When loss is gain: reduced presenilin proteolytic function leads to increased Abeta42/Abeta40. Talking Point on the role of presenilin mutations in Alzheimer disease
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Alzheimer's disease as homeostatic responses to age-related myelin breakdownInduced pluripotent stem cells for modeling neurological disordersApplications of Induced Pluripotent Stem Cells in Studying the Neurodegenerative DiseasesToward the structure of presenilin/γ-secretase and presenilin homologsPhenylbutyric acid rescues endoplasmic reticulum stress-induced suppression of APP proteolysis and prevents apoptosis in neuronal cellsTransgenic expression of the amyloid-beta precursor protein-intracellular domain does not induce Alzheimer's Disease-like traits in vivoMolecular profiling reveals diversity of stress signal transduction cascades in highly penetrant Alzheimer's disease human skin fibroblastsBapineuzumab alters aβ composition: implications for the amyloid cascade hypothesis and anti-amyloid immunotherapyPresenilin-dependent receptor processing is required for axon guidanceGeneration and initial characterization of FDD knock in miceAPP heterozygosity averts memory deficit in knockin mice expressing the Danish dementia BRI2 mutantAssembly, maturation, and trafficking of the gamma-secretase complex in Alzheimer's disease.A novel function for the presenilin family member spe-4: inhibition of spermatid activation in Caenorhabditis elegansThe large hydrophilic loop of presenilin 1 is important for regulating gamma-secretase complex assembly and dictating the amyloid beta peptide (Abeta) Profile without affecting Notch processing.A presenilin-1 mutation identified in familial Alzheimer disease with cotton wool plaques causes a nearly complete loss of gamma-secretase activityPharmacological and genetic reversal of age-dependent cognitive deficits attributable to decreased presenilin functionModeling presenilin-dependent familial Alzheimer's disease: emphasis on presenilin substrate-mediated signