormalities in vivo, so that disruption of the endocytic system is likely to contribute to basal forebrain cholinergic vulnerability.\n","Studies indicate that the core element of the majority of disease-related amyloid fibrils is a beta-strand-loop-beta-strand motif called beta-arch.\n","D3-FITC peptide-infused transgenic mice show a signi fi cant reduction in the number of plaques in the hippocampus, and in the amount of activated astrocytes and microglial cells surrounding amyloidbeta42 plaques compared to control infused mice.\n","an earlier onset of major depressive disorder may have a more serious abnormality in Abeta metabolism.\n","Endothelin-converting enzymes degrade intracellular beta-amyloid produced within the endosomal/lysosomal pathway and autophagosomes\n","The iron center and the porphyrin ring of heme exhibit distinct effects on ABETA fibrillation.\n","A loss of PS/gamma-secretase function to cleave Abeta42(43) may initiate Alzheimer's disease.\n","Although APP fragments appear to distribute similarly in neurons and peripheral blood leukocytes, the APP fragment species in these 2 tissues are not completely comparable.\n","Upon co-administration of amyloid (A)beta transgene and naturally-occurring antibodies to Abeta, no change in microglia viability is observed.\n","Amyloid beta precursor protein production was downregulated following edaravone administration, a free radical scavenger.\n","Events related to beta-amyloid activities lead to deregulation of homeodomain-interacting protein kinase 2 (HIPK2) signaling.\n","Abeta plaque might exacerbate activity-dependent neuronal Ca2+ signaling in hippocampal pyramidal neurons from APPSWE/PS1M146V transgenic mice.\n","Studies indicate that IAPP is one of the most amyloidogenic sequences known.\n","In contrast to N-terminal Asn of Amyloid peptides, Asp isomerization is significantly accelerated at acidic pH.\n","Data indicate that Abeta42 peptides sample quite heterogeneous secondary and tertiary structure ensembles.\n","A strong relationship is supported between the toxicity of Abeta for neurons and the total Abeta burden, including the soluble and fibrillar Abeta.\n","PuF may regulate the APP gene promoter\n","Studies indicate that mutations in the putative helical region alter the rate of amyloid formation.\n","Mutations in the APP precursor are associated with more medial temporal lobe loss in familial Alzheimer's disease patients compared to PSEN1 mutations.\n","lack of Npc1 protein can alter the expression profile of selected transcripts as well as proteins, and APP overexpression influences cerebral pathology by enhancing changes triggered by Npc1 deficiency in the bigenic line.\n","Prion protein-mediated toxicity of amyloid-beta oligomers requires lipid rafts and the transmembrane LRP1\n","identification of a new AbetaPP isoform in platelets as a potential Alzheimer's disease biomarker can provide an additional tool for the development of a reliable diagnostic test\n","Plasma from 5 Tangier disease patients and 5 controls were analyzed for Abeta1-40, Abeta1-42, AbetaX-40, and AbetaX-42 but no differences were found\n","yeast studies have provided major new insights into the effects of tau and Abeta and, at the same time, offered new approaches to rapidly search for chemicals that may be involved in prevention of Alzheimer's disease--{REVIEW}\n","Clinical and pathological features of CRC patients may indicated an association of these mutations with the risk and progression of colorectal cancer in Poland.\n","the role of Abeta in compensatory mechanisms of neuroplasticity restoration under normal physiological condition and Alzheimer's disease.\n","Evidence is provided that Abeta42 monomeric Abeta42 plays an important role in mediating structural transitions in the amyloid pathway and that fibrillization occurs via a combined mechanism of nucleated polymerization and secondary nucleation.\n","Structures of the E22Delta mutant-type Abeta40 and Abeta42 alloforms as well as the impact of E22Delta mutation on the wild-type Abeta40 and Abeta42 alloform structures are examined.\n","Soluble APPbeta could be potentially used as a new biomarker, which may potentially improve the diagnostic accuracy of existing markers of Alzheimer's disease.\n","Peptoid ligands IAM1 (inhibitor of amyloid) and dimeric form (IAM1)2 are synthesized and evaluated; IAM1 selectively binds to Abeta42, while the dimeric derivative (IAM1)2 has a higher affinity for Abeta42.\n","Binding of apolipoprotein E inhibits the oligomer growth of amyloid-beta peptide in solution as determined by fluorescence cross-correlation spectroscopy.\n","Cholesterol-dependent energy transfer between fluorescent proteins-insights into protein proximity of APP and BACE1 in different membranes in Niemann-Pick type C disease cells.\n","By using real-time (19)F NMR along with other techniques, the study shows that multiple oligomeric species can be detected during the lag phase of ABETA 1-40 fiber formation, consistent with a complex mechanism of aggregation.\n","mitochondrial ALDH2 in the endothelium is a target for the vascular effect of Abeta, including loss of barrier function and angiogenesis. ALDH2 activation, by restoring mitochondrial functions in the endothelium\n","Platelet APP ratios of Thai patients with Alzheimer disease (AD) are significantly lower than those of normal subjects, including significantly poorer cognitive functions; however, the ranges of the APP ratios from both groups markedly overlapped.\n","Studies indicate residue-specific information about amyloid intermediate states of IAPP, alpha-synuclein, and tau were characerized with Forster resonance energy transfer (FRET).\n","Activation of 5-HT4 receptors in Alzheimer's disease might stimulate alpha-secretase processing, which increases amyloid precursor protein (APP)alpha and reduces Abeta, according to the central dogma in APP processing.\n","The CA3 region of long-term ovariectomized rats was profoundly hypersensitive to the neurotoxic effects of amyloid-beta(1-42), the most amyloidogenic form of the amyloid-beta peptide.\n","This prospective cohort study finds that Abeta deposition is slow and protracted, likely to extend for more than two decades in an almost linear fashion.\n","Amyloid deposition in the preclinical stage of Alzheimer's appears to be associated with worse sleep quality but not with changes in sleep quantity.\n","Cerebrospinal fluid Abeta trimers are elevated in individuals at risk for Alzheimer disease and show stronger relationships with tau than does Abeta1-42, a surrogate for Abeta fibril deposition.\n","subjects with abnormal Abeta42 CSF levels and with high scores on cognitive reserve proxies may be tolerating a more advanced neurodegenerative process\n","A synergistic effect between cholinergic denervation and the presence of amyloid(Abeta)/presenilin-1 transgenes may trigger Abeta deposition and synergistically contribute to cognitive impairment in Alzheimer's disease.\n","This work provides insights into the mutual structure, dynamics, and interactions of both ABETA peptides and lipid bilayers at the atomic level, which expand our understanding of the complex behavior of amyloid-induced membrane disruption.\n","Slight increases in temperature can induce inhibitory and acceleratory effects of hydrophobic (polystyrene) and hydrophilic (silica) nanoparticles on the amyloid fibrillation process, resepctively.\n","The chirality and cation binding properties of Abeta aggregates should be capitalized for the development of novel amyloid labeling methods, adding to the arsenal of Alzheimer's imaging techniques and diagnostic tools.\n","Designing suitable ligands which modulate the aggregation of Abeta peptides toward minimally toxic pathways may be a possible therapeutic strategy for Alzheimer's disease.\n","While lower concentrations of iron oxide nanoparticles inhibit amyloid beta protein fibrillation, higher concentrations increase the rate of Abeta fibrillation.\n","ABETA aggregates formed in the presence of lipid membranes have a latent ability to trigger the uptake of raft components accompanied by phase separation of lipids.\n","acute lansoprazole treatment in wild type and AD transgenic mice promoted higher Abeta40 levels in brain, indicating that lansoprazole may also exacerbate Abeta production in vivo\n","OLE interferes with the Abeta aggregation skipping the appearance of toxic species, as already shown in vitro for Abeta42.\n","Demonstration of a specific association between Abeta40 and clusterin in Alzheimer's disease brain.\n","IDE-Met(1) links the mitochondrial biogenesis pathway with mitAbeta levels and organelle functionality.\n","Data indicate that glutamate carboxypeptidase II (GCPII) is not an amyloid peptide-degrading enzyme.\n","Data did not show any amyloid-beta (Abeta) peptide degradation activity of glutamate carboxypeptidase II (GCPII).\n","[review] Over the past decade, strong evidence has emerged that oligomeric forms of amyloid beta, the protein that accumulates in senile plaques in the Alzheimer brain, contributes to degeneration of synaptic structure and function.\n","Cerebrospinal fluid (CSF) and amyloid positron emission tomography measurement of Abeta are consistent in the majority of subjects in the cross-sectional and longitudinal populations.\n","Contrary to earlier claims, the Cu(II) complex with the soluble ABETA 16 peptide, and also that with ABETA 28 exhibit no phenol monooxygenase (tyrosinase-like) activity; the complexes neither exhibit superoxide dismutase activity.\n","Individuals with a vascular risk factor such as hypertension, in combination with a genetic risk factor for Alzheimer disease (apolipoprotein E epsilon4 allele), show greater beta-amyloid burden than those without such risk.\n","Amyloid precursor protein controls cholesterol turnover needed for neuronal activity.\n","Prophylaxis and treatment of Alzheimer's disease by delivery of an adeno-associated virus encoding a monoclonal antibody targeting the amyloid Beta protein\n","Altered secretory pattern in Abeta-induced senescent retinal epithelial cells may contribute to compromised barrier integrity and chronic inflammation in age related macular degeneration.\n","Prolyl oligopeptidase colocalizes with alpha-synuclein, beta-amyloid, tau protein and astroglia in the post-mortem brain samples with Parkinson's and Alzheimer's diseases\n","differences and similarities between MCI and AD patients were observed in several markers of platelet APP processing\n","These results demonstrate progressive neurodegeneration of the Alzheimer type in these animals.\n","In cognitively normal adults, Abeta*56 increases ahead of amyloid-beta dimers or amyloid-beta trimers and may play a pathogenic role very early in the pathogenesis of Alzheimer's disease.\n","Cerebrospinal fluid APP biomarker signals underlying Alzheimer disease pathology at least 7 years before the appearance of dementia symptoms.\n","a role for PrP(C) in regulating Abeta production\n","microglial functions progressively decline in Alzheimer's disease with the appearance of Abeta plaques\n","Disruption of neocortical histone H3 homeostasis by soluble Abeta implicates Alzheimer's disease.\n","Abeta can induce acute depression of basal glutamatergic synaptic transmission through both presynaptic and postsynaptic dysfunction via whole-cell voltage-clamping methods.\n","Structural similarities and differences between Abeta(1-42) oligomers and fibrils suggest that folded beta-strand peptide conformations form early in the course of self-assembly and that oligomers and fibrils differ primarily in intermolecular organization.\n","Both numbers of synapses per volume and synaptic morphology are affected in plaque-free regions of APP/presenilin-1 transgenic mice.\n","we review studies in vitro and in vivo that suggest that cerebral Abeta aggregation may indeed progress via prion-like templated misfolding--{REVIEW}\n","Large scale (20 mus) Coarse Grained simulations of 36 replicas of ABETA (1-40) performed within a model lipid bilayer palmitoy-oleyl-phosphatidylcoline matrix confirmed the formation of supramolecular assemblies which resemble a twisted ribbon.\n","Long-term exposure to Ginkgo biloba treatment does not affect the prevalence of cerebral amyloid-beta deposition in elderly, nondemented subjects aged older and younger than 82 years.\n","further detailed analyses of the interactions of Reelin and Lingo-1 with APP\n","The results reveal that the neuropeptides leucine enkephalin and galanin interact with both the monomeric and small oligomeric forms of ABETA(1-40) to create a range of complexes having diverse stoichiometries, while some tachyknins (substance P) do not.\n","Studies suggest a stable steady state characterized by low levels of Ca(2+) and amyloids, corresponding to a healthy situation, coexists with another 'pathological state' where the levels of both compounds are high.\n","Exposure to nanomolar concentrations of Abeta first induces increased expression and function of nicotinic acetylcholine receptor alpha7-nAChRs, and then induces neuronal hyperexcitation.\n","apoE influences sAbeta metabolism not through direct binding to sAbeta in solution but through its actions with other interacting receptors/transporters and cell surfaces\n","Data indicate the metabolism of neurotoxic amyloid beta (Abeta) oligomers in Alzheimer's disease (AD) brain and suggest insights into Abeta-targeted therapies for AD.\n","This review identifies and discusses critically the scientific issues contributing to the extensive inconsistencies reported in the literature on their purported in vivo amyloid beta probe specificity and potential utilization in patients.\n","The residues Asp 7 and Ser 8 of Abeta-peptide were found in close contact with Glu 384 of tACE along with Zn(2+).\n","Data indicate a reduction of IRS-1pS636 (serine phosphorylation at 636) level accompanied with decreased Abeta42 levels in the hippocampus of APP/PS1 transgenic mice after treatment with epigallocatechin-3-gallate (EGCG).\n","gamma-Secretase inhibition during repeated peripheral inflammation blocks central amyloid-beta accumulation and prevents cognitive dysfunction.\n","No difference is found in amyloid beta-peptide (1-40) cerebrospinal fluid levels between Alzheimer's disease patients and non-Alzheimer's disease patients.\n","findings suggest that a normal function of presenilin (PS)is to repress kinesin-1 and dynein motor activity during axonal transport of amyloid precursor protein (APP) vesicles; perturbations of APP/PS transport could contribute to early neuropatholog [...]","In asymptomatic individuals, amyloid-beta deposition in the brain is associated with gray-matter atrophy and memory impairment and is therefore not a benign process.\n","Data indicate that gamma-secretase inhibitors are selective for inhibition of amyloid beta generation over Notch.\n","Data indicate that crocin decreased the hydrophobic area in incubated Abeta42.\n","sAPPalpha rapidly and persistently regulates gene expression in rat hippocampus\n","caspase-2 is required for the cognitive decline seen in human amyloid precursor protein transgenic mice.\n","protein interactions between LRRTM3, APP and BACE1, as well as complex associations between mRNA levels of LRRTM3, CTNNA3, APP and BACE1 in humans might influence APP metabolism and ultimately risk of AD\n","Propranolol reduces cognitive deficits, amyloid and tau pathology in Alzheimer's transgenic mice.\n","This study demonistrated that Tooth loss induces memory impairment and neuronal cell loss in human app transgenic mice\n","When interacting with beta-structure promoting substances, such as surfactants, Abeta is kinetically driven toward an aggregation-prone state.\n","Amyloid-beta peptide (Abeta) engages alpha7 nicotinic acetylcholine receptors to induce release of astrocytic glutamate, which in turn activates extrasynaptic NMDA receptors on neurons, followed by reduction in evoked and excitatory postsynaptic currents.\n","Quantified white matter hyperintensities represent cerebrovascular disease, and cerebrospinal fluid beta-amyloid represents Alzheimer's disease pathology.\n","Lipidation states of apolipoprotein E (APOE) and Abeta peptides in the brain differ depending on apolipoprotein (APO)E genotype and cognitive diagnosis.\n","The uptake of intraperitoneally-administered monoclonal antibody 158 into the brain was age- and time-dependent, and saturable in AbetaPP transgenic mice with modest Abeta deposition.\n","In an amyloid beta precursor protein overexpressing transgenic rat model, quantification of amyloid beta load at 22 months indicated high levels of amyloid beta peptides.\n","Intensive protein synthesis in neurons and phosphorylation of beta-amyloid precursor protein and tau-protein are triggering factors of neuronal amyloidosis and Alzheimer's disease\n","catechol-type flavonoids could specifically suppress Abeta42 aggregation by targeting Lys residues.\n","The effect of human chorionic gonadotropin (hCG), an LH receptor agonist, on APP beta-cleavage in the SH-SY5Y neuroblastoma cell line.\n","beta-amyloid deposits in cerebral veins are observed in 78% of patients with cerebral amyloid angiopathy and intracerebral hemorrhage; veins may play a role in the elimination of beta-amyloid from the brain.\n","Amyloid beta may be released from axons of abnormal tau brainstem neurons in Alzheimer's disease.\n","Pathologic analysis reveals that Abeta deposition and production, oxidative stress, glial inflammation, and synaptic loss are not mitigated in the brain of exercised APP/presenilin (PS1) mice compared with the sedentary APP/PS1 animals.\n","peripheral Abeta peptides have a role in promoting platelet adhesion and activation in the initiation of thrombus formation\n","These results suggest that elevations in brain sAPPalpha levels are observed in subsets of individuals with autism and TgsAPPalpha mice display signs suggestive of gliosis and behavioral impairment.\n","The combined effect of cholesterol and Hcy in the presence of copper significantly increases the levels of reactive oxygen species and may render neurons more vulnerable to Abeta.\n","negative staggers are physiologically relevant structure of the amyloid beta fibrils\n","Synthetic dimeric Abeta(28-40) mimics the complex epitope of human anti-Abeta autoantibodies against toxic Abeta oligomers.\n","Genotype- and age-dependent effects of reproductive activity on cognition are associated with changes of neuropathology of Alzheimer's disease in APP transgenic mice, in expression of proteins related to synaptic plasticity and cognitive functions.\n","An amino acid sequence dependent role for amyloid-beta-40 in cytotoxicity in Alzheimer disease.\n","sAPP770 as a novel biomarker candidate of acute coronary syndrome\n","The use of the Abeta1-42/Abeta1-40 ratio could improve the differentiation of Alzheimer's disease from Parkinson's disease with dementia and dementia with Lewy bodies\n","The results mirror the temporal sequence and magnitude of Abeta and Tau changes in the CSF of patients with sporadic and dominantly inherited Alzheimer's disease.\n","Data suggest that, for 99-residue transmembrane C-terminal domain of APP in lipid bilayers, homodimerization and cholesterol binding are competitive processes centering on transmembrane glycine-zipper motif and adjacent glycine-709.\n","up-regulation of the KPI-containing APP isoforms is likely to contribute to the impairment of metabolic enzymes and mitochondrial function in Alzheimer's disease\n","These data demonstrate that hAPP-induced circuit disruption and subsequent recovery can occur rapidly and that behavior can provide a measure of circuit organization.\n","Determine human Abeta1-40 and Abeta1-42 peptides in transgenic mouse plasma.\n","Identification of the minimal zinc-binding center in natural isoforms of amyloid-beta domain 1-16 using ESI-MS\n","APP is an androgen-induced gene that promotes proliferation activity of breast carcinoma cells.\n","These data suggest that GCPII has two distinctive binding sites for two different substrates and that ABETA degradation occurs through binding to S1 pocket of GCPII.\n","Abeta oligomer increases sortilin gene and protein expression through p75(NTR) and RhoA signaling pathways\n","AChE is regulated in two neuronal cell lines by APP in a manner independent of the generation of sAPPalpha, sAPPbeta, and AICD.\n","50% of patients with Parkinson disease also develop sufficient numbers of amyloid-beta plaques and tau-containing neurofibrillary tangles for a secondary diagnosis of Alzheimer's disease.\n","disruptions in Ca(2+) homeostasis may influence Alzheimer disease pathogenesis directly through the modulation of Abeta production\n","Report early, preferential vulnerability of cells in rostral olfactory structures in APPxPS1 transgenic mice model of Alzheimer's disease.\n","familial Alzheimer's disease mutations modulate the flexibility of the APP transmembrane domain and the presentation of its gamma-site, modifying at the same time, the solvation of the epsilon-site.\n","these results clarify the mechanisms of amyloid precursor protein trafficking through the endosomal system in normal and pathological states.\n","charged clusters and hydrophobic regions of the prion protein were involved in binding to beta-amyloid1-40 and 1-42.\n","Ayloid beta mediates calpain cleavage of NCX3 in Alzheimer's disease brain.\n","COPS5 is a novel RanBP9-binding protein that increases APP processing and Abeta generation by stabilizing RanBP9 protein levels\n","A vicious cycle of inflammation has been formed between Abeta accumulation, activated microglia, and microglial inflammatory mediators\n","Data indicate that JTR-009, a benzimidazole, operated by preventing iron-regulatory protein-1 (IRP1) from binding to the iron-responsive element (IRE) in APP mRNA.\n","Data indicate that the initial U-shaped topology per amyloid-beta monomer is maintained over time in all oligomers.\n","Markov state model analyses reveal the complex network of conformational space of Abeta40 modulated by zinc binding, suggesting various misfolding pathways.\n","Escherichia coli maltose binding protein has inhibitory effects on beta-amyloid aggregation and cytotoxicity\n","Early deposition of soluble Abeta aggregates in the olfactory system together with early deficit in olfactory dysfunction have the potential to serve as molecular markers for early diagnosis of Alzheimer's disease..\n","In SH-SY5Y neuroblastoma cells intracellular Abeta is not preferentially localized to any particular organelle and, to a large extent, is secreted from the cells.\n","All functional parameters point to a severe bioenergetic impairment of the 7PA2 model ofAlzheimer cells, with the extent of mitochondrial dysfunction being correlated to the accumulation of Abeta peptides and oligomers.\n","reelin expression is altered by Abeta leading to impaired reelin signaling.\n","Data indicate that copper (Cu) down-regulated LRP1 and reduced amyloid-beta (Abeta) binding in brain endothelial cells.\n","Data indicate that the center region of amyloid beta (Abeta) peptide Abeta42 is first to aggregate, followed by the C and N termini.\n","Strict specificity for recruitment of the Mint3 adaptor by APP at the Golgi, a critical role for Tyr-682 (within the YENPTY motif) in Mint3 recruitment and export of APP from the Golgi, are demonstrated.\n","ABETA binds to the V domain of receptors for advanced glycation end-products (RAGE). Blocking of RAGE-ABETA interaction inhibited transport of peripheral ABETA into the brain.\n","SGMS activity impacts on amyloid precursor protein processing to produce amyloid-beta (Abeta) and it could be a contributing factor in Abeta pathology associated with Alzheimer's disease.\n","Factor V activator from Daboia russelli russelli venom destabilizes beta-amyloid aggregate, the hallmark of Alzheimer disease.\n","molecular dynamics simulations show aggregation-prone Osaka mutant (DeltaE22) barrels obtain the lipid-relaxed beta-sheet channel topology, indistinguishable from the WT Abeta1-42 barrels, as do the outer and pore dimensions of octadecameric (18-mer) [...]","molecular dynamics analysis of the Abeta-42 peptide in aqueous environment; findings show the E22Q (Dutch) mutation has a dramatic impact on the Abeta-42 structure; instead of a partially folded, but extended, conformation obtained with the wild type [...]","A lower CSF amyloid beta42/phospho-tau ratio and higher total tau were associated EEG abnormalities in dementia patients.\n","Down-regulation of APP and ADAM10 brought about similar results, as did batimastat treatment, thereby confirming that APP processing is important for growth and proliferation of these cells.\n","This review highlights the amyloid-nanoparticle interaction, its scope considered by scientists aiming for diagnostics and/or treatment of Alzheimer's disease, employing superparamagnetic iron oxide nanoparticles on the amyloid-beta fibrillation process.\n","Although cell toxicity was primarily driven by the D23N mutation, all Abeta isoforms tested were capable, albeit at different time frames, of eliciting comparable apoptotic pathways with mitochondrial engagement and cytochrome c release\n","Enhanced fibril formation of Abeta40 peptide can be explained in the dimer by the enhanced group of turns in the region 20-30; it does not hold for the Abeta42 peptide, where the most significant change is the decrease of turn in the region 4-10.\n","Acceleration of the depolymerization of amyloid beta fibrils by ultrasonication.\n","The gas-phase structures of doubly and triply protonated Amyloid beta (12-28)peptides have been investigated through the combination of ion mobility, electron capture dissociation mass spectrometry, and infrared spectroscopy.\n","a novel mechanism by which reduction of a PI(4,5)P2-degrading enzyme, synj1, improves amyloid-induced neuropathology and behavior deficits through accelerating cellular Abeta clearance.\n","Increase in mRNA levels of the APP gene is associated with Alzheimer's disease.\n","AP-2/PICALM complex functions as an autophagic cargo receptor for the recognition and shipment of APP-CTF from the endocytic pathway to the LC3-marked autophagic degradation pathway.\n","Gpr3 stimulates Abeta production via interactions with APP and beta-arrestin2.\n","New thiosemicarbazone-pyridylhydrazine based ligands that incorporate functional groups designed to bind amyloid-beta plaques have been synthesized\n","Amyloid-beta42 fragment modifies tight junction protein expression and functionally alters barrier properties in vitro, an effect not conditioned by other pathogenic Alzheimer's disease events taking place in the complex brain microenvironment.\n","The -491 T allele of APOE polymorphism may be associated with a risk of POAG occurrence in the Polish population.\n","A subset of genomic loci in differentiated human neurons shows a significant change in DNA methylation following Abeta treatment that contributes to the brain shrinkage and memory loss seen in Alzheimer's disease.\n","Patients with Alzheimer disease had lower levels of CSF Abeta42 than healthy controls and non-AD demented controls. The difference in CSF Abeta40 was not significant.\n","that upregulation of Nebula/DSCR1 is neuroprotective in the presence of APP upregulation and provides evidence for calcineurin inhibition as a novel target for therapeutic intervention in preventing axonal transport impairments associated with AD\n","A strategy focused on MAPT, APP, NCSTN and BACE1 to build blood classifiers for Alzheimer's disease.\n","Entrapping of AbetaPP in growth factor receptor (GRB)2-bound cellular vesicles and its clearance via autophagosomes is important for cell survival in an Alzheimer's disease type scenario.\n","Altered CpG methylation in sporadic Alzheimer's disease is associated with APP dysregulation.\n","APP with the Osaka mutation potentiates cholesterol-dependent exacerbation of intracellular Abeta toxicity\n","Inflammatory processes in Alzheimer disease may be different considering different levels of amyloid beta protein--{REVIEW}\n","amyloid-b (Ab) peptide aggregate accumulation in the brain parenchyma. There is strong evidence indicating that Ab is able to disrupt membranes, causing pore formation.\n","no above-average backbone dynamics was found for the APP transmembrane helix\n","Autosomal-dominant Alzheimer's disease-associated APP mutations at the 716 codon alter APP processing and Abeta generation by different mechanisms\n","A673T variant in APP is not involved in longevity in Chinese individuals.\n","Mass spectrometry results show that beta-Sheet ABETA(25-35) Oligomers Emerge at the Dimer, and the Transition from Isotropic to beta-Sheet Oligomers Is Completed at the ABETA(25-35) Pentamer\n","prefrontal amyloid beta deposition correlates with apathy\n","Cell-extrinsic effects of Abeta accumulation are thought to underlie the breakdown of hippocampal neurogenesis observed in Alzheimer's models.\n","prenatal zinc deficiency as a risk factor for autism spectrum disorder may unfold through the deregulation of zinc-binding ProSAP/Shank family members\n","The structural changes in the fibrillar state of ABETA42 peptide observed to occur upon introduction of single point mutations can be accompanied by changes in the dominance of the microscopic processes by which these aggregates are themselves formed.\n","Abnormal cerebrospinal fluid levels of amyloid beta-protein (1-42) are related to greater impairment in mood and behavior in Alzheimer's disease.\n","Data indicate that wild type and mutant amyloid precursor proteins (APP) expression enhances the induction in cathepsin B after administration of proteasome inhibitor MG132.\n","Pulse pressure elevation in cognitively normal older adults is associated with reduced cerebrospinal fluid (CSF) levels of beta-amyloid(1-42).\n","these data provide a thorough characterization of all intermediate steps in Abeta production in native cell membranes and provide key mechanistic insights to genetic and pharmacological modulation of Abeta generation.\n","an increased stability for the E22G Abeta42 peptide and a decreased stability for D23G compared to wild-type Abeta42, while D23G has the largest membrane-disruptive effect.\n","the high kinetic stability of Abeta protofibrils toward dissociation into monomers and supports the delineation of the Abeta folding and assembly energy landscape.\n","A reduction in peripheral amyloid-beta can lower brain amyloid-beta, thereby reducing formation of plaques predominantly composed of insoluble amyloid-beta.  This is the so-called peripheral sink hypothesis.\n","The structure function analysis identified intracellular domain of Crb to be required for Abeta42-mediated-neurodegeneration.\n","Dihydrochalcone could effectively reduce the cytotoxicity induced by Abeta.\n","The APP/PS1/htau mice displayed mild, age-dependent, Amyloid beta plaques and tau hyperphosphorylation, thus successfully recapitulating the late-onset Alzheimer's disease pathological hallmarks.\n","Report describes a novel neuroprotective function of mGlu3 receptors related to their ability to promote the non-amyloidogenic pathway of APP cleavage in astrocytes, thus enhancing sAPPalpha production\n","Amyloid beta protein fragment (1-38) is deposited in the brains of the majority of patients with sporadic Alzheimer's disease.\n","purified recombinant N-terminal 18-285 amino acid residues of human amyloid precursor protein from the methylotrophic yeast Pichia pastoris with a high yield of 50 mg/L.\n","These results suggest that HIV-1 Tat may contribute to HAND by interacting with and modifying APP processing, thereby increasing Abeta production.\n","Study described hyperlocomotion, reduced anxiety, and an impairment in spatial memory in the cheeseboard task in female APPxPS1 mice\n","The quantitative analysis of SMFS data demonstrated that Abeta interaction leads to the formation of dimers with a lifetime in the range of a second.\n","the nature of the catalytic subunit in the complex affects both activities. Interestingly, PSEN2 complexes discriminate between the Abeta40 and Abeta38 production lines, indicating that Abeta generation in one or the other pathway can be dissociated\n","These studies also raise interesting issues about the solubility and detection of long Abeta, as well as the use of truncated substrates for assessing relative potency of gamma-secretase inhibitors.\n","BACE1 activity evolved at least 360 My before Abeta.\n","The acidic fragment of human Abeta (Abeta1-11) and a phosphorylated fragment of beta-Casein induced tau fibrillization in vitro.\n","It is regarded as the critical component associated with AD pathogenesis, which is derived from the amyloid precursor protein (APP) cleavage.\n","study defines Rheb as a novel physiological regulator of BACE1 levels and Abeta generation, and the Rheb-BACE1 circuitry may have a role in brain biology and disease.\n","Turnover of C99 is controlled by a crosstalk between endoplasmic reticulum-associated degradation and ubiquitin-independent lysosomal degradation in human neuroglioma cells.\n","Using biophysical experiments, the present study shows that simultaneous D-isomerization of Asp residues at positions 7 and 23 (D-Asp(7,23)) enhances oligomerization, fibril formation, and neurotoxic effect of Abeta1-42.\n","Familial Alzheimer's mutations within APPTM increase Abeta42 production by enhancing accessibility of epsilon-cleavage site.\n","Report increased platelet amyloid precursor protein expression in subjects with Alzheimer's disease and frontotemporal lobar degeneration.\n","CSF Abeta42 levels were similar across patients with Alzheimer's disease subtypes amnestic, logopenic progressive aphasia, and posterior cortical atrophy.\n","Met35 oxidation decreases the beta-strand content of the C-terminal hydrophobic region (residues 29-40), with a specific effect on the secondary structure of residues 33-35, thus potentially impeding aggregation.\n","Abeta is one of the pathological hallmarks of Alzheimer's disease, and as a result Abeta neuroimaging in vivo with positron emission tomography (PET) provides an important tool for the evaluation of the causes.  [review]\n","Dentate gyrus principal cells in APP transgenic mice may contribute to early Alzheimer's hippocampal network hyperexcitability via a presynaptic mechanism with cognitive defects.\n","The histidine-rich domain of selenoprotein P is capable of binding Cu ions in both oxidation states of Cu(+) and Cu(2+) with high affinity and of modulating Cu(+) and Cu(2+)-mediated ABETA aggregation, reactive oxygen species production, neurotoxicity.\n","Study seeks to elucidate the Abeta-dependent changes in wild-type human tau that cause synaptic loss and cognitive decline in Alzheimer's disease, focusing on changes in synaptic proteins in the Fyn kinase pathway\n","Subtle memory impairment with a positive beta-amyloid scan identifies healthy individuals at high risk for mild cognitive impairment (MCI) or Alzheimer's disease (AD).\n","Conformational changes induced by the A21G Flemish mutation in the amyloid precursor protein lead to increased amyloid-beta peptides production.\n","It is a key player in neuronal differentiation.\n","These new thermodynamic data strengthen structural interpretations for the Cu-ABETA complexes and provide valuable insights into the molecular mechanism by which copper chemistry may induce oxidative stress in Alzheimer's disease.\n","The soluble building blocks of the abnormal brain structures in Alzheimer disease pathogeneisis are amyloid-beta (Abeta) peptides for plaques and tau for neurofibrillary tangles.\n","This article reviews studies on the structure, expression and post-translational processing of beta-amyloid precursor protein (APP)--{REVIEW}\n","Structure and concentration of amyloid-beta play an important role in the effect of intravenous immunoglobulin (IVIG) on blood-brain barrier tightening and cytokine neutralization.\n","Larger assemblies of amyloid-beta or additional non-amyloid-beta components may play a role in binding of amyloid-beta42 to prion PrP(C) in Alzheimer's disease.\n","A hierarchical, biochemical sequence of amyloid-beta aggregation and accumulation is related to disease progression and may be relevant for an increasing toxicity of amyloid-beta aggregates.\n","The presence of ApoE4 may attenuate amylin's capacity to remove Abeta, especially Abeta1-40, from the Alzheimer's disease brain.\n","Study of secretory forms of human Abeta1-40 and Abeta1-42 expressed in Drosophila neurons and the preferential localization of Abeta1-42 within AEL (autophagy-endosomal-lysosomal)vesicles\n","Capturing a reactive state of amyloid aggregates: NMR-based characterization of copper-bound Alzheimer disease amyloid beta-fibrils in a redox cycle.\n","We now show that the amyloid beta-peptide clearance protein transthyretin is also epigenetically up-regulated by amyloid precursor protein intracellular domain\n","Its gene variant, A673T (rs63750847) was recently reported to protect against Alzheimer's disease and age-related cognitive decline.\n","beta-APP may thus contribute to the pathogenesis of refractory epilepsy.\n","Data indicate that the interaction of nicotine molecule with the beta-sheet of amyloid beta-protein (Abeta) peptide transforms the beta-sheet to an alpha-helical structure, which helps prohibit the aggregation of Abeta-protein.\n","mass spectrometry data and molecular dynamics simulations consistently identified the 17-21 Abeta1-40 portion as the location of the interaction region between peptide and the Ac-LPFFN-NH2 beta-sheet breaker.\n","Data show that contact of platelets with soluble beta-amyloid peptide (Ass) leads to Ass production in platelet culture.\n","Data indicate taht reelin interacts with amyloid beta-protein(1-42) and is sequestered by fibrils.\n","Abeta accumulation is non-cell autonomous, with the primary age-dependent contribution to cerebral Abeta deposition arising from mutant presenililn 1-dependent cleavage of APP within cells other than excitatory neurons.\n","the existence of a structurally related family of quasi-fibrillar conformers of Abeta42, which is stabilized both by curcumin and by Zn(2+.)\n","copper promotes APP trafficking by promoting a GSK3beta-dependent phosphorylation\n","results provide a mechanistic connection between lipid alterations in these microdomains and amyloidogenic processing of amyloid precursor protein\n","results suggest amyloid-beta oligomers induce neuronal death by triggering methylglyoxal(MG) production; increased release of MG is a direct consequence of triosephosphate isomerase nitrotyrosination due to amyloid-beta peptide action at the 2 tyrosi [...]","This study demonstrates that phosphorylation at serine 26 (S26) impairs ABETA fibrillization while stabilizing its monomers and nontoxic soluble assemblies of nonfibrillar morphology.\n","Data show the interaction between amyloid-beta peptide fragment and hydrophobic substrate binding site of phospholipase A2 (PLA2) involving H bond and van der Waals interactions.\n","Our results suggest that APP overexpression, and not Abeta overproduction, is responsible for EEG abnormalities in our transgenic mice and can be rescued independently of pathology.\n","seven novel frameshift mutations in exons 16 and 17 of the APP gene in Moroccan patients with Alzheimer's disease;mutations may eventually become genetic markers for Alzheimer's disease predisposition\n","Results indicate APP-driven alterations in hippocampal and amygdala c-Fos expression during memory acquisition and retrieval, confirm detrimental effects of early-stage amyloid synaptic pathology on neural network dynamics in a mouse model\n","TGFbeta2 causes death in neuronal cells expressing wild-type APP, but not in those expressing the Alzheimer disease-protective mutant of APP\n","Inhibition of PLD2 ameliorated ABETA-induced reduction of soluble amyloid precursor protein alpha secretion.\n","Its mutation is the major causes of eraly-onset familial Alzheimer's disease.\n","These results demonstrate the ability of Abeta to accumulate iron, offering an explanation for previously observed local increases in iron concentration associated with AD lesions.\n","Results showed that in fibroblasts from normal subjects as well as from Lesch-Nyhan syndrome patients: the real profile of APP isoforms accounted for epigenetic mechanisms in the regulation of alternative APP pre-mRNA splicing.\n","soluble Abeta oligomers disturb long-term depression induction and cerebellar function in a transgenic Alzhiemer disease mouse model\n","Greater systemic arterial stiffness is associated with the extent of Abeta accumulation in the brain during 2 years of follow-up.\n","Demonstration of APP expression level is a safe and effective approach for reducing Abeta deposition in Alzheimer disease transgenic model mice.\n","This study demonistrated that knock-in mice that harbor Swedish and Beyreuther/Iberian mutations with and without the Arctic mutation in the APP gene. The mice showed Abeta pathology, neuroinflammation and memory impairment in an age-dependent manner.\n","effects of structural changes at the center of the turn, Gly25-Ser26, on Abeta42 conformational dynamics and assembly\n","3D structures and redox potentials of Cu2+-ABETA(1-16) complexes at different pH are determined using homology modeling and quantum-mechanics-based methods.\n","CSF levels of Abeta1-42 were decreased, but Abeta1-28 levels were increased in Down syndrome patients.\n","The C-terminal threonine of Abeta43 nucleates toxic aggregation via structural and dynamical changes in monomers and protofibrils.\n","Data suggest that link between amyloid beta dimers and Alzheimer's disease results from ability of dimers to further assemble and form synaptotoxic assemblies that persist for long periods of time; synthetic peptides, Abeta(1-40), were used here.\n","The results of this study indicated that overexpression of mutant hAbetaPP initiates a cascade of pathologic events well before the appearance of visible Abeta plaques.\n","Amyloid-beta alters ongoing neuronal activity and excitability in the frontal cortex.\n","Interaction of the protein with homer3 protein is regulated by calcium homeostasis.\n","Transmission electron microscopy identifies a larger number of prefibrillar aggregates of Pyroglutamylated ABETA at early stages of aggregation and suggests that Pyroglutamylated ABETA affects the fibrillogenesis even at low molar fractions.\n","Our results support the view that DR6 functions with APP to modulate synaptic density in the adult CNS\n","These results provide direct support for the model that APP and DR6 function cell autonomously and in the same pathway to control pruning\n","Microbleeds are present with cerebrospinal fluid (CSF) beta-amyloid 42 (Abeta42), total tau, and tau phosphorylated at threonine 181 (P-tau181) as well as a subset of APOE epsilon4 carriers and noncarriers.\n","MicroRNA-384 regulates both amyloid precursor protein and BACE-1 expression.\n","The periphery of parenchymal amyloid plaques was largely composed of CAA mutant Abeta. Non-mutated Abeta fibril seeds promoted CAA mutant Abeta fibril formation in vitro.\n","APP modulates FoxO-mediated cell death through AICD, which acts as a transcriptional co-activator of FoxO.\n","intracellular Abeta undergoes pathological oligomerization through critical conformations formed inside the endoplasmic reticulum.\n","These findings show that the AD-like phenotype of NPC model cells can be partly reverted by promoting a non-amyloidogenic processing of APP through the upregulation of GGA1 supporting its preventive role against AD\n","sAPP modulates iron efflux from brain microvascular endothelial cells by stabilizing the ferrous iron exporter ferroportin.\n","N-terminally truncated Abeta(x-42) induced the phagocytosis of microbeads significantly more effectively than did Abeta(x-40).\n","the nuclear translocation of Abeta42 impacts gene regulation, and deleterious effects of Abeta42 in Alzheimer disease pathogenesis may be influenced by altering the expression profiles of disease-modifying genes\n","This study demonistrated that the APP transgenic rat have the intraneuronal development of AD-like amyloid pathology includes a mixture of molecular species ; and that the early presence of these species within neurons has deleterious effects in the CNS.\n","The results demonstrate a complex interaction between tau and AICD involving activation of GSK3beta in promoting cell death, and the ability of Hirano bodies to modulate this process.\n","Data suggest that activity/structure of HET-S/prion/amyloid are very robust; only a few key mutations are able to corrupt structure/function; while some mutations strongly destabilize folding, many substitutions in fact increase stability of folding.\n","Exogenous Abetas stimulate the normal cortical adult astrocytes to produce and secrete VEGF-A through a CaSR-mediated mechanism. Abetas in the AD brain may make astrocytes into multi-agent AD-driving \"machines\" via a CaSR signaling mechanism(s).\n","Carriers of the apolipoprotein E (APOE) epsilon4 allele, the major genetic risk for Alzheimer's disease (AD), harbor an increased load of beta-amyloid (Abeta) plaque burden that is felt to be a major instigator of AD development.\n","study provides a detailed atomistic picture of the H6R-mediated conformational changes that are consistent with the experimental findings and highlights the important role of the N-terminal in Abeta peptide aggregation\n","Role of N-terminal residues in Abeta interactions with integrin receptor and cell surface\n","the Abeta amyloid plaques in the brains of bigenic mice inoculated with Abeta42 prions prepared in the presence of SDS were similar to those found in mice that received Abeta40 prions.\n","at least two distinct strains of Abeta prions can be discerned in the brains of AD patients and that strain fidelity was preserved on serial passage in mice.\n","ABETA 42 increased uptake of H3N2 and H1N1 influenza A virus by neutrophils. ABETA 42 reduced viral protein synthesis in monocytes and reduced H3N2 and H1N1 influenza A virus -induced interleukin-6 production by these cells.\n","Many adults with Down syndrome can tolerate amyloid-beta deposition without deleterious effects on cognitive functioning.\n","These studies indicate that it is possible to prevent the generation of neurotoxic oligomers by targeting the cholesterol-binding domain of Abeta peptides. [review]\n","In this review, we present some examples of APP associations and the role played by these interactions, which are generally involved in the pathological progression of Alzheimer's disease.\n","R-cysteine modification suppresses the adsorption, nucleation, and fiber elongation processes of ABETA(1-40) and thus largely inhibits amyloid fibril formation on the surface, while S-modification promotes these processes.\n","A probabilistic generative model predicts with high confidence that the cerebrospinal fluid biomarkers become abnormal in a distinct sequence: amyloid-beta1-42, phosphorylated tau, total tau.\n","Its K724M mutation causes Chinese early-onset familial Alzheimer's disease.\n","Naturally occurring antibodies against amyloid beta (Abeta) protein play a role in Abeta-clearance, and such a mechanism appears to be impaired in Alzheimer's disease.\n","RanBP9 relocates APP intracellular domain to Tip60-enriched nuclear speckles and prevented the formation of nuclear spots formation; results place RanBP9 as an important player in the multiple steps of AbetaPP signaling\n","The results demonstrated that the A2V mutation in amyloid-beta (Abeta) 1-42 is able to promote a peculiar oligomerization process pathway of Abeta1-42 that leads to the formation of annular structures with a higher hydrophobicity profile.\n","This study indicates a regulatory role of the D678H mutation in APP sorting and processing, and provides genetic evidence for the importance of APP sorting in Alzheimer's disease pathogenesis.\n","Data suggest that aggregation of amyloid beta(1-42) can be prevented by dietary antioxidant such as quercetin; in these studies, expression of amyloid beta(1-42) in muscle of transgenic Caenorhabditis elegans is used as model for Alzheimer disease.\n","Study found increased levels of ATBF1 in the cytoplasm of hippocampal pyramidal neurons in Alzheimer's disease brains and that ATBF1 binds to the C-terminal of A-beta-PP, increasing the steady state levels of A-beta-PP and resulting in increased A-be [...]","Abeta25-35 can induce the release from human neutrophils of pro-MMP-9, a metalloprotease involved in the onset of inflammation\n","Effect of the Interaction of the amyloid beta (1-42) peptide with short single-stranded synthetic nucleotide sequences: morphological characterization of the inhibition of fibrils formation and fibrils disassembly.\n","Non-chaperone proteins prevent amyloid formation and reduce the cytotoxicity of the Abeta peptide.\n","These findings demonstrate the therapeutic potential of Abeta-specific DARPins for the treatment of Alzheimer disease.\n","each Abeta42 protein forms a single beta-sheet with three beta-strands in an antiparallel arrangement.\n","kidney is involved in peripheral clearance of Abeta, and dialysis might be a potential therapeutic approach of Abeta removal.\n","7-Ketocholesterol, an oxidized derivative of cholesterol, majorly enhances the fluidity of the cell membrane and beta-amyloid distribution.\n","Kinetic network analysis of biased simulations resulted in a kinetic model that encompasses all ABETA segments essential for fibril formation.\n","Data (including data from studies of mutant proteins found in Alzheimer patients) suggest that binding of Zn2+ to amyloid beta and amyloid beta fragments follows conformational selection mechanism and, thus, is independent of domain motions.\n","Genetic studies in 2 Iranian families with Alzheimer's disease show that a valine-to-isoleucine substitution in the APP gene was detected in 14 subjects including 6 with Early-onset disease suggesting the importance of APP in early detection.\n","Data show that recombinant gastrokine 1 (GKN1) interacts with amyloid-beta peptide (1-40) preventing its aggregation.\n","Study demonstrates that AbetaPP/BACE1 association is significantly favored, if not promoted, by the physical microenvironment of lipid rafts in the early neuropathological stages of Alzheimer's disease\n","Studies indicate that amyloid-beta (Abeta) can be internalized into neurons through unidentified Abeta receptors and induces malfunction of subcellular organelles, which explains some part of Abeta neurotoxicity.\n","Cerebrospinal fluid Abeta42 is correlated with cortical Abeta deposition identified by PET scan in patients with mild cognitive symptoms.\n","Results show that APP mutations in the E1 copper binding domain had no impact on alpha- or beta-secretase processing but mutation of histidine 14 down-regulated beta-secretase processing without impacting on non-amyloidogenic proteolysis\n","The conformational heterogeneity of the beta-amyloid peptide(1-42) monomers has been found to affect the translational and rotational motions of hydration water molecules in a nonuniform manner.\n","DNAJB6 interacts with growing amyloid-beta 42 (Abeta42) aggregates, which leads to sub-stoichiometric inhibition of amyloid formation\n","APP regulates migration and ADAM10/ADAM17 gene expression in prostate cancer cells.\n","findings suggest that Abeta42-induced impairment of glutamatergic synaptic function depends on its internalization and intracellular accumulation.\n","Data suggest that amyloid beta peptides significantly reduce levels of glutathione in both astrocytes and neurons, effects which are dependent on external calcium. [REVIEW]\n","Consistent with the expression of APP in pre-synaptic vesicles, the synaptic APP intracellular domain interactome is predominantly constituted by pre-synaptic, rather than post-synaptic, proteins.\n","A2T is a mutation in APP that modulates kinetic and thermodynamic properties of amyloid-beta (Abeta) aggregation\n","A673T, a protective allele of APP, reproducibly reduces amyloidogenic processing of APP and also mildly decreases Abeta aggregation\n","the immune response to Abeta42 fibrils is diverse and reflects the structural polymorphisms in fibrillar amyloid structures\n","data demonstrate that cyclopamine alters APP processing and Abeta generation by inducing changes in APP subcellular trafficking and APP-CTF degradation.\n","Data indicate that transgenic mouse with human mutant Alzheimer disease protein (APP)/presenilin 1 (PS1) exhibited an abnormal neurochemical profile.\n","APP may be a novel regulator of protein synthesis in dividing human cells.\n","Data indicate the intermediate state of amyloid beta (Abeta) in Alzheimer's disease.\n","Hydrogen sulfide can induce APP processing.\n","APP likely represents one of a range of copper binding proteins that PCa cells employ in order to ensure efficient proliferation despite elevated concentrations of the metal within the tumour microenvironment.\n","Abeta-mediated effects on both MT and actin networks are reviewed with a focus on the relevance of the elicited cytoskeletal signaling events targeted in AD pathology. Review.\n","Vascular Abeta load was significantly increased in the brains of aged individuals with a history of hypercholesterolaemia.\n","These findings give new insights on the molecular mechanism of the amyloid/membrane interaction, highlighting the peculiar role of cholesterol.\n","The alpha-helical propensity of residues 15-25 may play a determinant role in the aggregative ability of Amyloid beta peptides.\n","Data (including data from studies using hydroxyl radical footprinting) suggest individual fibrils of Abeta40 (a fragment of APP) exhibit structural heterogeneity; regions of two-filament structure alternate with regions of three-filament structure.\n","Wnt signaling might be implicated in Abeta42 toxicity.\n","Data indicate that the secretion of APP and its proteolytic processing products traverse different pathways in the somatodendritic compartment before axonal entry.\n","This study reports atomic-resolution fibril structure of the ABETA 1-40 peptide with the Osaka mutation (E22Delta), associated with early-onset Alzheimer's disease.\n","structural basis behind interactions between the beta amyloid (Abeta) peptides and cellular membrane bilayers, resulting in distinct evolution pathways\n","The correlation between N-terminal interactions and capping of the height of the Abeta oligomers provides insights into the mechanism of inhibition and the pathway of Abeta aggregation.\n","The clinical utility of the CSF biomarkers amyloid-beta-1-42, t-tau, and p-tau (phosphorylated tau protein) for Alzheimer's disease diagnosis has been well documented; progress in use of these biomarkers for early diagnosis is discussed. [REVIEW]\n","These findings highlight the role of neuronal exosomes in Abeta clearance, and suggest that their downregulation might relate to Abeta accumulation and, ultimately, the development of AD pathology.\n","a function of SNX27 in regulating beta-amyloid (Abeta) generation by modulating gamma-secretase activity.\n","RPE iron overload could contribute to Abeta accumulation in the retina.\n","Data suggest that sub-stoichiometric copper ions (Cu2+) affect misfolding of Abeta(1-40) and the more toxic Abeta(1-42) in markedly different ways; Cu2+ accelerates Abeta(1-40) fiber formation; mature Abeta(1-42) fibers disassemble with added Cu2+.\n","the increase of APP expression is causally linked to tumorigenicity as well as invasion of aggressive breast cancer and, therefore, the targeting of APP may be an effective therapy for breast cancer.\n","ABETA (16-22) is observed to organize into anti-parallel and parallel beta-sheet arrangements. Confinement in the sodium bis(2-ethylhexyl) sulfosuccinate reverse micelles stabilizes extended peptide conformations and enhance peptide aggregation.\n","some brain regions show periods of accelerated volume loss well before the CSF Abeta42 threshold. This implies that signs of brain atrophy develop before the current conventional definition of \"preclinical Aalzheimer's disease\"\n","The present results add to the growing evidence of AbetaPP-related hyper-excitability, and further implicate both soluble Abeta and non-Abeta AbetaPP metabolites in its early emergence.\n","Structural analysis of membrane-bound hECE-1 dimer using molecular modeling techniques: insights into conformational changes and Abeta1-42 peptide binding.\n","Amyloid Precursor Protein appears to play a central role in regulating cell cycle entry with the rate of protein synthesis\n","The E1 domain of APP shows pH-dependent conformations; the pH-dependent structure of APP seems to influence its trafficking and processing\n","The APP A673T variant is extremely rare in US cohorts and does not play a substantial role in risk for AD in this population.\n","Utilizing atomic force microscope controlled tip-enhanced Raman scattering, the study directly shows the secondary structure information for ABETA(1-40) assembly in situ at the nanoscale.\n","Golgi fragmentation in Alzheimer's disease accelerates APP trafficking and amyloid-beta production. [Review]\n","Overexpression of heparanase lowers the amyloid burden in amyloid-beta precursor protein transgenic mice\n","Data show that co-expression with sodium-hydrogen antiporter NHE6 or treatment with the Na(+)/H(+) ionophore monensin shifted amyloid precursor protein (APP) away from the trans-Golgi network into early and recycling endosomes in HEK293 cells.\n","There were significant differences in CSF Abeta42 between patients with Alzheimer's disease and non-demented controls.\n","Altered genomic mosaicism in single, sporadic Alzheimer's disease (AD) neurons characterized by increases in DNA content and amyloid precursor protein (APP) gene copy number, are reported.\n","molecular dynamics simulations of the solvated wild-type (WT), A2V, and A2T Abeta monomers; simulations reveal that although all 3 variants remain as collapsed coils in solution, there exist significant structural differences among them at shorter timescales\n","elevating klotho expression decreases premature mortality and network dysfunction in human amyloid precursor protein transgenic mice\n","we show that Abeta species can hyperexcite corticotropin releasing hormone neurons, providing a mechanism by which Abeta influences stress-related symptoms\n","The soluble ABETA(1-42) species were analyzed by various liquid-state NMR methods. Transient formation of a micelle species was observed at the onset of the aggregation kinetics.\n","Interaction of Zn(2+) with the metal-binding domain of the English (H6R) amyloid-beta mutant results in the formation of peptide dimers.\n","we review the recent multitarget strategies for the drug discovery in the treatment of Alzheimer's disease by focusing on the involvement of Abeta--{REVIEW}\n","Study applied a pathway scoring method to a large-scale siRNA screen aimed at identifying regulators of APP processing; identification of these processes/pathways, their differential impact on APP processing, and their relationships to each other, pr [...]","Interaction of C60 fullerene-polyvinylpyrrolidone complex and brain Abeta(1-42)-peptide in vitro\n","Cerebrospinal fluid APP shows a robust association with ventricular size in preterm infants treated for post-hemorrhagic hydrocephalus of prematurity.\n","A 500 ns molecular dynamics simulation was performed for the system consisting of nine helices of ABETA 13-23.\n","APP enhances Nav1.6 sodium channel cell surface expression through a Go-coupled JNK pathway\n","Abeta42-mediated contact system activation is driven by factor XII and can occur in the AD circulation\n","results of this exploratory investigation suggest that an APP SNP and an APH1B SNP are marginally associated with PD CSF Abeta42 levels in APOE varepsilon4 noncarriers\n","findings suggest that the folded Abeta40-Zn(2+) complex modulates the fibril ends, where elongation takes place, which efficiently retards fibril formation.\n","Beta amyloid peptide is suggested by some to be important in maintaining synaptic function, learning and memory.\n","The APP c.*331_*332del variant affected APP messenger RNA structure and binding of two microRNAs (miR-582-3p and miR-892b), providing a mechanism for the development of cerebral amyloid angiopathy.\n","Zn(2+) and to a larger degree also Cu(2+) enhance the binding of heparin to APP E2, consistent with an extracellular regulation of the function of APP by both metal ions.\n","The high energy demands associated with neuronal functions such as memory formation and protection from oxidative stress put these cells at particular risk from Abeta-induced hypometabolism\n","The work reveals the significant side effect of Tris on the interaction of Abeta with Cu(2+), which will greatly improve the quantitative investigation on Abeta-Cu(2+) interaction\n","CSF levels of Abeta1-42 were moderated by ApoE4 genotype in a minority of patients with HIV dementia.\n","No difference in CSF Abeta levels was found between patients with Creutzfeldt-Jakob disease and other neurodegenerative disorders.\n","Solid-state NMR data indicate an antiparallel beta-sheet within the C-Terminal Region of 42-Residue Alzheimer's amyloid-beta peptides when they form 150-kDa oligomers.\n","Atorvastatin prevents amyloid beta oligomer-induced neurotoxicity in cultured rat hippocampal neurons by inhibiting calpain- and caspase-mediated Tau cleavage.\n","cleavage of BRICHOS in a loop region that is cleaved during proSP-C biosynthesis results in increased capacity to delay Abeta(42) fibril formation.\n","In this review, we highlight various structural ensembles of A beta peptide revealed and characterized by computational approaches in order to find converging structures of A beta monomer.\n","The study explores the uptake of ganglioside GM1 into two types of ABETA aggregates and the related membrane damage.\n","Natural human anti-ABETA IgG binding readily binds ABETA oligomers but does not bind monomers.\n","These experiments suggest that Abeta(1-42) C-terminal Ala42 of , absent in Abeta(1-40), forms a salt bridge with Lys28 to create a self-recognition molecular switch that excludes Abeta(1-40).\n","Results show that insulin-like growth factor II (IGF-II) overexpression enhanced the levels of amyloid precursor protein (APP) in SK-N-AS neuroblastoma cells.\n","In a family with Alzheimer's disease, the APP mutation was found to be autosomal dominant.\n","It is likely that Zn(2+) and Cu(2+) play as a key-mediating factor in pathophysiology of the synaptic dysfunction in which ABETA is involved. [review]\n","tau allows Abeta oligomers to inhibit axonal transport through activation of GSK3beta, possibly by facilitating aberrant neuronal activity.\n","Lower levels of cerebrospinal fluid ABeta42 are associated with reduced cognitive functions in early Parkinson's Disease.\n","The result also shows that Apolipoprotein E4 induces the aggregation of ABETA 42 more specifically and rapidly than that of ABETA 40.\n","Competition between Fibrillation and Induction of Vesicle Fusion for the Membrane-Associated 40-Residue beta-Amyloid Peptides.\n","A highly aggregation prone ABETACu(II) species is formed on the sub-second timescale at mildly acidic pH. This observation might be central to the molecular origin of the known detrimental effect of acidosis in Alzheimer's disease.\n","Amyloid precursor protein gene the second most common gene of the autosomal-dominant cases of Early onset familial Alzheimer Disease.\n","the early ESCRT machinery has a dual role in limiting intracellular Abeta accumulation through targeting of APP and processing products to the lysosome for degradation, and promoting Abeta secretion.\n","Abeta appears to be necessary, but not sufficient, to cause Alzheimer's disease --{REVIEW}\n","These results demonstrate a stage-dependent plasma Abeta increase that is augmented by loss of glomerulotubular integrity, low body weight, and inflammation, demonstrating a multifaceted role of renal dysfunction in Abeta retention.\n","The assembly state of Abeta during the lag phase, the time required by an Abeta solution to reach the exponential growth phase of aggregation, was characterized by a dominant monomer fraction below 1 S and a population of oligomeric species between 4 and 16 S\n","Abeta down regulates basal BDNF levels via Abeta-induced CREB transcriptional down regulation.\n","Staufen 1 (STAU1) is demonstrated to have interaction with APP, using yeast two-hybrid screening and co-immunoprecipitation in mammalian system.\n","APP levels then decrease progressively as a function of age in close relationship with the gradual normalization of FMRP and hnRNP C levels.\n","the importance of interaction of zinc ions with the metal-binding domain 1-16 of Abeta as a molecular mechanism that leads to Abeta aggregation.\n","Experiments described in this article provide new information about the structural properties of intermediates in the ABETA 40 assembly process.\n","Beta-Sheet secondary structure develops during the irreversible lateral association of the oligomers of ABETA 42. The first step in this conversion is the formation of an antiparallel beta-hairpin stabilized by intramonomer hydrogen bonding.\n","Report alternative splicing of APP in colorectal cancer.\n","In contrast to anionic lipids, zwitterionic lipids, which are typical of neuronal soma, did not induce any significant conformational difference in ABETA 40 fibrils.\n","findings from this study suggest a close relation between the severity of regional atrophy and cognitive and language impairment, but argue against a strong association between regional beta-amyloid burden and such deficits in aphasic Alzheimer's dis [...]","The authors report that both Abeta42 and Abeta43 spontaneously aggregate into mature amyloid fibrils via sequential appearance of the same series of oligomeric and protofibrillar intermediates, the earliest of which appears to lack beta-structure.\n","APP functionally cooperates with PIKfyve in vivo. This regulation is required for maintaining endosomal and neuronal function.\n","Data presented a novel model to link phospholipid metabolism to APP processing and also suggested that PLTP played an important role in Abeta metabolism and would be useful to further elucidate functions of PLTP in Alzheimer's disease susceptibility.\n","Lipid insertion domain regulates protein membrane orientational transitions.\n","A dominant negative mutant of Arf6 blocks direct transport of APP to lysosomes, but does not affect classical endocytosis to endosomes.\n","The computational models support the cross-sequence interactions between ABETA and IAPP pentamers, which would lead to the complex hybrid ABETA-IAPP assemblies.\n","FE65 influences APP degradation via the proteasome, and phosphorylation of FE65 Ser(610) by SGK1 regulates binding of FE65 to APP, APP turnover and processing.\n","Wild-type and Italian-mutant Abeta both form fibrils characterized by the cross-beta architecture, but with distinct beta-sheet organizations.\n","Results indicate that persistent rab5 overactivation through beta-cleaved carboxy-terminal fragment of APP-APPL1 interactions constitutes a novel APP-dependent pathogenic pathway in Alzheimer's disease\n","Sex steroid hormones distinctively increase mitochondrial bioenergetics in APP/ABETA and TAU-overexpressing cells.\n","These results suggest that yonk could rescue cognitive deficits by ameliorated amyloid burden through regulating APP processing, inhibited the over-activation of microglia and astrocytes as well as restored neurogenesis.\n","ApoE expression attenuated intracellular trafficking of APP and Alcbeta\n","The PIKfyve complex is required for APP trafficking, suggesting a feedback loop in which APP, by binding to and stimulating phosphatidylinositol-3,5-bisphosphate vesicle formation may control its own trafficking.\n","synthesized four singly substituted Tyr variants in different positions across the Abeta42 sequence and studied the stability of the resulting cross-linked oligomers as well as procedures for fractionating the oligomers to obtain different sizes\n","Tyr 10 residue is pivotal in Abeta-Cu(II) complex and shows important relevance to oxidative stress, implicating the novel significance of Tyr 10 residue as well as Abeta-Cu(II) complex in the pathology of AD.\n","variants in FRA10AC1 associated with CSF Abeta1-42 level passing the genome-wide significance threshold, were identified.\n","Alternative splicing of APP, VEGFA and NUMB may play an important role in pathogenesis of pancreatic ductal adenocarcinoma.\n","The membrane-active amphibian peptide caerin 1.8 inhibits fibril formation of amyloid beta1-42.\n","A decrease in amounts of WASF1 mRNA was also observed in human Alzheimer's disease brains, suggesting clinical relevance of the negative feedback circuit involved in homeostatic regulation of Abeta production\n","Data suggest that expression of beta-amyloid peptide in neurons is up-regulated in G1/S phase and down-regulated in G2/M phase.\n","more than one-third of APOE4 noncarriers with the primary clinical diagnosis of mild to moderate Alzheimer dementia had minimal Abeta plaque accumulation in the cerebral cortex\n","The search for the genetic factors contributing to Alzheimer disease (AD) has evolved tremendously throughout the years. It started from the discovery of fully penetrant mutations in Amyloid precursor protein, Presenilin 1, and Presenilin 2 as a caus [...]","description of a new physiological APP processing pathway, which generates proteolytic fragments capable of inhibiting neuronal activity within the hippocampus\n","This study shows by Atomic Force Microscopy that attachment of ApoE4/ABETA complexes to basement membrane laminin is significantly weaker than ApoE3/ABETA complexes.\n","The pattern of development of cerebral amyloid angiopathy in the human brain suggests expansion of ABETA from the basement membranes to progressively replace all tissue elements in the artery wall.\n","Asian patients with APP mutations presented less frequently with aphasia. Thus, clinical features could be modified by underlying mutations, and Asian familial Alzheimer's disease patients may have different clinical features when compared with white [...]","distribution and activity of TRPC6 can be regulated by cardiotonic steroids like ouabain and the naturally occurring peptide Abeta(1-40) which underlines the pathophysiological significance of these processes.\n","that Abeta1-42 oligomers could cause disturbances in insulin/Akt/EAAT signaling in astrocytes\n","a considerable amount of evidence goes against the classical amyloid hypothesis and illustrates a new picture in which the Abeta loss of function, rather than its accumulation, has a pathogenic role in AD.\n","results suggest that a kind of Abeta40 dimer with a parallel beta-sheet might not be pathological\n","study reports that sAbetaPPalpha, the product of the cleavage of AbetaPP by alpha-secretase, is a potent endogenous direct inhibitor of the BACE enzyme, and that its inhibition is likely by an allosteric mechanism\n","Results suggest that TMEFF2 is a brain-enriched endogenous modulator of Abeta neurotoxicity and an enhancer of alpha-secretase processing of AbetaPP\n","This study demonstrated that the AbetaPP M722K mutation contributed to the cause of Early-Onset Familial Alzheimer's Disease in this Chinese pedigree mediated by increased Abeta 42/Abeta 40.\n","None of the homodimers was cleaved in vitro by purified gamma-secretase, strongly suggesting that homodimerization protects amyloid precursor protein C-terminal fragment C99 fragment from cleavage.\n","The study explored ABETA functional brain networks Alzheimer's disease and Mild Cognitive Impairment patients.\n","Nef exosomes isolated from the plasma of individuals with HIV-associated dementia (HAD) can induce amyloid beta (1-42) secretion in cultured neurons.\n","The very tight fm affinity of Cu(2+) for Abeta(11-40/42) explains the high levels of Cu(2+) observed in Alzheimer disease plaques.\n","evidence that HFD, by regulation of subcellular trafficking of BACE1, promotes APP cleavage.\n","a magic angle spinning solid-state NMR study demonstrating that the NSAID sulindac sulfide interacts specifically with Alzheimer disease Abeta fibrils.\n","Using surface plasmon resonance and atomic force microscopy the study demonstrates that Ca(2+) ions, in conjunction with lipid bilayer, lower the threshold concentration for ABETA aggregation.\n","Studies indicate that a common pathway of beta-amyloid precursor protein (APP) is associated with the development of beta-amyloidopathy in structural elements of the eye and the brain.\n","IGF-I showed a significant negative correlation with age (beta = -0.357, P = 0.002) and a positive correlation with Abeta42/Abeta40 ratio (beta = 0.318, P = 0.007).\n","Study elucidated alterations in TTR, APP and the global gene expression profile in the frontal cortex between idiopathic normal pressure hydrocephalus patients and nondemented control brain\n","findings may suggest that these multiple transporters/receptors and IDE expressed on the choroid plexus epithelium, ventricular ependymal cells and brain microvessels complementarily or cooperatively contribute to the clearance of amyloid-beta peptid [...]","ACAT1 has a role in regulating the dynamics of free cholesterols in plasma membrane which leads to the APP-alpha-processing alteration\n","MSCs from APP695 mice have higher neuronal differentiation efficiency than MSCs from wild type mice (WT MSCs). The expression of Notch-1 signaling decreased during the differentiation process.\n","This study found evidence of mitochondrial dysfunction (i.e. decreased mitochondrial membrane potential (MMP), increased production of reactive oxygen species (ROS) and oxidative DNA damage) at 6 months of age\n","Cell viability and ROS assays indicate that graphene oxide can indeed mitigate cytotoxicity of Abeta peptide amyloids.\n","Study suggests that ABCA2 modulation of sphingolipid metabolism activates a signaling pathway that regulates amyloid precursor protein transcription\n","The reduction of connectivity of the dorsal PCC [Posterior cingulate cortex ]with the retrosplenial cortex on the right side was closely related to decreased CSF Abeta1-42 levels in patients with AD.[Alzheimer's disease]\n","The purpose of this review article is to summarize recent research on how cerebral vascular ABETA and amyloid beta precursor protein influence cerebral hemostasis. [review]\n","modulation of proteostasis is a distinct biological function of sAPPalpha and does not require surface-bound holo-APP.\n","PrP-Abeta oligomers binding might be the underlying mechanism of the prion diseases and Alzheimer's disease. [review]\n","Male heterozygous (HET) APP23 mice, overexpressing human APP 751 carrying the Swedish double mutation (K670M/N671L) were used for all experiments.  The ABETA 1-42/ABETA 1-40 ratio spikes at 2 distinct ages: 1.5 months and 18 months. An initial build  [...]","The effect of different Abeta concentrations, Abeta:ThT ratios, differences between the 40 (Abeta40) and 42 (Abeta42) residue long variants of Abeta, and the effect of stirring were also examined.\n","TRPC6 specifically interacts with APP leading to inhibition of its cleavage by gamma-secretase and reduction in Abeta production.\n","Mutant SOD1 Increases APP Expression and Phosphorylation in Cellular and Animal Models of ALS\n","Study identifies a common mechanism of transport into neurites of proteins linked to the pathology of Alzheimer's disease (i.e. sAPP) and ALS (i.e. FUS, TDP-43 and SOD1)\n","Results demonstrate the differential effects of Alzheimer's disease biomarkers p-tau and amyloid-beta on brain functional connectivity networks, supporting a possible division of labour between the cardinal pathologies\n","Abeta binds to NCAM2 at the cell surface of cultured hippocampal neurons and induces removal of NCAM2 from synapses. Abeta-dependent disruption of NCAM2 functions in Alzheimer's disease hippocampus contributes to synapse loss.\n","Abeta activates FXII, resulting in FXI activation and thrombin generation in human plasma, thereby establishing Abeta as a possible driver of prothrombotic states\n","REVIEW: evidence links amyloid-beta to functional change, progressive brain atrophy, and cognitive decline\n","the antibody NT4X is therapeutically beneficial in Alzheimer mouse models showing that N-truncated Abeta starting with position four in addition to pyroglutamate Abeta3-x is a relevant target to fight Alzheimer's disease.\n","the Alzheimer's disease-protective 'Icelandic' mutation greatly attenuates APP-BACE-1 interactions, suggesting a mechanistic basis for protection.\n","SPIONs with a positive charge have dual effects on the Abeta fibrillation process\n","A+ and A- oligomers display a similar lateral diffusion on the plasma membrane of living cells. However, only the toxic A+ oligomers appear to interact and alter the mobility of GM1.\n","The APP Intracellular Domain Is Required for Normal Synaptic Morphology, Synaptic Plasticity, and Hippocampus-Dependent Behavior.\n","These findings suggest that apolipoprotein E-genotype exerts its impact on cerebral blood flow at least partly independently from amyloid beta-deposition.\n","p38alpha MAPK plays a critical role in the regulation of BACE1 degradation and Abeta generation in Alzheimer Disease pathogenesis\n","PrP(C) is highly enriched on exosomes and that exosomes bind amyloid beta via PrP(C) . Exosomes showed highest binding affinity for dimeric, pentameric, and oligomeric Abeta species.\n","Data suggest amyloid-beta peptides (Ab) occur in several forms (monomeric, oligomeric, fibrillar); oligomeric Ab forms interact with cell surface receptors for (1) transcytosis outside of cells, (2) formation of aggregates/plaques, or (3) both. [REVIEW]\n","Astrocytic expression of the mutant APP is involved in the down-regulation of synaptic transmission in cell aging.\n","Redox-mediated posttranslational modification of brain proteins link Abeta and hyperglycaemia to cognitive dysfunction in metabolic syndrome/type 2 diabetes and Alzheimer disease.\n","report kinetic parameters of five different forms of ACE with various amyloid beta (Abeta) substrates together with high resolution crystal structures of the N-domain in complex with Abeta fragments\n","AD-like APP processing yielding to levels of APP, betaCTF and Abeta42/Abeta40 ratio similar to those observed in AD patients\n","Pharmacophore-based screening targeted at upregulated FN1, MMP-9, APP reveals therapeutic compounds for nasopharyngeal carcinoma.\n","This work represents an extensive and quantitative study on the initial events of Abeta oligomerization at physiological concentration.\n","KFERQ motif is important for normal processing and degradation of APP\n","esults suggest that P-gp plays important role in mediating rivastigmine non-cholinergic beneficial effects, including Abeta brain load reduction, neuroprotective and anti-inflammatory effects in the AD mouse models.\n","It plays a role of in the modulation of the proliferation of human somatic cells.\n","Data suggest that both the higher aggregation propensity of amyloid beta protein Abeta42 and the importance of Abeta42 to Abeta40 ratio in the pathogenesis of Alzheimer's disease.\n","Studies indicate that amyloid precursor-like protein 2 (APLP2) and amyloid precursor protein (APP) are linked to increased tumor cell proliferation, migration, and invasion.\n","Hyperglycemia enhances APP expression with increased Abeta production, which downregulates junctional proteins causing increased intercellular permeability in endothelial cells\n","Data (including data from studies using recombinant proteins) suggest that C99 (99-residue C-terminal domain fragment of amyloid beta-protein precursor) exhibits little tendency to partition into liquid-ordered domains of giant unilamellar vesicles.\n","we found Abeta-related increases in frontoparietal control regions compared with baseline activity\n","this study provides support for the conformational selection mechanism of Abeta peptide self-assembly.\n","Bipolar disorder-mild cognitive impairment patients had a non-significant reduction in CSF Abeta1-42 compared to controls, but this was still higher than in the Alzheimer disease group.\n","data show that p-FTAA promoted the formation of insoluble and stable Abeta species that were nontoxic which indicates that p-FTAA might have therapeutic potential.\n","APP overexpression is associated with Down syndrome.\n","The monomer to oligomer transition and the radius of gyration were studied using SANS. A hydrodynamic radius of 1.8+/-0.3 nm was found for Abeta1-40 and 3.2+/-0.4 nm for Abeta1-42 including a surface layer of dHFIP solvent molecules.\n","the downregulation of two validated genes, PSMA5 and PSMB7, inhibits cell proliferation, suggesting that the downregulation of PSMA5 and PSMB7 is involved in APP-induced cell proliferation impairment.\n","Sporadic Abeta accumulation may be partly associated with increased amyloidogenic APP production, especially in APOE varepsilon4-negative subjects.\n","Study with MDR1A knockout mice were crossed with Tg2576 APP transgenic mice indicate that Abeta accumulates to a greater degree in brains of mice lacking MDR1A\n","Study demonstrates the effect of betaAPP/Abeta on the metabolism of arginine, shows for the first time that betaAPP/Abeta simultaneously down-regulated both arginases and increased constitutive NOS isoforms, suggests that the significance of arginase [...]","Data suggest that amyloid beta peptide fragments associated with Alzheimer disease [Abeta(16-22) and Abeta(11-25)] exhibit high degree of polymorphism in forming hydrogen-bonded networks.\n","The authors now show that the very little Abeta generated by PS1 L435F mutant consists primarily of Abeta43, a highly amyloidogenic species which was overlooked in previous studies of this mutant.\n","Data suggest that light-chain subunits/fragments of kinesin-1 inhibit the pathological aggregation of amyloid(beta).\n","these results offer an explanation for the reduced aggregation rate of the Abeta1-40 A2V-WT peptides and the protective effect of A2V in heterozygotes\n","The conformational dynamics of large fatty acids derived oligomers (Abeta42) correlates with their ability to replicate and to induce apoptosis in human neuroblastoma cells, with 12mers being more neurotoxic and prone to replication than 12-24mers.\n","The cumulative data emphasizes the critical importance of Abeta42, yet establishes Abeta40 as a regulator of Abeta42 aggregation.\n","Overexpression of human APP in mice reduce cortical free cholesterol under normal diet and HFD.\n","These findings identify Syt1 as a novel Ca(2+)-sensitive PS1 modulator that could regulate synaptic ABETA, opening avenues for novel and selective synapse targeting therapeutic strategies.\n","Data suggest that the driving forces for beta-amyloid (Abeta) peptides aggregation and Abeta-membrane interactions may be similar at the molecular level.\n","evaluated Abeta-induced DNA methylation status of HMOX1 at -374 promoter CpG site in blood samples from Alzheimer disease patients, patients with mild cognitive impairment, and control individuals\n","Data show that overexpression of wild-type netrin receptor UNC5C (UNC5C) causes low-grade death, which is intensified by an Alzheimer Disease-linked mutation T835M, and mediated by amyloid beta precursor protein (APP).\n","Obstructive Sleep Apnea, and particularly Obstructive Sleep Apnea+Obesity, are associated with increased plasma levels of Alzheimer Disease biomarkers, which decline upon treatment of OSA in a representative, yet not all- encompassing subset of patie [...]","SEPT8 modulates beta-amyloidogenic processing of APP through a mechanism affecting the intracellular sorting and accumulation of BACE1.\n","elevated levels of plasma homocysteine /homocysteine thiolactone contribute to AD pathology via the Abeta-fibrin(ogen) interaction\n","in Alzheimer's disease (AD) brains, elevated DAPK1 levels showed co-relation with the increase of APP phosphorylation. Combined together, these results suggest that DAPK1 promotes the phosphorylation and amyloidogenic processing of APP, and that may  [...]","This study reports the discovery of a TTR mutant, N98A, that was more effective at inhibiting ABETA aggregation than wild-type (WT) TTR, although N98A and WT bound ABETA equally.\n","analysis of the structural basis linking alpha-helicity of the alpha/beta-discordant segment with the conformational conversion propensity of Abeta protein\n","The mechanism involved in the interaction of HSP60-Ass conjugate with HLA-DR-DRB allele considering the fact that Ass (1-42) is highly immunogenic in human and interactions evoked highly robust T-cell response through MHC class II binding predictions.\n","Photoinduced electrons of g-C3 N4 generate reactive oxygen resulting in photooxidation of amyloid peptides that blocks Abeta aggregation.\n","Multifunctional quinoline-triazole derivatives as potential modulators of amyloid-beta peptide aggregation.\n","This review reveled that Mutations in APP and PS-1 and PS-2 genes that are associated with early-onset, autosomal, dominantly inherited AD\n","Data showed that in both PC12 cells and primary neurons, human Abeta1-42 oligomers triggered endoplasmic reticulum stress, leading to insulin signaling impairment mediated by JNK-dependent IRS-1 serine phosphorylation, ultimately resulting in Tau hyp [...]","Taken together, these results suggest that ApoE4 enhances Abeta inhibition of insulin-stimulated AMPA receptor function, which accelerates memory impairment in ApoE4xAPP mice.\n","ABCG1 and ABCG4 alter the distribution of gamma-secretase on the plasma membrane, leading to the decreased gamma-secretase activity and suppressed Abeta secretion\n","The authors demonstrate that pathological PS1 loss-of-function impinges on neurite formation through a selective APP gain-of-function that could impact on axodendritic connectivity and contribute to aberrant axonal sprouting observed in Alzheimer's d [...]","This article reviews the evidence for the role of the Alzheimer's disease -associated peptide ABETA in promoting inflammation and thrombosis in Alzheimer's disease via its interaction with the circulating proteins factor XII and fibrinogen. [review]\n","Abeta phosphorylation at serine 8 causes structural changes in the N-terminal region of Abeta aggregates in favor of less compact conformations. Structural changes induced by serine 8 phosphorylation can provide a mechanistic link between phosphoryla [...]","the amyloid cascade hypothesis in Alzheimer disease should be expanded to include cross-interactions between Abeta and other amyloid proteins.\n","Study of an MPTP-induced cell model of Parkinson's disease, discovered the interactions between hsa-miR-144-3p and APP. MiR-144-3p was found to be down-regulated, along with its target gene APP that participates in regulating MPTP-induced mitochondri [...]","results suggest that co-oligomers are a common form of aggregate when Abeta isoforms are present in solution and may potentially play a significant role in Alzheimer's disease.\n","alpha-synuclein (Parkinson) and Abeta peptide (Alzheimer) no longer form Ca(2+)-permeable pores in presence of drugs that target either cholesterol or ganglioside or both membrane lipids.\n","APP processing is regulated throughout differentiation of cortical neurons and that amyloidogenic APP processing, as reflected by Abeta1-40/42, is associated with mature neuronal phenotypes.\n","APP + PS1 double transgenic rats had altered serum Abeta42 and Abeta42/Abeta40 levels, brain histopathology and cognitive behavior. APP rat brain had many histopathogical abnormalities that are often seen in Alzheimer's disease brains, but their memo [...]","The conditional thermodynamic parameters suggest that, under the experimental conditions, the formation of the Cu(2+)- Abeta(5-16) complex is both an enthalpy and entropy driven process.\n","Flexibility and Solvation of Amyloid-beta Hydrophobic Core.\n","electrostatic interactions in the center of the Abeta peptide sequence play a crucial role in the three-dimensional fold of the fibrils, and by inference, fibril-induced neuronal toxicity and AD pathogenesis\n","using a transgenic model we could not provide evidence to support the hypothesis that PrPC regulates amyloid-beta production\n","data therefore imply that the formation of beta-sheet-rich aggregates is a prerequisite for Abeta(1-42) uptake and cytotoxicity.\n","APP may cooperate with c-KIT mutation/overexpression in the regulation of cell apoptosis but not proliferation in AML1ETO-positive leukemia via the PI3K/AKT signaling pathway.\n","This study presented that Seizures are a common feature of early-onset Alzheimer disease , especially in cases of APP duplication.\n","various proteins have been identified that interact with APP and modulate its cleavage by the secretases.\n","Overall, these findings suggest that the ability of apoE fragments to promote Abeta42 intraneuronal accumulation is specific for both the apoE4 isoform and the particular structural and thermodynamic properties of the fragment.\n","Using mouse olfactory models in which large-scale neurodegeneration is readily observable, we show here that the intrinsic apoptosis pathway is clearly activated in olfactory sensory neurons overexpressing hAPP, supporting this link and further sugge [...]","The data suggest that miR-106b inhibits Amyloid-beta (1-42)-induced tau phosphorylation at Tyrosine 18 by targeting Fyn.\n","APP does not modulate Orai-dependent store-operated calcium entry following quantitative calcium store depletion.\n","aggregating proteins, such as amyloid-beta (Abeta) and alpha-synuclein (alpha-syn), proteins associated with Alzheimer's disease and synucleinopathies, respectively, share similar biophysical and biochemical properties with PrP(Sc) that influence-{REVIEW}\n","while Reelin expression is enhanced in the Alzheimer's brain, the interaction of Reelin with Abeta hinders its biological activity\n","the precise and complex regulation of APP phosphorylation, abundance, and cleavage impacts the generation of nuclear spheres, which are under discussion of being of relevance in neurodegeneration and dementia.\n","These findings thus provide new insights into Abeta-induced mitochondrial defects that may contribute to neuronal dysfunction and Alzheimer's disease pathogenesis.\n","Our study provides insight into the observed dependence of C99 protein cleavage by gamma-secretase, critical to the formation of amyloid-beta protein, on membrane thickness and lipid composition\n","RHBDL4-mediated APP processing provides insight into APP and rhomboid physiology and qualifies for further investigations to elaborate its impact on Alzheimer disease pathology.\n","APP substrate occupancy of these three pockets of gamma-secretase occurs after initial substrate binding but precedes catalysis, suggesting a conformational change in substrate may be required for cleavage.\n","both apolipoprotein E and Abeta1-42 abundance can differ depending upon the type of CJD.\n","Data show that presenilin 1 (PS1)/anterior-pharynx-defective protein 1 (Aph1b), presenilin 2 (PS2)/Aph1aL, PS2/Aph1aS and PS2/anterior pharynx defective 1 homolog B (Aph1b) gamma-secretase produced amyloid beta peptide (Abeta) with a higher Abeta42+A [...]","increased pCRMP2 may underlie the axonal pathology of Lewy body dementias.\n","Data show that valproic acid (VPA) treatment enhanced gender-dependent learning and memory impairment in the human amyloid beta precursor protein/presenilin 1 (APP/PS1) double transgenic mice.\n","Complicated function of dopamine in Abeta-related neurotoxicity: Dual interactions with Tyr(10) and SNK(26-28) of Abeta\n","analysis suggests that some familial Alzheimer's disease mutations in APP are amyloidogenic and/or amyloidolytic via selection of alternative BACE1 cleavage sites\n","Our results suggested that hAPP was more likely an important factor inhibiting adult neurogenesis, and Abeta was not the major factor affecting neurogenesis in the adult hippocampus of hAPP mice.\n","It may contribute to the pathophysiology of late-onset epilepsy of unknown origin.\n","BECN1-APP association and BECN1-dependent APP endocytosis and degradative trafficking were negatively regulated by active AKT.\n","use replica exchange molecular dynamics simulations to test five modern force fields, OPLS, AMBER99SB, AMBER99SB*ILDN, AMBER99SBILDN-NMR and CHARMM22*, in their ability to model Abeta42 , an intrinsically disordered peptide associated with Alzheimer's disease\n","ABETA oxidation by the Cu-ABETA complex triggers a positive feedback loop that leads to a more deleterious oxidative stress due to both an enhanced reactive oxygen species production rate and a decreased HO scavenging ability.\n","Decreased lipoprotein endocytosis and transcytosis of APP to the axon suggest that a neuron-specific impairment in endocytic axonal delivery of lipoproteins and other key materials might compromise synaptic maintenance in familial Alzheimer's disease.\n","genotype and severity of depressive and anxiety symptoms in cognitively normal older persons\n","Mice overexpressing the Swedish (K594M/N595L) mutation of human APP together with PS1 deleted in exon 9 were used in this study which traces age- and brain region-specific changes of glucose metabolic disorder, learning, and memory dysfunction in ear [...]","APP mutations are associated with specific AD phenotype.\n","plasma amyloid beta protein level may predicti cognitive decline in patients suffering from chronic kidney disease.\n","Three early-onset Alzheimer's disease (EOAD) causative genes (APP, PSEN1, and PSEN2) were discovered in Asian countries. Most of the EOAD-associated mutations have been detected in PSEN1, and several novel PSEN1 mutations were recently identified in  [...]","different Ramachandran angle values could possibly be traced to the unique conformational folding avenues sampled by the Abeta42 peptide owing to the presence of its two extra residues.\n","prion protein-derived cell-penetrating peptide cytotoxicity is modulated by pH but independent of amyloid formation\n","The effects of Abeta and its modified forms containing isomerized Asp7, phosphorylated Ser8, or both, were studied in SH-SY5Y human neuroblastoma cells. Asp7 isomerization of was shown to increase cytotoxicity of both the intact and phosphorylated Abeta.\n","Han Chinese EOFAD patients carrying the APPV717I mutation exhibited a specific clinical phenotype that was mainly characterized by prominent early affective symptoms, executive dysfunction, and disorientation in their 50s, as well as frequent late sp [...]","This is the first evidence of cortical calcification in patients with an APP mutation other than the Iowa mutation.\n","in vitro BACE1-activity assays demonstrate that palmitoylation-dependent dimerization of APP promotes beta-cleavage of APP in lipid-rich detergent resistant cell membranes (DRMs), when compared to total APP.\n","All binary complexes (KLC1:APP, KLC1:JIP1, and APP:JIP1) contain conformations with favorable binding free energies indicating that KLC1 and JIP1 may take part in APP transport in Alzheimer's disease patients.\n","The overexpression of MTERF4 induced a significant increase in the levels of APP protein and secreted Abeta 42 in HEK293-APPswe cells compared with control cells these results suggest that MTERF4 promotes the amyloidogenic processing of APP by inhibi [...]","findings demonstrate that only Abeta(1-42) contains unique structural features that facilitate membrane insertion and channel formation, now aligning ion channel formation with the differential neurotoxic effect of Abeta(1-40) and Abeta(1-42) in Alzh [...]","Study found that FERMT2 (a beta3-integrin co-activator) was significantly associated with a variation in cerebrospinal fluid Abeta peptide levels in 2886 Alzheimer's disease cases.Under-expression of FERMT2 increases Abeta peptide production by raisi [...]","High-affinity binding of amyloid-beta protein (Abeta) Abeta(1-40) to GM1 containing nanodiscs, with dissociation constants, KD, in the range from 25 to 41 nM, in a ganglioside GM1 concentration-dependent manner.\n","Nuclear HSP70 leads to enhancement of vaccinia H1-related phosphatase (VHR) activity via protein-protein interaction rather than its molecular chaperone activity, thereby suppressing excessive ERK activation. Downregulation of either VRK3 or HSP70 re [...]","These results suggest that APPsw transgenic zebrafish well simulate the pathological characters of Alzheimer's disease and can be used as an economic Alzheimer's disease transgenic model.\n","glycoprotein quality control-related proteins have strong affinity for Abeta monomers.\n","The amyloid hypothesis proposes that Alzheimer's Disease is caused by altered beta-amyloid precursor protein expression or APP-mutation-induced Ab aggregation, following an imbalance between Ab production and Ab clearance.\n","Data suggest that aggregates of amyloid beta(1-40) induce excessive generation of reactive oxygen species, MAPK/NFkappaB signaling activation, and NLRP3 inflammasome activation in retinal pigment epithelial cells mimicking changes seen in age-related [...]","HCN2 has a role in maturation and processing of the amyloid precursor protein\n","Data show that the positron emission tomography (PET) signal of the (18)F-labelled tracer florbetaben binds to amyloid-beta plaques inversely correlates with CSF levels of amyloid peptide Ass42, which is a biomarker for Alzheimer's disease (AD).\n","Western diet (WD) dramatically increases ABETA levels and generates pyroglutamate-ABETA deposits.\n","Familial Alzheimer's Disease mutations falling within the Amyloid Precursor Protein sequence lead to dramatic changes in aggregation kinetics and influence the ability of Amyloid-beta Peptide to form immunologically and morphologically distinct amylo [...]","results demonstrate the existence of a specific predominant Abeta40 fibril structure in typical prolonged-duration form-AD and posterior cortical atrophy variant-AD, suggest that rapidly progressive form-AD may relate to additional fibril structures  [...]","These data suggest that excess O-glycosylation on APP by GalNAc-T6 inhibits Abeta production.\n","brain. In the present study, two familial Ab42 mutations, namely A2V (harmful) and A2T (protective) have been analyzed and compared with the wild-type (WT) by performing all-atom molecular dynamics (MD) simulations in the absence and presence of curc [...]","The authors show that APP can physically interact with KCC2, a neuron-specific K(+)-Cl(-) cotransporter that is essential for Cl(-) homeostasis and fast GABAergic inhibition.\n","It is suggested that the metal-binding domain may serve as a zinc-dependent site of beta-amyloid interaction with biological polyanions including DNA, RNA, and glycosaminoglycans.\n","The addition of recombinant heat-shock protein HSP70 reduces TNFalpha production induced by Abeta, which leads to a decrease in neuronal cell damage at the organism level.\n","The dissociation constant of amyloid-beta peptide Abeta1-42 binding to norepinephrine (NE) was determined by simulating a series of binding curves obtained at different Abeta1-42 concentrations.\n","For the first time, natural ABETA (1-42) fibrils (WT) implicated in Alzheimer's disease, as well as two synthetic mutants forming less toxic amyloid fibrils (L34T) and highly toxic oligomers (oG37C), are chemically characterized at the scale of a sin [...]","zinc, copper inhibited Abeta production by directly targeting the subunits presenilin and nicastrin in the gamma-secretase complex\n","Our findings provide evidence that induction of APP shedding via Ang II/AT1 receptor stimulation is effected by G protein activation with Gbg subunits playing important roles.\n","Data describe a novel signal transduction pathway in neurons whereby ApoE activates a non-canonical MAP kinase cascade that enhances APP transcription and amyloid-beta synthesis; using embryonic stem cell-derived human neurons, show that ApoE secrete [...]","Shape complementarity between close-packed residues plays a critical role in the amyloid aggregation process. This study probes such \"steric zipper\" interactions in amyloid-beta (ABETA 40), whose aggregation is linked to Alzheimer's disease, by repla [...]","The short-chain lipid dilauroyl phosphatidylcholine (DLPC) bilayers remodeled preformed amyloid fibrils into a pseudo-unfolded, molten globule state, which resembled on-pathway, protofibrillar aggregates. These results provide mechanistic insights in [...]","Compared with noncarriers, carriers of the APPswe mutation have significantly decreased CSF levels of sAPPalpha and Abeta42 whereas the levels of Abeta38 and Abeta40 were not significantly different.\n","common in cognitively normal older adults. However, evidence of pathological effects on episodic memory has largely been limited to beta-amyloid (Abeta). Because Abeta and tau often cooccur in older adults, previous research offers an incomplete unde [...]","Data suggest that, at neutral pH, amyloid fibril formation is destabilized by substitution of any histidine residue to alanine in amyloid beta-protein (1-40) by a factor of 4-12 compared to wild-type; however, none of His-Ala variants impact the stab [...]","A physical interaction between nicastrin (hNCT) and the gamma-secretase substrate amyloid beta-protein precursor (APPC100) confirmed the functionality of hNCT as a substrate recognizer.\n","Our study provides new insights into the regulation of APP pre-mRNA processing, supports the role for nELAVLs as neuron-specific splicing regulators and reveals a novel function of AUF1 in alternative splicing.\n","Data suggest that amyloid-beta/pyroglutamylated-amyloid-beta hetero-oligomers/aggregates exert unsurpassed cytotoxic effect on neurons as compared to homo-oligomers/aggregates of individual peptides; the peptides form unusual beta-sheet hetero-oligom [...]","The circular RNA ciRS-7 promotes APP and BACE1 degradation in an NF-kappaB-dependent manner.\n","Mitochondria are devoid of amyloid beta-protein-producing secretases; the evidence presented for unlikely occurrence within mitochondria of amyloid beta generation from amyloid precursor protein.\n","results establish a novel toxic impact ofAbeta oligomers on neuronal metabolism and suggest that Abeta oligomers-induced, NMDA receptor-mediated AMPK inhibition may play a key role in early brain metabolic defects in AD.\n","The results suggest that SelS is required for C99 degradation through endoplasmic reticulum-associated degradation, resulting in inhibition of amyloid beta production.\n","HMGCS2 shares with ketone bodies common features in autophagic clearance of APP, suggesting that ketone bodies play an important role in HMGCS2 regulation of the autophagy.\n","Fe65 is an adaptor protein involved in both processing and signaling of the Alzheimer-associated amyloid-beta precursor protein, APP. Here, the subcellular localization was further investigated using TAP-tagged Fe65 constructs expressed in human neur [...]","bis(sulfosuccinimidyl) suberate (BS3) was used to cross-link Abeta1-42 oligomers prior to electrophoresis. When compared to a previously reported Abeta cross-linking agent, glutaraldehyde, it was quite apparent that BS3 is more suitable for detecting [...]","findings are in agreement with the pathology literature, which suggests that tau tangles but not amyloid-beta plaques correlate with cognition and clinical symptoms of early Alzheimers disease patients\n","Results show that Drosophila APPL-RNAi largely mimics transgenic amyloid beta in various phenotypes which include eye degeneration, reduced longevity and motor neuron deficit functions. This is the first report showing comparable phenotypes between A [...]","Results show that concerted signaling by both APP and Abeta is necessary for aberrant neuronal cell cycle entry. Thus, APP plays a central role in promotion of neurodegeneration, through activation of Ras-ERK signaling axis as well as GSK-3, and inte [...]","Besides, the promoting effect of Zn2+ on ABETA42 fast aggregation peaked at pH 6.8-7.8, which includes the pH values of the cerebrospinal fluid (pH 7.3) and hippocampus (pH 7.15-7.35). The findings demonstrate the significant effect of Zn2+ on ABETA  [...]","data point to a scenario where neuroinflammatory processes together with direct synaptotoxic effects are caused by posttranslational modification of soluble oligomeric Abeta and contribute synergistically to the onset of synaptic dysfunction in Alzhe [...]","Structural and biochemical differences between the Notch and the amyloid precursor protein transmembrane domains.\n","Data suggest that post-translational modifications (phosphorylation, oxidation, and nitrosylation) of RyR2 (ryanodine receptor 2) occur downstream of production of amyloid beta-peptides through ADRB2 (beta2-adrenergic receptor) Ca2+ signaling cascade [...]","Fibrillation of CysC therefore likely initiates from the monomer and does not require domain-swapping. The non-swapped oligomers likely represent a dead-end offshoot of the amyloid pathway and must dissociate to monomers prior to rearranging to amylo [...]","Recombinant mutant KPI(R13I) domain of ABPP was ineffective in the inhibition of pro-thrombotic proteinases and did not inhibit the clotting of plasma in vitro.\n","Young healthy adults carrying APOE epsilon4 and APP/presenilin-1/2 displayed different hippocampus functional connectivity patterns\n","These results provide evidence for an emerging role of BAG-1M in the regulation of BACE1 expression and AD pathogenesis and that targeting the BAG-1M-NF-kappaB complex may provide a mechanism for inhibiting Abeta production and plaque formation.\n","This is the first report to show decreased Amyloid beta levels in plasma in Amyloid beta Precursor Protein A673T carriers and thus provides evidence that lower Abeta levels throughout life may be protective against Alzheimer Disease.\n","Data suggest that antiinflammatory agents, non steroidal (NSAIDs) bind to amyloid beta (Abeta) protein leading to the blockage of hydrophobic site which might prevent incoming Abeta molecules from extending the fibril.\n","Mass spectrometry analysis of APP intracellular domains revealed differential processing of APP-C83, APP-C89, and APP-C99 by gamma-secretase already at the epsilon-cleavage stage. This mechanistic insight could aid in developing substrate-targeted mo [...]","enzymes known to act in other metabolic pathways, such as meprin beta, have been found to cleave APP to yield products known to participate in AD pathologies. This review provides an overview of current knowledge of conventional and novel APP processing.\n","O-GlcNAcylation at Thr 576 residue regulates APP trafficking from the trans-Golgi network to plasma membrane.\n","data suggests that the hydrophobic interactions between beta-casein and Abeta1-42 play an important role in the burial of the hydrophobic part of the Abeta1-42.\n","Combining a murine APP-deficient and a human APP-transgenic strain, we were able to analyse the progression of the cortical amyloidosis independent of the murine variant. The lack of endogenous mAPP resulted in accelerated deposition and, thus, incre [...]","activation of mTOR signalling via RHEB over-expression inhibited the starvation-induced autophagy but did not affect trafficking of tf-Amyloid precursor protein (APP). These results show tf-APP can be used to determine how APP is trafficked through t [...]","Remarkably, the cyclic neuroendocrine peptide somatostatin-14 (SST14) was observed to be the most selectively enriched oligomeric Abeta1-42 binder.\n","beta-amyloid interacts with fibrinogen and factor XII. These interactions can lead to increased clotting, abnormal clot formation, persistent fibrin deposition, and generation of proinflammatory molecules.\n","PKCdelta knockdown reduces BACE1 expression, BACE1-mediated APP processing, and Abeta production.\n","ethanol-induced eIF2alpha phosphorylation stimulates COX-2 expression and PGE2 production which induces the BACE1 expression and Abeta production via EP-2 receptor-dependent PKA/CREB pathway.\n","Covalent modifications of the amyloid beta peptide by hydroxynonenal: Effects on metal ion binding by monomers and insights into the fibril topology.\n","Data suggest that single aromatic/hydrophobic amino acid residues within IAPP (islet amyloid polypeptide) amyloid core region are able to control its interaction with amyloid-beta(1-40) or amyloid-beta(1-42) but not IAPP self-assembly; four aromatic/ [...]","The authors found that as already shown for oligomeric Abeta, also oligomeric Tau can bind to amyloid precursor protein (APP). Moreover, efficient intra-neuronal uptake of oligomeric Abeta and oligomeric Tau requires expression of APP.\n","Here, using a library of short heparin polysaccharides modified at specific sites, the authors show that the N-sulfate or 6-O-sulfate of glucosamine, but not the 2-O-sulfate of iduronate within heparin is required for binding to Abeta40 fibrils with  [...]","specific balance between the concentrations of monomeric and fibrillar alpha-synuclein determines the outcome of the Abeta42 aggregation reaction\n","Data suggest that the substitution of alanine by valine at position 2 of the amyloidogenic peptide affect the lateral interactions between fibrils, promoting a more compact, aligned and uniform structure which explains its aggressiveness in homozygou [...]","A comprehensive understanding of the still undefined contribution of Abeta truncations to the disease pathogenesis and their potential as novel therapeutic targets.\n","Phosphorylation of amyloid precursor protein by mutant LRRK2 promotes AICD activity and neurotoxicity in Parkinson's disease.\n","This study structurally characterized ABETA 40 and ABETA 42 monomers through pentamers which were converted from previously derived coarse-grained (DMD4B-HYDRA) simulations into all-atom conformations and subjected to explicit-solvent Molecular Dynamics.\n","These studies support the hypothesis that the ratio of Abeta monomers to Abeta oligomers is a critical factor that regulates synapse damage.\n","review up-to-date structural knowledge about amyloid-beta peptides, focusing on data acquired using solution and solid state NMR techniques.\n","Using purified PSEN1/Aph1A gamma-secretase and the APPC99-3XFLAG substrate, authors show that substrate shortening progressively destabilizes the consecutive enzyme-substrate complexes that characterize the sequential gamma-secretase processing of AP [...]","Study showed that the APP Osaka mutation has dual effects: it causes a loss-of-function of APP and gain-of-toxic-function of Abeta, though the latter seems to come out only after the former causes GABAergic depletion. Also present OSK-KI mice as a mo [...]","Study demonstrated that Alzheimer's disease (AD) cell membranes differ in their nanoscale structure and physical properties than healthy cell membranes, and interact differently with Abeta1-42 . Based on data, authors propose a new hypothesis that ch [...]","These results confirm the involvement of amyloid precursor protein (APP) in synaptogenesis and provide evidence to suggest that human APP overexpression specifically disturbs the structural and functional organization of active zone and results in al [...]","This case study reports the first detailed clinical description of Val717Phe mutation, demonstrating amnestic AD phenotype with seizures, myoclonus, and Parkinsonism, and yields an overview of related autosomal dominantly inherited exonic mutations i [...]","UBQLN4, APP, CTNNB1, SHBG, and COL1A1 might be involved in the development of nonalcoholic fatty liver disease, and are proposed as the potential markers for predicting the development of this condition\n","Authors measured cerebral morphological and neurochemical alterations using structural magnetic resonance imaging (MRI) and proton magnetic resonance spectroscopy ((1)H-MRS) in an AD model of APP/PS1 transgenic mice.\n","These results provide an unprecedented view of how albumin interacts with Abeta and illustrate the potential of dark-state exchange saturation transfer NMR in mapping the interactions between amyloid-inhibitory proteins and amyloidogenic peptides.\n","Data show that amyloid precursor protein (APP) dimerization affects its interaction with LDL receptor related protein 1 (LRP1) and LDL-receptor related protein SorLA (SorLA), suggesting that APP dimerization modulates its interplay with sorting molec [...]","This study reports the transition dipole strengths and frequencies of the amyloid beta-sheet amide I mode for the aggregated proteins amyloid-beta1-40, calcitonin, alpha-synuclein, and glucagon.\n","this study presents the structure of an Abeta(1-42) fibril composed of two intertwined protofilaments determined by cryo-electron microscopy to 4.0-angstrom resolution, complemented by solid-state nuclear magnetic resonance experiments.\n","xplored structural details of fibrils formed by a mutated amyloid beta (Abeta(1-40)) peptide carrying a Phe19 to Lys19 mutation. Although morphologically very robust, local perturbations of the Abeta(1-40) sequence lead to moderate structural alterat [...]","We found that individuals with elevated beta-amyloid aggregation had a blunted cerebrovascular response compared to non-elevated individuals\n","A Toxic Conformer of Abeta42 with a Turn at 22-23 is a Novel Therapeutic Target for Alzheimer's Disease.\n","overall results and observations regarding human serum albumin, amyloid-beta, and metal ions advance our knowledge of how protein-protein interactions associated with amyloid-beta and metal ions could be linked to Alzheimer's disease pathogenesis\n","These findings indicate that under physiological conditions, expression of APP in cerebral vascular endothelium plays an important protective function by maintaining constitutive expression of eNOS .\n","The findings reveal a novel mechanism whereby GSK3beta stimulates amyloidogenic processing of APP by phosphorylation of FE65 at threonine 579.\n","the AOEP2 peptide binds to Abeta monomers and inhibits the formation of Abeta oligomers and beta-sheet structure, reduces Abeta42-induced neurotoxicity, and decreases the release of proinflammatory cytokines.\n","The neuronal specific alpha3 (alpha3)-subunit of the plasma membrane enzyme Na, K-ATPase (NKA) is a new binding partner of sAPPalpha.\n","The authors show that lipoproteins including brain (apoE) and circulating (high-density lipoprotein, HDL) synergize to facilitate beta-amyloid transport across bioengineered human cerebral vessels.\n","a 99-aa C-terminal fragment of APP,C99, in addition to its localization in endosomes, can also be found in mitochondria-associated endoplasmic reticulum (ER) membranes, where it is normally processed rapidly by gamma-secretase.\n","Data suggest that kinetics of degradation/proteolysis versus of aggregation of amyloid beta(1-40) and amyloid beta(1-42) at specific concentrations of amyloid beta, cathepsin B, and cystatin C can be modeled and predicted.\n","CSF Abeta levels and white matter lesion loads (WM-LL) suggests a direct link between amyloid pathology and WM macrostructural and microstructural damage in Alzheimer's disease. There was increased WM-LL in Abeta(+) compared with both, healthy contro [...]","Data, including data from studies using cadaver tissue, suggest that matriptase and matriptase mRNA are expressed in several regions of the brain with an enrichment in neurons; higher levels of matriptase RNA are expressed in young individuals as com [...]","This review highlights the existing link between oxidative stress and Alzheimer's disease, and the consequences towards the ABETA peptide and surrounding molecules in terms of oxidative damage.  [review]\n","Overexpression of SNX7 in HEK293T cells reduces the levels of secreted Abeta and beta-cleaved N-terminal APP fragments (sAPPbeta). Moreover, SNX7 overexpression caused a significant reduction of the steady-state levels of APP as well as of the cell s [...]","Abeta fibrils start to accumulate predominantly within certain parts of the default mode network in preclinical Alzheimer's disease and already then affect brain connectivity.\n","In Alzheimer's Disease brain, amyloid Beta-protein binds to synapses and requires the expression of amyloid precursor protein to disrupt synaptic activity.\n","study provides molecular insights into the design of amyloidogenic inhibitors to cure various neurodegenerative and amyloid-associated diseases, as NABi would regulate aggregation of other toxic beta-sheet proteins other than Abeta.\n","APP-deficient cells exhibited elevated resting calcium levels in the ER and prolonged emptying of ER calcium stores upon the cyclopiazonic acid-induced inhibition of sarco-endoplasmic reticulum calcium-ATPase. These effects could be ascribed to lower [...]","The results of study demonstrate that different degradation pathways play distinct roles in the removal of Abeta42 aggregates and in disease progression. These findings also suggest that pharmacologic treatments that are designed to stimulate cellula [...]","Amyloid precursor protein (APP) binds the HIV-1 Gag polyprotein, retains it in lipid rafts and blocks HIV-1 virion production and spread.\n","Enhancing mitochondrial proteostasis reduces amyloid-beta proteotoxicity\n","This study applies methodologies on the initial stages of aggregation of a hexamer of Alzheimer's amyloid beta fragment 25-35 (ABETA 25-35) and finds that transitions within the hexameric aggregate are dominated by entropic barriers and speculates th [...]","Aggregation processes of ABETA on living cells and cytotoxic events were monitored by fluorescence techniques. ABETA formed amyloids after forming oligomers composed of approximately 10 ABETA molecules. The formation of amyloids was necessary to acti [...]","we show that F-actin depolymerization in spines leads to a breakdown of the nano-organization of outwardly radiating F-actin rods in cortical neurons from APPswe/PS1DeltaE9 mice\n","uncovered for the first time a phenomenon of chaperone antagonism on BACE1-mediated Abeta42 generation.\n","Solution NMR allowed us to define the secondary structure of this Abeta dimer, which shows interlocking contacts between C-terminal peptide strands. Thus, we present a novel Abeta oligomer that resists conversion to fibrils and remains stable for mor [...]","Prior work has shown that beta-amyloid and Apolipoprotein E epsilon4 combine to influence memory decline in nondemented older adults. This study indicate that increasing age may further exacerbate these effects.\n","Overexpression of AbetaPP in Muller cells (MC) induced strong antioxidant and anti-ER stress (PERK downregulation and GADD34 upregulation) responses accompanied by activation of the prosurvival branch of the unfolded protein response. It was also ass [...]","Data show that phospholipase D3 (PLD3) functions in endosomal protein sorting and plays an important role in regulating amyloid precursor protein (APP) processing.\n","c-Abl is activated in AbetaOs exposed neurons and in Alzheimer's disease patient's brain, and the inhibition of activated c-Abl ameliorates cognitive deficits\n","X-box binding protein 1 overexpression at an early stage reversed Abeta-induced early death without affecting learning performance in the Abeta42 transgenic flies. PERK activation was determined to only enhance Abeta-induced learning deficits.\n","Downregulation of C9orf72 in non-neuronal human cells overexpressing amyloid-beta protein precursor (AbetaPP) resulted in increased levels of secreted AbetaPP fragments and Abeta, while levels of AbetaPP or its C-terminal fragments (CTFs) remained un [...]","Analysis of biochemical fractions of Alzheimer's disease brain extract indicate that the seeding-activity correlated with the presence of ABETA peptide and ABETA-derived aggregates. In vitro-formed fibrils were also active but their activity was low  [...]","Overall these data suggest that the assembly of mixtures of Abeta peptides into different Abeta seeds leads to the formation of distinct subtypes of amyloid having distinctive physicochemical and biological properties which result in the generation o [...]","overexpression of APP may promote the onset of seborrhoeic keratosis and is a marker of skin ageing and UV damage.\n","ABETA(1-42) doses >5 microM inhibited the growth of U87 cells compared with the 0 microM group after 24 and 48 h treatment.\n","N-terminal mutations can affect Abeta fibril and oligomer formation, despite lying outside the core amyloid region of Abeta. Of the three factors that may influence Abeta-mediated toxicity (primary structure of Abeta, assembly structure and cellular  [...]","ASIC1a modulates the ABETA-mediated increase in intrinsic excitability of CA1 pyramidal neurons. The study was performed on APP transgenic mice (Tg2576) expressing high levels of human mutant (K670N/M671L) APP transgene (hAPPK670N/M671L).\n","genetic manipulation of Sirt3 revealed that amyloid-beta increased levels of total tau acetylated tau through its modulation of Sirt3.\n","findings show adverse effects of one-night sleep deprivation on brain ABB and expand on prior findings of higher Abeta accumulation with chronic less sleep.\n","Immature intracellular aggregates are more toxic than mature fibrillar ABETA(1-42).\n","We found amyloid measures to be sensitive early on in predicting subsequent early tau deposition\n","Amyloid fibrils of Abeta1-40 peptide can effectively initiate amyloid formation in different globular proteins and metabolites, converting native structures into beta-sheet rich assemblies. Structural and biophysical properties of the resultant prote [...]","Synaptic dysfunction caused by presenilin-1 mutant and amyloid precusor protein duplication secretomes is mediated by Abeta peptides, whereas trisomy of chromosome 21 (trisomy 21) neuronal secretomes induce dysfunction through extracellular tau.\n","The differing patterns in cerebral amyloid angiopathy within individuals may relate to the relative tissue burdens of the two major forms of Abeta, with higher levels of Abeta40 promoting a more 'aggressive' form of CAA, and higher levels of Abeta42( [...]","This study presents nonequilibrium molecular dynamics data of the Amyloid beta (1-40) peptide, periodically driven by an oscillating electric field\n","APP-Knockout astrocytes have reduced cholesterol and elevated levels of sterol regulatory element-binding protein (SREBP) target gene transcripts and proteins, which were both downstream consequences of reduced lipoprotein endocytosis.\n","these data reveal an important role for APP in the amyloidogenic aspects of AD but challenge the idea that increased APP levels are solely responsible for increasing specific phosphorylated forms of tau or enhanced neuronal cell death in Down syndrom [...]","The primary conclusion is that, under copper-limiting conditions, the M1 site in domain E2 dominates the properties of the entire APP ectodomain with comparable picomolar affinities for both oxidation states Cu(I) and Cu(II).\n","On the role of sidechain size and charge in the aggregation of Abeta42 with familial mutations.\n","Gnetin C may thereby prevent Abeta toxicity by suppressing BACE1 and enhancing MMP-14, together with reducing both internalization and oligomerization of exogenous Abeta monomers.\n","This article reviews the current applications of Mass Spectrometry (MS) in the search for possible ABETA biomarkers of Alzheimer's disease to help the diagnosis of the disease. Recent examples of the important contributions that MS has given to prove [...]","Super-resolution transient amyloid binding microscopy was used to image amyloid fibrils from multiple polypeptides, oligomeric, and fibrillar structures formed during different stages of amyloid-beta aggregation.\n","the inhibition of APPswe-induced secretion of inflammatory cytokines and the suppression of NF-kappaB activation by miR-15b were validated...Our study suggests that miR-15b inhibits Abeta accumulation through targetting NF-kappaB signaling and BACE1  [...]","Study shows attenuated pain-like behaviour in a transgenic mouse model of Alzheimer's disease (bearing mutant human amyloid precursor protein (APP) (695-aa isoform)) due to alterations in the opioidergic system and central plasticity mechanisms of pe [...]","in cholinergic neurons from Drosophila, beta-amyloid (Abeta) peptides Abeta40 and Abeta42 both induce an increase in spontaneous activity.\n","Abeta oligomers bind herpesvirus surface glycoproteins, accelerating beta-amyloid deposition and leading to protective viral entrapment activity in 5XFAD mouse and 3D human neural cell culture infection models against neurotropic herpes simplex virus [...]","In vitro neuroprotective effects of naringenin nanoemulsion against beta-amyloid toxicity through the regulation of amyloidogenesis and tau phosphorylation.\n","CIP2A-mediated PP2A inhibition drives tau/APP hyperphosphorylation and increases APP beta-cleavage and Abeta production.\n","these results suggest an important role of the allosteric sodium binding site for GPR3 activity and open a possible avenue for the modulation of Abeta production in the Alzheimer's Disease.\n","This study data demonstrate that low expression of APP is sufficient to drive histopathological and cognitive changes in mice without overexpression or excessive plaque deposition.\n","The 11-strand beta-strip helix resembles a trans-membrane beta-barrel which could explain the ability of small oligomers of Abeta(1-40) to form toxic ion channels.\n","This study explores the mechanism of ABETA (1-40) fiber elongation. A Markov state model shows that the unfolded monomer is trapped at the end of the fiber in a set of interconverting antiparallel beta hairpin conformations.\n","Identified TMEM30A as a candidate partner for beta-carboxyl-terminal fragment (betaCTF) of amyloid-beta precursor protein (APP). TMEM30A physically interacts with betaCTF in endosomes and may impair vesicular traffic, leading to abnormally enlarged e [...]","In invasive cells, MT1-MMP endocytosis to the endolysosomal reservoir compartment requires flotillin 1 and flotillin 2.\n","These results suggest a role of cPLA2 activation in facilitating oligomeric Abeta endocytosis by microglial cells through regulation of the membrane-cytoskeleton connectivity.\n","we provide a novel method to convert standardized uptake value ratios-levels into PET-Abeta phase estimates that can be easily translated into neuropathological phases of Abeta-deposition\n","These data indicate that the sAbeta1-42 may play a dual role during inflammatory process, wherein, it may be involved in protecting the cells from inflammatory damage due to TNF-alpha.\n","These findings suggest a role for TREM2 in the brain of HIV+ individuals may deserve more investigation as a biomarker for HIV-associated neurocognitive disorders and as a possible therapeutic\n","This study demonstrated that the APP21 transgenic rats develop age-dependent cognitive impairment and accelerated white matter inflammation.\n","APP facilitate an early step in thrombus formation when amyloid beta (Abeta) peptides accumulate in cerebral vessel walls or atherosclerotic plaques.\n","The Swedish variant was a more potent co-activator of Wnt-PCP signalling than wild-type APP and, unlike wild-type APP, which co-activates Wnt beta-catenin signalling, APPSwe suppressed this branch of Wnt.\n","This review includes brief discussions with regards to the levels of Cu and Zn in an Alzheimer's disease affected brain, structures of ABETA peptides, and the coordination of ABETA peptides with Cu and Zn.  [review]\n","We observed that over-expression of PIEZO1 in HEK293 cells increased cell migration velocity ~10-fold, and both enantiomeric A-beta peptides and GsMTx4 independently inhibited migration, demonstrating involvement of PIEZO1 in cell motility.\n","Among hip fracture patients, 88.6% of the cognitively normal (Clinical Dementia Rating-CDR 0; n = 70) and 98.8% with mild cognitive impairment (CDR 0.5; n = 81) fell in the abnormal biomarker categories by CSF Abeta42/40 ratio, p-tau, and t-tau measures.\n","This study showed a direct interaction between statins and Abeta protofibrils, which may underlie the protective role of this widely used class of drugs against amyloidogenesis and Abeta-mediated neurodegeneration.\n","This study showed that 24-month-old AppNL/NL mice, despite presenting an age dependent increase in insoluble amyloid-beta oligomers in the prefrontal cortex, they do not develop amyloid plaque deposition, reactive gliosis, or cognitive deficits.\n","Using Western blotting, kinetic assays, and microfluidic analyses, the study shows that FXIIIa covalently cross-links ABETA40 into dimers and oligomers (k cat/Km = 1.5 x 10(5) m(-1)s(-1)), as well as to fibrin, platelet proteins, and blood clots unde [...]","recombination of APP in human neurons, occurring mosaically as thousands of variant 'genomic cDNAs' (gencDNAs); gencDNAs lacked introns and ranged from full-length cDNA copies of expressed, brain-specific RNA splice variants to myriad smaller forms t [...]","These results demonstrated the contributory role of APP cleavage on its oncogenic roles in breast cancer. ADAM10 was the key alpha-secretase. APP and ADAM10 co-expression was associated with worse survival in non-luminal breast cancers.\n","miR-346 plays a role in upregulation of APP in the CNS and participates in maintaining APP regulation of Fe, which is disrupted in late stages of AD.\n","results confirm the presence of Abeta seeds in archived c-hGH vials and are consistent with the hypothesized iatrogenic human transmission of Abeta pathology; this experimental confirmation has implications for both the prevention and the treatment o [...]","The results showed that EGR1 overexpression increased Abeta40 secretion in vitro, possibly through increasing BACE1 expression. Based on these results, EGR1 might be a promising therapeutic target for the AD.\n","These data demonstrate a key role for proteolysis of the C-terminal of APP by gamma-secretase in neuronal dysfunction in monogenic Alzheimer's disease.\n","a Drosophila Alzheimer's disease (AD) model expressing a secreted form of human amyloid-beta42 peptide showed that it recapitulates key aspects of AD pathology, including neuronal death and impaired long-term memory.\n","High carboxypeptidase A4 (CPA4) expression in triplenegative breast cancer (TNBC) cases is associated with low expression of E-cadherin and with the expression of cancer stem cell markers. Patients with TNBC and high levels of CPA4 expression have po [...]","This study investigated the assembly mechanisms of dimeric ABETA 16-22 and found that the fibril formation rate is predominantly controlled by the total beta-strand content.\n","Findings suggest that the polymorphisms of amyloid-beta (Abeta) fibril structures are caused by differences in the surrounding ionic environment.\n","Fpn and Heph co-localize, and FRET analysis indicated that the two proteins form an iron-efflux complex; in contrast, none of the full-length, cellular APP proteins exhibited Fpn co-localization or FRET\n","analysis of the interaction between monomeric Abeta40/42 and HSA using surface plasmon resonance spectroscopy\n","the presence of ApoEepsilon4 allele might also have a possible effect on the amyloid beta phagocytosis efficiency of the macrophages.\n","The familial D678H APP gene mutation resulted in a more potent amyloid burden than in the patients with sporadic Alzheimer's Disease.\n","Solid-state NMR reveals a comprehensive view of the dynamics of the flexible, disordered N-terminal domain of amyloid-beta fibrils.\n","Influence of the familial Alzheimer's disease-associated T43I mutation on the transmembrane structure and gamma-secretase processing of the C99 peptide\n","These data provide valuable insights in understanding GRN-3's ability to modulate Abeta-induced toxicity under redox control and presents a new perspective toward AD pathology.\n","results may explain the role of hAChE-S in Abeta deposition and aggregation, as amyloidogenic hAChE-S beta-sheet species might seed Abeta aggregation.\n","results uncover a mechanism by which PP2A Aalpha regulates Abeta protein stability and activity\n","The B6.Cg-Tg(PDGFB-APPSwInd)20Lms/2Mmjax (J20) mouse strain (#006293: Jackson Laboratory) carries a human APP695 transgene harboring the aggressive Swedish and Indiana substitutions. Sex-specific biochemical and behavioral phenotypes are observed in  [...]","results indicate that N-terminal Abeta1-42 pyroglutamation and Abeta1-40 deposition are critical events in priming and maturation of pathogenic Abeta from diffuse into cored plaques, underlying neurotoxic plaque development in Alzheimer's disease.\n","Thirteen of 148 (8.8%) individuals had possible pathogenic APP, PSEN1, or PSEN2 variants, including 2 (15.4%) APP variants, 8 (61.5%) PSEN1 variants, and 3 (23.1%) PSEN2 variants\n","Amyloid beta in nasal secretions may be a potential biomarker of Alzheimer's disease.\n","We report here an essentially complete atomic model of C99 within wild-type gamma-secretase that respects all the experimental constraints and additionally describes loop, helix, and C99 substrate dynamics in a realistic all-atom membrane. Our model  [...]","APP 3'UTR polymorphisms can affect the regulation of APP expression by miRNAs and thus affect the occurrence of Alzheimer's disease\n","Analysis of microRNAs (miRNAs) revealed that miR-9 and miR-181a negatively coregulated BACE1 and TGFBIp, which was directly associated with the pathogenesis of AD and GCD2, respectively. Immunohistochemical analysis indicated that APP and BACE1 were  [...]","This review summarizes the current understanding of transition metal interactions with ABETA obtained from computational chemistry studies. [review]\n","oligomeric Abeta can profoundly disrupt the bilayer, visualized as widespread lipid extraction and subsequent deposition, which can be likened to an effect expected from the action of a detergent.\n","As indicated by a comparison between experiment and computation, the number of adjacent beta-strands per peptide molecule is two for ABETA40 oligomers and two or more for ABETA42 oligomers. These results are well explained by regular, antiparallel be [...]","Familial Alzheimer's disease patient-derived neurons reveal distinct mutation-specific effects on amyloid beta.\n","BIN1 rs744373 SNP is associated with increased tau but not beta-amyloid pathology, suggesting that alterations in BIN1 may contribute to memory deficits via increased tau pathology\n","Cortical beta-amyloid protein was associated with faster cognitive decline in the absence of beta-amyloid deposits, which supports the role of cortical soluble beta-amyloid as a neurotoxic agent in aging. The lack of protein association with paired h [...]","It was evident that on average only a single histidine residue coordinates Cu(II) in monomeric ABETA(1-42) at pH 6.1, in addition to 3 other oxygen or nitrogen ligands. Cu(II) coordination in ABETA(1-42) at pH 7.4 is similarly 4-coordinate with oxyge [...]","HIV and Alzheimer's disease: complex interactions of HIV-Tat with amyloid beta peptide and Tau protein.\n","Individuals over 80 years of age had the lowest amounts of prion-like Abeta and phosphorylated tau.\n","Structural dynamics of dipeptides and ABETA (25-35) in aqueous solution were demonstrated\n","There was no statistically significant difference in the levels of CSF A[beta]1-42 between the former athletes with multiple concussions group and healthy control group.\n","In this study, the analytical capabilities of MALDI-TOF/TOF mass spectrometry for relative quantitation of isoAsp7 in ABETA (1-42) and ABETA(1-16) were investigated.\n","High-speed atomic force microscopy (HS-AFM) is used to directly visualize the dynamic interactions between single ABETA 42 oligomers and aggregates. Analysis of HS-AFM movies reveals up to three different ABETA 42 species, in addition to the appearan [...]","human Abeta1-40 and rat Abeta1-42 affect cognitive activity via extracellular Zn(2+)-independent mechanism at low micromolar concentration.\n","there is an increase in CSF Abeta42 early in Alzheimer's disease before its decline while tau pathology progresses; this pattern is particularly observed in non-APOE4 subjects\n","These results suggest that Abeta could induce autophagy in RPE cells, which provided a potential protective mechanism for the retina cells that encountered Abeta deposition.\n","Synaptic Abeta was increased by apoE4 in control and AD samples. These results are consistent with uptake of apoE/Abeta complex and associated lipids into synaptic terminals, with subsequent Abeta clearance in control synapses and accumulation in AD synapses.\n","Beta-amyloid peptide(1-42) (Abeta1-42) : phosphorylated Tau (p-Tau) ratio has potential for being implemented in the clinical routine for differential diagnosis between AD and other dementias and to distinguish underling pathology such as neurodegene [...]","The present results suggested that APP knockdown may significantly inhibit the development of nasopharyngeal carcinoma by suppressing cell viability, migration and invasion, and by inhibiting the epithelialmesenchymal transition process via downregul [...]","This study found the L723P mutation to cause local unfolding of the C-terminal turn of the APP Transmembrane Domain helix and increase its accessibility to water required for cleavage of the protein backbone by gamma-secretase in the epsilon-site, th [...]","Molecular dynamics simulation of aluminium binding to amyloid-beta and its effect on peptide structure.\n","The impact of H2O2 on ABETA aggregation in the presence of lipids was associated with a reduced affinity of ABETA for the vesicle surface. However, this reduced vesicle affinity was predominately associated with lipid peroxidation rather than ABETA oxidation.\n","\"\"Dual Disease\"\" TgAD/GSS mice exhibit enhanced Alzheimer's disease pathology and reveal PrP(C)-dependent secretion of Abeta.\n","MMP9 inhibition can facilitate Abeta clearance across the blood brain barrier.\n","Abelmoschus esculentus is potential to prevent Abeta-induced neuron damage by regulating DPP-4 and the insulin resistance cascades.\n","This paper discusses the structure of the ABETA(11-42) amyloid fibril.\n","results indicate a modulating effect of PTB-APs on PICALM-mediated APP endocytosis and localization.\n","Platelet Amyloid-beta Protein Precursor (AbetaPP) Ratio and Phosphorylated Tau as Promising Indicators for Early Alzheimer's Disease.\n","Both wild-type and L-isoAsp23 protofilaments adopt beta-helix-like folds with tightly packed cores, resembling the cores of full-length fibrillar Abeta structures, and both self-associate through two distinct interfaces.\n","Structure and Physicochemical Properties of the Abeta42 Tetramer: Multiscale Molecular Dynamics Simulations.\n","Results indicate that GULP, engulfment adaptor PTB domain containing 1 (GULP1) threonine 35 (T35) phosphorylation is a mechanism for the regulation of GULP1-amyloid beta precursor protein (APP) interaction and thereby APP processing.\n","The G37V mutation reduced toxicity but did not accelerate the aggregation rate or change the content of secondary structures.  The G37V mutation formed an ellipse-like aggregate rather than a network-like fibril. Using the replica exchange molecular  [...]","The Interaction Between Neuroinflammation and beta-Amyloid in Cognitive Decline in Parkinson's Disease.\n","Cognitive decline was slower and started earlier in APP mutation carriers, whereas decline was relatively rapid in PSEN1 mutation carriers.\n","In APP mutant neurons, endosomal dysfunction correlated with accumulation of APP beta C-terminal fragments, not Abeta.\n","Attached were six lysines (6K) to the C-terminus of native ABETA (1-42) to create a more soluble, monomeric form of ABETA (1-42) called ABETA42C6K. These results indicate that ABETA42C6K stays monomeric at high concentrations (unlike ABETA(1-42) and  [...]","Connections Between Amyloid Beta and the Meningeal Lymphatics As a Possible Route for Clearance and Therapeutics.\n","ABETA (25-35) induced cell injury and increased the expression level of SNHG1 in neuronal cells.\n","Role of GABAA receptors in EEG activity and spatial recognition memory in aged APP and PS1 double transgenic mice.\n","we reveal that the APOE4 genotype has a profound impact on several aspects of microglial functionality, whereas PSEN1DeltaE9 and APPswe mutations trigger minor alterations. The APOE4 genotype impairs phagocytosis, migration, and metabolic activity of [...]","doxycycline tightly binds the exposed hydrophobic amino acids of the Abeta42 amyloid fibrils, partly leading to destabilization of the fibrillar structure. Clarifying the molecular determinants of doxycycline binding to Abeta42 may help devise furthe [...]","Apolipoprotein E impairs amyloid-beta fibril elongation and maturation.\n","The Amyloid Precursor Protein C-Terminal Domain Alters CA1 Neuron Firing, Modifying Hippocampus Oscillations and Impairing Spatial Memory Encoding.\n","As meprin beta cleavage of APP has been shown to result in formation of highly aggregation-prone, truncated Abeta2-40/42 peptides, enhanced APP processing by this enzyme could contribute to Alzheimer's disease pathology.\n","Dual Bioorthogonal Labeling of the Amyloid-beta Protein Precursor Facilitates Simultaneous Visualization of the Protein and Its Cleavage Products.\n","Insulin quiescently incubated with ABETA 42 attenuates both ABETA 42 fibril formation and the ability of ABETA 42 to disrupt membranes in a concentration-dependent manner.\n","The Molecular Misreading of APP and UBB Induces a Humoral Immune Response in Alzheimer's Disease Patients with Diagnostic Ability.\n","The role of innate immune responses and neuroinflammation in amyloid accumulation and progression of Alzheimer's disease.\n","The N-terminal sequence Xaa-Xaa-His is known as an amino terminal copper and nickel binding motif (ATCUN), which avidly binds Cu(II). Cu(II) bound to this particular ATCUN site is redox silent, but the second Cu(II) site is redox active and can be re [...]","the present findings suggested that APP could affect the migration and invasion of human breast cancer cells by mediating the activation of the MAPK signaling pathway, thereby promoting the EMT process.\n","Amyloid-beta, Tau, and 18F-Fluorodeoxyglucose Positron Emission Tomography in Posttraumatic Stress Disorder.\n","NMR-based site-resolved profiling of beta-amyloid misfolding reveals structural transitions from pathologically relevant spherical oligomer to fibril.\n","These findings show that amyloid-beta and tau have different spatial affinities, which can be used to understand how they accumulate in the brain and potentially damage the brain's connections.\n","Histidine 131 in presenilin 1 is the pH-sensitive residue that causes the increase in Abeta42 level in acidic pH.\n","The antioxidant 2,3-dichloro,5,8-dihydroxy,1,4-naphthoquinone inhibits acetyl-cholinesterase activity and amyloid beta42 aggregation: A dual target therapeutic candidate compound for the treatment of Alzheimer's disease.\n","Alzheimer-like amyloid and tau alterations associated with cognitive deficit in temporal lobe epilepsy.\n","This study found that African American individuals had lower levels of tau-based biomarkers that were not likely explained by the degree of mild cognitive impairment (MCI) disease stage or neurodegeneration. For a comparable level of cognitive impair [...]","Predicting clinical decline and conversion to Alzheimer's disease or dementia using novel Elecsys Abeta(1-42), pTau and tTau CSF immunoassays.\n","Targeting alpha synuclein and amyloid beta by a multifunctional, brain-penetrant dopamine D2/D3 agonist D-520: Potential therapeutic application in Parkinson's disease with dementia.\n","PSEN1, PSEN2, and APP mutations in 404 Chinese pedigrees with familial Alzheimer's disease.\n","Plasma levels of Interleukin 18 but not amyloid-beta or Tau are elevated in female depressive patients.\n","MicroRNA-298 reduces levels of human amyloid-beta precursor protein (APP), beta-site APP-converting enzyme 1 (BACE1) and specific tau protein moieties.\n","An increased interaction force between finger 3 of Sp1 (Sp1-f3)and the APP promoter in Pb(2+) solutions was consistent with a lower binding free energy, as determined by computer-assisted analysis.\n","Reduced Influence of apoE on Abeta43 Aggregation and Reduced Vascular Abeta43 Toxicity as Compared with Abeta40 and Abeta42.\n","Cereblon-mediated degradation of the amyloid precursor protein via the ubiquitin-proteasome pathway.\n","Dysregulation of Amyloid Precursor Protein Impairs Adipose Tissue Mitochondrial Function and Promotes Obesity.\n","Serum levels of Abeta42 and tau protein in Parkinson's disease may be a useful marker for the assessment of cognitive impairments\n","Changes in plasma Abeta concentration are time-dependent, whereas changes in hyperphosphorylated tau protein levels paralleled the clinical progression of mild cognitive impairment\n","Galectin 3-binding protein suppresses amyloid-beta production by modulating beta-cleavage of amyloid precursor protein.\n","Beta secretase 1-dependent amyloid precursor protein processing promotes excessive vascular sprouting through NOTCH3 signalling.\n","Extracellular vesicle-mediated amyloid transfer to neural progenitor cells: implications for RAGE and HIV infection.\n","Systematic validation of variants of unknown significance in APP, PSEN1 and PSEN2.\n","Relationship Between Tau, beta Amyloid and alpha-Synuclein Pathologies:  discuss how the presence of multiple pathological lesions can affect the pathological and clinical phenotype of neurodegenerative disorders\n","Amyloid-beta and Tau at the Crossroads of Alzheimer's Disease\n","The Amyloid, Tau, and Neurodegeneration (A/T/N) Classification Applied to a Clinical Research Cohort with Long-Term Follow-Up.\n","Effect of Piedmont mutation (L34V) on the structure, dynamics, and aggregation of Alzheimer's Abeta40 peptide.\n","A Preliminary Study of Cu Exposure Effects upon Alzheimer's Amyloid Pathology.\n","Decrease in 130 kDa- amyloid protein precursor protein (APP) and APP protein ratio in schizophrenia platelets.\n","Cerebrospinal beta-amyloid peptides(1-40) and (1-42) in severe preeclampsia and HELLP syndrome - a pilot study.\n","Metal ion coordination delays amyloid-beta peptide self-assembly by forming an aggregation-inert complex.\n","The cellular expression and proteolytic processing of the amyloid precursor protein is independent of TDP-43.\n","SIRT5 impairs aggregation and activation of the signaling adaptor MAVS through catalyzing lysine desuccinylation.\n","Lesch-Nyhan disease: I. Construction of expression vectors for hypoxanthine-guanine phosphoribosyltransferase (HGprt) enzyme and amyloid precursor protein (APP).\n","A Spectroscopic Marker for Structural Transitions Associated with Amyloid-beta Aggregation.\n","An APP mutation family exhibiting white matter hyperintensities and cortical calcification in East China.\n","Investigating APOE, APP-Abeta metabolism genes and Alzheimer's disease GWAS hits in brain small vessel ischemic disease.\n","Amyloid-beta oligomers are captured by the DNAJB6 chaperone: Direct detection of interactions that can prevent primary nucleation.\n","Cerebral Microhemorrhage at MRI in Mild Cognitive Impairment and Early Alzheimer Disease: Association with Tau and Amyloid beta at PET Imaging.\n","Intramitochondrial proteostasis is directly coupled to alpha-synuclein and amyloid beta1-42 pathologies.\n","Acute zoster plasma contains elevated amyloid, correlating with Abeta42 and amylin levels, and is amyloidogenic.\n","Elevated circulating amyloid concentrations in obesity and diabetes promote vascular dysfunction.\n","Zinc binding promotes greater hydrophobicity in Alzheimer's Abeta42 peptide than copper binding: Molecular dynamics and solvation thermodynamics studies.\n","Presynaptic APP levels and synaptic homeostasis are regulated by Akt phosphorylation of huntingtin.\n","High-Throughput Screening at the Membrane Interface Reveals Inhibitors of Amyloid-beta.\n","Since the retinal nerve fiber layer (RNFL) is depleted in established Alzheimer's disease (AD), we tested whether its thickness can predict whether cognitively healthy (CH) individuals have a normal or pathological cerebrospinal fluid (CSF) Ab42 (A)  [...]","Advent of Proteomic Tools for Diagnostic Biomarker Analysis in Alzheimer's Disease.\n","Dcf1 alleviates C99-mediated deficits in drosophila by reducing the cleavage of C99.\n","Presence of intrinsically disordered proteins can inhibit the nucleation phase of amyloid fibril formation of Abeta(1-42) in amino acid sequence independent manner.\n","Amyloid precursor protein 770 is specifically expressed and released from platelets.\n","ORAI2 Down-Regulation Potentiates SOCE and Decreases Abeta42 Accumulation in Human Neuroglioma Cells.\n","Integrated Bioinformatics Analysis Identifies ELAVL1 and APP as Candidate Crucial Genes for Crohn's Disease.\n","Alix and Syntenin-1 direct amyloid precursor protein trafficking into extracellular vesicles.\n","Modification of lipid rafts by extracellular vesicles carrying HIV-1 protein Nef induces redistribution of amyloid precursor protein and Tau, causing neuronal dysfunction.\n","Differences in the free energies between the excited states of Abeta40 and Abeta42 monomers encode their aggregation propensities.\n","Fyn Tyrosine Kinase Elicits Amyloid Precursor Protein Tyr682 Phosphorylation in Neurons from Alzheimer's Disease Patients.\n","Fluorescence-Labeled Amyloid Beta Monomer: A Molecular Dynamical Study.\n","Association of CSF Abeta, amyloid PET, and cognition in cognitively unimpaired elderly adults.\n","The inhibition of cellular toxicity of amyloid-beta by dissociated transthyretin.\n","A pilot study investigating the effects of voluntary exercise on capillary stalling and cerebral blood flow in the APP/PS1 mouse model of Alzheimer's disease.\n","The Alzheimer's disease-associated C99 fragment of APP regulates cellular cholesterol trafficking.\n","Internalisation and toxicity of amyloid-beta 1-42 are influenced by its conformation and assembly state rather than size.\n","Amyloid-beta1-43 cerebrospinal fluid levels and the interpretation of APP, PSEN1 and PSEN2 mutations.\n","Behavioral and neural network abnormalities in human APP transgenic mice resemble those of App knock-in mice and are modulated by familial Alzheimer's disease mutations but not by inhibition of BACE1.\n","Small Vessel Disease and Associations with Cerebrospinal Fluid Amyloid, Tau, and Neurodegeneration (ATN) Biomarkers and Cognition in Young Onset Dementia.\n","Amyloid, tau and risk of Alzheimer's disease: a Mendelian randomization study.\n","The role of hypoxia on Alzheimer's disease-related APP and Tau mRNA formation.\n","Exploring the Role of Aggregated Proteomes in the Pathogenesis of Alzheimer's Disease.\n","Familial Alzheimer's disease mutations at position 22 of the amyloid beta-peptide sequence differentially affect synaptic loss, tau phosphorylation and neuronal cell death in an ex vivo system.\n","Mitochondrial Calcium Deregulation in the Mechanism of Beta-Amyloid and Tau Pathology.\n","Kinetic fingerprints differentiate the mechanisms of action of anti-Abeta antibodies.\n","APP Binds to the EGFR Ligands HB-EGF and EGF, Acting Synergistically with EGF to Promote ERK Signaling and Neuritogenesis.\n","Alzheimer's protection effect of A673T mutation may be driven by lower Abeta oligomer binding affinity.\n","Amyloid precursor protein is a restriction factor that protects against Zika virus infection in mammalian brains.\n","Accumulation of amyloid precursor protein C-terminal fragments triggers mitochondrial structure, function, and mitophagy defects in Alzheimer's disease models and human brains.\n","Structural rearrangement of amyloid-beta upon inhibitor binding suppresses formation of Alzheimer's disease related oligomers.\n","Enlightening amyloid fibrils linked to type 2 diabetes and cross-interactions with Abeta.\n","Chia seeds as a potential cognitive booster in the APP23 Alzheimer's disease model.\n","Evidence for aggregation-independent, PrP(C)-mediated Abeta cellular internalization.\n","Self-assembly of N-terminal Alzheimer's beta-amyloid and its inhibition.\n","Amyloid-beta oligomers induce Parkin-mediated mitophagy by reducing Miro1.\n","Post-Translational Modifications of Platelet-Derived Amyloid Precursor Protein by Coagulation Factor XIII-A.\n","Flow cytometry method to quantify the formation of beta-amyloid membrane ion channels.\n","Circulating Amyloid Beta 1-40 Is Associated with Increased Rate of Progression of Atherosclerosis in Menopause: A Prospective Cohort Study.\n","Binding of Cu(2+) to Abeta1-29 causes aggregation and toxicity in SH-SY5Y cells.\n","Megadalton-sized Dityrosine Aggregates of alpha-Synuclein Retain High Degrees of Structural Disorder and Internal Dynamics.\n","Performance of Markov State Models and Transition Networks on Characterizing Amyloid Aggregation Pathways from MD Data.\n","Inactive variants of death receptor p75(NTR) reduce Alzheimer's neuropathology by interfering with APP internalization.\n","Alzheimer's Abeta42 and Abeta40 form mixed oligomers with direct molecular interactions.\n","An \"\"epitomic\"\" analysis of the specificity of conformation-dependent, anti-Ass amyloid monoclonal antibodies.\n","Neuroprotective effect of emodin against Alzheimer's disease via Nrf2 signaling in U251 cells and APP/PS1 mice.\n","Amyloid beta, alpha-synuclein and the c subunit of the ATP synthase: Can these peptides reveal an amyloidogenic pathway of the permeability transition pore?\n","Cu(2+)-binding to S100B triggers polymerization of disulfide cross-linked tetramers with enhanced chaperone activity against amyloid-beta aggregation.\n","Effect of Amyloid-beta Monomers on Lipid Membrane Mechanical Parameters-Potential Implications for Mechanically Driven Neurodegeneration in Alzheimer's Disease.\n","Lentivirus-Mediated Expression of Human Secreted Amyloid Precursor Protein-Alpha Promotes Long-Term Induction of Neuroprotective Genes and Pathways in a Mouse Model of Alzheimer's Disease.\n","Amyloid-beta, cortical thickness, and subsequent cognitive decline in cognitively normal oldest-old.\n","Single Point Mutation from E22-to-K in Abeta Initiates Early-Onset Alzheimer's Disease by Binding with Catalase.\n","Molecular structure of a prevalent amyloid-beta fibril polymorph from Alzheimer's disease brain tissue.\n","Familial Alzheimer's disease mutations in amyloid protein precursor alter proteolysis by gamma-secretase to increase amyloid beta-peptides of >/=45 residues.\n","Cu, Fe, and Zn isotope ratios in murine Alzheimer's disease models suggest specific signatures of amyloidogenesis and tauopathy.\n","Significant Overlap of alpha-Synuclein, Amyloid-beta, and Phospho-Tau Pathologies in Neuropathological Diagnosis of Lewy-related Pathology: Evidence from China Human Brain Bank.\n","Different Aggregation Pathways and Structures for Abeta40 and Abeta42 Peptides.\n","Highly Expressed Amyloid Beta-42 Of Aqueous Humor In Patients With Neovascular Macular Degeneration.\n","Amyloid cross-sequence interaction between Abeta(1-40) and alphaA(66-80) in relation to the pathogenesis of cataract.\n","Mitochondrial fission is a critical modulator of mutant APP-induced neural toxicity.\n","Role of Retinal Amyloid-beta in Neurodegenerative Diseases: Overlapping Mechanisms and Emerging Clinical Applications.\n","Polymorphic SERPINA3 prolongs oligomeric state of amyloid beta.\n","Promotion and Inhibition of Amyloid-beta Peptide Aggregation: Molecular Dynamics Studies.\n","Binding of Amyloid beta(1-42)-Calmodulin Complexes to Plasma Membrane Lipid Rafts in Cerebellar Granule Neurons Alters Resting Cytosolic Calcium Homeostasis.\n","Retinal ganglion cell dysfunction in preclinical Alzheimer's disease: an electrophysiologic biomarker signature.\n","Associations of AT(N) biomarkers with neuropsychiatric symptoms in preclinical Alzheimer's disease and cognitively unimpaired individuals.\n","Interplay between stress-related genes may influence Alzheimer's disease development: The results of genetic interaction analyses of human data.\n","Plasma Amyloid-Beta Levels in a Pre-Symptomatic Dutch-Type Hereditary Cerebral Amyloid Angiopathy Pedigree: A Cross-Sectional and Longitudinal Investigation.\n","Degradation of Alzheimer's Amyloid-beta by a Catalytically Inactive Insulin-Degrading Enzyme.\n","Detecting beta-amyloid glycation by intrinsic fluorescence - Understanding the link between diabetes and Alzheimer's disease.\n","The Protective A673T Mutation of Amyloid Precursor Protein (APP) in Alzheimer's Disease.\n","Insoluble Vascular Amyloid Deposits Trigger Disruption of the Neurovascular Unit in Alzheimer's Disease Brains.\n","Plasma amyloid beta levels are driven by genetic variants near APOE, BACE1, APP, PSEN2: A genome-wide association study in over 12,000 non-demented participants.\n","Non-productive angiogenesis disassembles Ass plaque-associated blood vessels.\n","Crosstalk between astrocytes and microglia results in increased degradation of alpha-synuclein and amyloid-beta aggregates.\n","Abeta receptors specifically recognize molecular features displayed by fibril ends and neurotoxic oligomers.\n","MT5-MMP controls APP and beta-CTF/C99 metabolism through proteolytic-dependent and -independent mechanisms relevant for Alzheimer's disease.\n","Molecular insight into the early stage of amyloid-beta(1-42) Homodimers aggregation influenced by histidine tautomerism.\n","Utilizing magnetic resonance techniques to study membrane interactions of amyloid peptides.\n","KL-VS heterozygosity is associated with lower amyloid-dependent tau accumulation and memory impairment in Alzheimer's disease.\n","Default mode network dissociation linking cerebral beta amyloid retention and depression in cognitively normal older adults.\n","CK1delta-Derived Peptides as Novel Tools Inhibiting the Interactions between CK1delta and APP695 to Modulate the Pathogenic Metabolism of APP.\n","Regulation of PPARalpha by APP in Alzheimer disease affects the pharmacological modulation of synaptic activity.\n","Structural and mechanistic insights into amyloid-beta and alpha-synuclein fibril formation and polyphenol inhibitor efficacy in phospholipid bilayers.\n","Carboxy-terminal fragment of amyloid precursor protein mediates lipid droplet accumulation upon gamma-secretase inhibition.\n","Structural and Functional Impairments of Reconstituted High-Density Lipoprotein by Incorporation of Recombinant beta-Amyloid42.\n","Role of cholesterol in substrate recognition by [Formula: see text]-secretase.\n","The Amyloid Precursor Protein C99 Fragment Modulates Voltage-Gated Potassium Channels.\n","Endo-lysosomal Abeta concentration and pH trigger formation of Abeta oligomers that potently induce Tau missorting.\n","Dysregulated clock gene expression and abnormal diurnal regulation of hippocampal inhibitory transmission and spatial memory in amyloid precursor protein transgenic mice.\n","Deficiency in MT5-MMP Supports Branching of Human iPSCs-Derived Neurons and Reduces Expression of GLAST/S100 in iPSCs-Derived Astrocytes.\n","Mutations in the Amyloid-beta Protein Precursor Reduce Mitochondrial Function and Alter Gene Expression Independent of 42-Residue Amyloid-beta Peptide.\n","Alzheimer's disease BIN1 coding variants increase intracellular Abeta levels by interfering with BACE1 recycling.\n","Elevated Expression of MiR-17 in Microglia of Alzheimer's Disease Patients Abrogates Autophagy-Mediated Amyloid-beta Degradation.\n","Microglial activation and tau propagate jointly across Braak stages.\n","Exosomal tau with seeding activity is released from Alzheimer's disease synapses, and seeding potential is associated with amyloid beta.\n","Amyloid beta acts synergistically as a pro-inflammatory cytokine.\n","Overexpression of wild-type human amyloid precursor protein alters GABAergic transmission.\n","A mass spectrometric approach to study the interaction of amyloid beta peptides with human alpha-2-macroglobulin.\n","Spreading of Alzheimer tau seeds is enhanced by aging and template matching with limited impact of amyloid-beta.\n","The role of the half-turn in determining structures of Alzheimer's Abeta wild-type and mutants.\n","The localization of amyloid precursor protein to ependymal cilia in vertebrates and its role in ciliogenesis and brain development in zebrafish.\n","Accumulation of amyloid beta (Abeta) and amyloid precursor protein (APP) in tumors formed by a mouse xenograft model of inflammatory breast cancer.\n","Low prevalence of amyloid and tau pathology in drug-resistant temporal lobe epilepsy.\n","Distinct conformers of amyloid beta accumulate in the neocortex of patients with rapidly progressive Alzheimer's disease.\n","Human cerebral vascular amyloid contains both antiparallel and parallel in-register Abeta40 fibrils.\n","In Silico Modeling of the Influence of Environment on Amyloid Folding Using FOD-M Model.\n","alphaS Oligomers Generated from Interactions with a Polyunsaturated Fatty Acid and a Dopamine Metabolite Differentially Interact with Abeta to Enhance Neurotoxicity.\n","Data Mining of Molecular Simulations Suggest Key Amino Acid Residues for Aggregation, Signaling and Drug Action.\n","Performance of the plasma Abeta42/Abeta40 ratio, measured with a novel HPLC-MS/MS method, as a biomarker of amyloid PET status in a DPUK-KOREAN cohort.\n","Structural differences in amyloid-beta fibrils from brains of nondemented elderly individuals and Alzheimer's disease patients.\n","The apolipoprotein receptor LRP3 compromises APP levels.\n","Dysregulated expression levels of APH1B in peripheral blood are associated with brain atrophy and amyloid-beta deposition in Alzheimer's disease.\n","Network Meta-analysis on the Changes of Amyloid Precursor Protein Expression Following SARS-CoV-2 Infection.\n","Zinc Induced Abeta16 Aggregation Modeled by Molecular Dynamics.\n","Tauhe Greek Variant in APP Gene: The Phenotypic Spectrum of APP Mutations.\n","Amyloid beta protein negatively regulates human platelet activation induced by thrombin receptor-activating protein.\n","A longitudinal investigation of Abeta, anxiety, depression, and mild cognitive impairment.\n","No evidence of aberrant amyloid beta and phosphorylated tau expression in herpes simplex virus-infected neurons of the trigeminal ganglia and brain.\n","Anchoring of Amyloid-beta onto Polyunsaturated Phospholipid Membranes.\n","Perivascular space dilation is associated with vascular amyloid-beta accumulation in the overlying cortex.\n","Probing the Influence of Single-Site Mutations in the Central Cross-beta Region of Amyloid beta (1-40) Peptides.\n","Near-Wall Aggregation of Amyloidogenic Abeta 1-40 Peptide: Direct Observation by the FRET.\n","Hybrid Bis-Histidine Phenanthroline-Based Ligands to Lessen Abeta-Bound Cu ROS Production: An Illustration of Cu(I) Significance.\n","Synthesis and Characterization of Andrographolide Derivatives as Regulators of betaAPP Processing in Human Cells.\n","The APOE epsilon4 Allele Affects Cognitive Functions Differently in Carriers of APP Mutations Compared to Carriers of PSEN1 Mutations in Autosomal-Dominant Alzheimer's Disease.\n","Conformational Models of APP Processing by Gamma Secretase Based on Analysis of Pathogenic Mutations.\n","In vitro coordination of Fe-protoheme with amyloid beta is non-specific and exhibits multiple equilibria.\n","Altered succinylation of mitochondrial proteins, APP and tau in Alzheimer's disease.\n","Cryo-EM structures of amyloid-beta 42 filaments from human brains.\n","The amyloid concentric beta-barrel hypothesis: Models of amyloid beta 42 oligomers and annular protofibrils.\n","A PDK-1 allosteric agonist neutralizes insulin signaling derangements and beta-amyloid toxicity in neuronal cells and in vitro.\n","Segregation of the membrane cargoes, BACE1 and amyloid precursor protein (APP) throughout the Golgi apparatus.\n","Revisiting APP secretases: an overview on the holistic effects of retinoic acid receptor stimulation in APP processing.\n","Differentiation of Amyloid Plaques Between Alzheimer's Disease and Non-Alzheimer's Disease Individuals Based on Gray-Level Co-occurrence Matrix Texture Analysis.\n","A comparison between tau and amyloid-beta cerebrospinal fluid biomarkers in chronic traumatic encephalopathy and Alzheimer disease.\n","The Ubiquitin E3 Ligase Nedd4 Regulates the Expression and Amyloid-beta Peptide Export Activity of P-Glycoprotein.\n","Meta-Analysis of APP Expression Modulated by SARS-CoV-2 Infection via the ACE2 Receptor.\n","A Palette of Fluorescent Abeta42 Peptides Labelled at a Range of Surface-Exposed Sites.\n","Blood amyloid and tau biomarkers as predictors of cerebrospinal fluid profiles.\n","APP and DYRK1A regulate axonal and synaptic vesicle protein networks and mediate Alzheimer's pathology in trisomy 21 neurons.\n","Effects of microRNA-298 on APP and BACE1 translation differ according to cell type and 3'-UTR variation.\n","Alzheimer's disease amyloid-beta pathology in the lens of the eye.\n","Epigenetic Studies in the Male APP/BIN1/COPS5 Triple-Transgenic Mouse Model of Alzheimer's Disease.\n","Endothelial expression of human amyloid precursor protein leads to amyloid beta in the blood and induces cerebral amyloid angiopathy in knock-in mice.\n","beta-Amyloid activates reactive astrocytes by enhancing glycolysis of astrocytes.\n","Long non-coding RNA MALAT1 protects against Abeta1-42 induced toxicity by regulating the expression of receptor tyrosine kinase EPHA2 via quenching miR-200a/26a/26b in Alzheimer's disease.\n","Microglial amyloid beta clearance is driven by PIEZO1 channels.\n","Study on the correlation between PPARgamma, Abeta1-42, miR-155 and the occurrence and development of diabetes.\n","Does Loss of Integrity of the Cingulum Bundle Link Amyloid-beta Accumulation and Neurodegeneration in Alzheimer's Disease?\n","Correlation Between Plasma Oligomeric Amyloid-beta and Performance on the Language Neutral Visual Cognitive Assessment Test in a Southeast Asian Population.\n","Amyloid-beta misfolding and GFAP predict risk of clinical Alzheimer's disease diagnosis within 17 years.\n","Tau Mediates Synergistic Influence of Vascular Risk and Abeta on Cognitive Decline.\n","The AICD fragment of APP initiates a FoxO3a mediated response via FANCD2.\n","Clinical course and serum amyloid beta levels in elderly patients with major depressive disorder.\n","Astrocyte biomarker signatures of amyloid-beta and tau pathologies in Alzheimer's disease.\n","Amyloid- beta and tau deposition influences cognitive and functional decline in Down syndrome.\n","Focal-type, but not Diffuse-type, Amyloid Beta Plaques are Correlated with Alzheimer's Neuropathology, Cognitive Dysfunction, and Neuroinflammation in the Human Hippocampus.\n","Precocious emergence of cognitive and synaptic dysfunction in 3xTg-AD mice exposed prenatally to ethanol.\n","Impact of A2T and D23N mutations on C99 homodimer conformations.\n","beta-Amyloid and Tau Imaging in Chronic Traumatic Brain Injury: A Cross-sectional Study.\n","Predicting conversion of brain beta-amyloid positivity in amyloid-negative individuals.\n","A CHCHD6-APP axis connects amyloid and mitochondrial pathology in Alzheimer's disease.\n","Rare Amyloid Precursor Protein Point Mutations Recapitulate Worldwide Migration and Admixture in Healthy Individuals: Implications for the Study of Neurodegeneration.\n","Cardiolipin released by microglia can act on neighboring glial cells to facilitate the uptake of amyloid-beta (1-42).\n","Soluble amyloid-beta precursor peptide does not regulate GABAB receptor activity.\n","Potential Protective Function of Abeta42 Monomer on Tauopathies.\n","Amyloid precursor protein CTF accumulates in synapses in sporadic and genetic forms of Alzheimer's disease.\n","Knockdown of Amyloid Precursor Protein Increases Ion Channel Expression and Alters Ca[2+] Signaling Pathways.\n","Interplay between APP and glypican-1 processing and alpha-synuclein aggregation in undifferentiated and differentiated human neural progenitor cells.\n","How Single Site Mutations Can Help Understanding Structure Formation of Amyloid beta1-40.\n","Molecular dynamics simulations reveal the importance of amyloid-beta oligomer beta-sheet edge conformations in membrane permeabilization.\n","Tau, beta-Amyloid, and Glucose Metabolism Following Service-Related Traumatic Brain Injury in Vietnam War Veterans: The Australian Imaging Biomarkers and Lifestyle Study of Aging-Veterans Study (AIBL-VETS).\n","Receptor for Advanced Glycation End Products: Dementia and Cognitive Impairment.\n","Age-Dependent Dysregulation of APP in Neuronal and Skin Cells from Fragile X Individuals.\n","circRNA from APP Gene Changes in Alzheimer's Disease Human Brain.\n","Long-term effects of amyloid-beta deposits in human iPSC-derived astrocytes.\n","Detecting amyloid-beta positivity using regions of interest from structural magnetic resonance imaging.\n","Association of APP gene polymorphisms and promoter methylation with essential hypertension in Guizhou: a case-control study.\n","Cellular cholesterol loss by DHCR24 knockdown leads to Abeta production by changing APP intracellular localization.\n","Retromer Proteins Reduced in Down Syndrome and the Dp16 Model: Impact of APP Dose and Preclinical Studies of a gamma-Secretase Modulator.\n","Assessment of tau phosphorylation and beta-amyloid pathology in human drug-resistant epilepsy.\n","Respective influence of beta-amyloid and APOE epsilon4 genotype on medial temporal lobe subregions in cognitively unimpaired older adults.\n","Amyloid beta peptides (Abeta) from Alzheimer's disease neuronal secretome induce endothelial activation in a human cerebral microvessel model.\n","Distinct and joint effects of low and high levels of Abeta and tau deposition on cortical thickness.\n","Protective Alzheimer's disease-associated APP A673T variant predominantly decreases sAPPbeta levels in cerebrospinal fluid and 2D/3D cell culture models.\n","Amyloid-beta accumulation in relation to functional connectivity in aging: A longitudinal study.\n","Structural Dynamics of Amyloid-beta Protofibrils and Actions of Anti-Amyloid-beta Antibodies as Observed by High-Speed Atomic Force Microscopy.\n","Whole-exome sequencing detected a novel APP variant in a Han-Chinese family with Alzheimer's disease.\n","Enlarged perivascular spaces and plasma Abeta42/Abeta40 ratio in older adults without dementia.\n","Phenotype and imaging features associated with APP duplications.\n","APP in the Neuromuscular Junction for the Development of Sarcopenia and Alzheimer's Disease.\n","Identification of Catechins' Binding Sites in Monomeric Abeta42 through Ensemble Docking and MD Simulations.\n","beta-Secretase-1: In Silico Drug Reposition for Alzheimer's Disease.\n","Plasma amyloid-beta biomarkers are associated with Alzheimer's disease comorbidity in Lewy body disease.\n","Amyloid-beta is a cytokine.\n","Astrocyte reactivity influences amyloid-beta effects on tau pathology in preclinical Alzheimer's disease.\n","Amyloid Precursor Protein: A Regulatory Hub in Alzheimer's Disease.\n","The temporal balance between self-renewal and differentiation of human neural stem cells requires the amyloid precursor protein.\n","APP-BACE1 Interaction and Intracellular Localization Regulate Abeta Production in iPSC-Derived Cortical Neurons.\n","Revisit the E2 Domain of Amyloid Precursor Protein: Ferroxidase, Superoxide and Peroxynitrite Scavenging Activities.\n","Effects of the APOEvarepsilon4 Allele on the Relationship Between Tau and Amyloid-beta in Early- and Late-Onset Alzheimer's Disease.\n","Sugar distributions on gangliosides guide the formation and stability of amyloid-beta oligomers.\n","The complex pathway between amyloid beta and cognition: implications for therapy.\n","Individual regional associations between Abeta-, tau- and neurodegeneration (ATN) with microglial activation in patients with primary and secondary tauopathies.\n","Physiological expression of mutated TAU impaired astrocyte activity and exacerbates beta-amyloid pathology in 5xFAD mice.\n","Amyloid and tau pathology are associated with cerebral blood flow in a mixed sample of nondemented older adults with and without vascular risk factors for Alzheimer's disease.\n","Spatial cognition is associated with levels of phosphorylated-tau and beta-amyloid in clinically normal older adults.\n","N-Acetyltransferase 9 ameliorates Abeta42-mediated neurodegeneration in the Drosophila eye.\n","Amyloid beta1-42 Oligomers Induce Galectin-1[S8] O-GlcNAcylation Leading to Microglia Migration.\n","Distinct Molecular Signatures of Amyloid-Beta and Tau in Alzheimer's Disease Associated with Down Syndrome.\n","Physical activity and amyloid beta in middle-aged and older adults: A systematic review and meta-analysis.\n","Amyloid Beta Peptides Lead to Mast Cell Activation in a Novel 3D Hydrogel Model.\n","Blood-Brain Barrier Dysfunction and Abeta42/40 Ratio Dose-Dependent Modulation with the ApoE Genotype within the ATN Framework.\n","Neurophysiological alterations in mice and humans carrying mutations in APP and PSEN1 genes.\n","Abnormal interaction of Rlip with mutant APP/Abeta and phosphorylated tau reduces wild-type Rlip levels and disrupt Rlip function in Alzheimer's disease.\n","The molecular spectrum of amyloid-beta (Abeta) in neurodegenerative diseases beyond Alzheimer's disease.\n","Capillary dysfunction in healthy elderly APOE epsilon4 carriers with raised brain Abeta deposition.\n","Cerebrospinal fluid amyloid beta with amyloid positron emission tomography concordance rates in a heterogeneous group of patients including late-onset psychotic disorders: a retrospective cross-sectional study.\n","Identification and characterization of the conformation and size of amyloid-beta (42) oligomers targeting the receptor LilrB2.\n","Detection the severity of organophosphate intoxication using sensitive serum biomarkers S100B and amyloid beta (Abeta) in Egyptian subjects.\n","The Abeta42 Peptide and IAPP Physically Interact in a Yeast-Based Assay.\n","Serum matrix metalloproteinase-9 (MMP9) and amyloid-beta protein precursor (APP) as potential biomarkers in children with Fragile-X syndrome: A cross sectional study.\n","Integrating TSPO PET imaging and transcriptomics to unveil the role of neuroinflammation and amyloid-beta deposition in Alzheimer's disease.\n","Plasma Abeta level alterations after sleep deprivation correspond to brain structural remodeling in medical night shift workers.\n","Arrangement of lipid vesicles and bicelle-like structures formed in the presence of Abeta(25-35) peptide.\n","Axon-Autonomous Effects of the Amyloid Precursor Protein Intracellular Domain (AICD) on Kinase Signaling and Fast Axonal Transport.\n","Amyloid Precursor Protein and Alzheimer's Disease.\n","The role of melatonin in amyloid beta-induced inflammation mediated by inflammasome signaling in neuronal cell lines.\n","Plasma biomarkers predict Alzheimer's disease before clinical onset in Chinese cohorts.\n","Associations Between Blood Nutritional Biomarkers and Cerebral Amyloid-beta: Insights From the COGFRAIL Cohort Study.\n","CSF biomarker analysis of ABCA7 mutation carriers suggests altered APP processing and reduced inflammatory response.\n","Physical Performance and Amyloid-beta in Humans: A Systematic Review and Meta-Analysis of Observational Studies.\n","Amyloid and Tau PET Positivity in Progressive Agrammatic Aphasia and Apraxia of Speech.\n","Elevated Ghrelin Promotes Hippocampal Ghrelin Receptor Defects in Humanized Amyloid-beta Knockin Mice During Aging.\n","Molecular modeling of apoE in complexes with Alzheimer's amyloid-beta fibrils from human brain suggests a structural basis for apolipoprotein co-deposition with amyloids.\n","GDP dissociation inhibitor 1 (GDI1) attenuates beta-amyloid-induced neurotoxicity in Alzheimer's diseases.\n","Abeta Amyloid Fibers Drastically Alter the Topography and Mechanical Properties of Lipid Membranes.\n","APOE3ch alters microglial response and suppresses Abeta-induced tau seeding and spread.\n","Age of onset predicted by Abeta profiling in a novel PSEN1 (I180F) mutation.\n","Spatiotemporal Correlation between Amyloid and Tau Accumulations Underlies Cognitive Changes in Aging.\n","Potentially Pathogenic SORL1 Mutations Observed in Autosomal-Dominant Cases of Alzheimer's Disease Do Not Modulate APP Physiopathological Processing.\n","Proteolytic cleavage of amyloid precursor protein by ADAM10 promotes proliferation and migration via activating MAPKs pathway in tongue squamous cell carcinoma in vitro.\n","Potential links between platelets and amyloid-beta in the pathogenesis of Alzheimer's disease: Evidence from in vitro, in vivo, and clinical studies.\n","Interaction Between Arteriosclerosis and Amyloid-beta on Cognitive Function.\n","Amyloid-beta deposits in human astrocytes contain truncated and highly resistant proteoforms.\n","Updates on Abeta Processing by Hsp90, BRICHOS, and Newly Reported Distinctive Chaperones.\n","Nuclear SphK2/S1P signaling is a key regulator of ApoE production and Abeta uptake in astrocytes.\n","Amyloid beta interferes with wound healing of brain microvascular endothelial cells by disorganizing the actin cytoskeleton.\n","Amyloid-beta aggregates activate peripheral monocytes in mild cognitive impairment.\n","The contribution of beta-amyloid, Tau and alpha-synuclein to blood-brain barrier damage in neurodegenerative disorders.\n","Signal peptide peptidase-like 2b modulates the amyloidogenic pathway and exhibits an Abeta-dependent expression in Alzheimer's disease.\n","Exploring the Association between Amyloid-beta and Memory Markers for Alzheimer's Disease in Cognitively Unimpaired Older Adults.\n","Edge Substitution Effects of Histidine Tautomerization Behaviors on the Structural Properties and Aggregation Properties of Abeta(1-42) Mature Fibril.\n","Alzheimer's Amyloid-beta Accelerates Cell Senescence and Suppresses SIRT1 in Human Neural Stem Cells.\n","Subsequent correlated changes in complement component 3 and amyloid beta oligomers in the blood of patients with Alzheimer's disease.\n","Consequences of Amyloid-beta Deficiency for the Liver.\n","Chronic pain exacerbates memory impairment and pathology of Abeta and tau by upregulating IL-1beta and p-65 signaling in a mouse model of Alzheimer's disease.\n","Single-cell transcriptomic analysis in clear cell renal cell carcinoma: Deciphering the role of APP within the tumour microenvironment.\n","Dementia and depression: Biological connections with amyloid beta protein.\n","Probable Novel APP Met671Leu Mutation in a Chinese Han Family with Early-Onset Alzheimer's Disease.\n","Amyloid precursor protein combinatorial phosphorylation code regulates AMPA receptor removal during distinct forms of synaptic plasticity.\n","Sex-specific associations between AD genotype and the microbiome of human amyloid beta knock-in (hAbeta-KI) mice.\n","Trajectories of amyloid beta accumulation - Unveiling the relationship with APOE genotype and cognitive decline.\n","The Co-oligomers of Abeta42 and Human Islet Amyloid Polypeptide Exacerbate Neurotoxicity and Alzheimer-like Pathology at Cellular Level.\n","CNTN4 modulates neural elongation through interplay with APP.\n","G-protein coupled estrogen receptor 1, amyloid-beta, and tau tangles in older adults.\n","The presenilin 1 mutation P436S causes familial Alzheimer's disease with elevated Abeta43 and atypical clinical manifestations.\n","Distinctive contribution of two additional residues in protein aggregation of Abeta42 and Abeta40 isoforms.\n","Decreased extrasynaptic delta-GABAA receptors in PNN-associated parvalbumin interneurons correlates with anxiety in APP and tau mouse models of Alzheimer's disease.\n","Are Women with Polycystic Ovary Syndrome at Increased Risk of Alzheimer Disease? Lessons from Insulin Resistance, Tryptophan and Gonadotropin Disturbances and Their Link with Amyloid-Beta Aggregation.\n","Cellular prion protein acts as mediator of amyloid beta uptake by caveolin-1 causing cellular dysfunctions in vitro and in vivo.\n","Elevated concentrations of amyloid-beta oligomers and their proapoptotic effects on age-related cataract.\n","Entorhinal cortex vulnerability to human APP expression promotes hyperexcitability and tau pathology.\n","Structural Insight into Melatonin's Influence on the Conformation of Abeta42 Dimer Studied by Molecular Dynamics Simulation.\n","Unveiling the effect of CaCl2 on amyloid beta aggregation via supercritical angle Raman and fluorescence spectroscopy and microscopy.\n","Pathology of Amyloid-beta (Abeta) Peptide Peripheral Clearance in Alzheimer's Disease.\n","The link between amyloid beta and ferroptosis pathway in Alzheimer's disease progression.\n"],"discontinued":null,"gene_no":351,"geneconstraints_lof":0.999,"start_pos":"25880550","geneconstraints_missense":2.252,"genesymbol":"APP","chromosome":21,"geneconstraint":1,"end_pos":"26171128","type":"protein-coding","changed_to":null}]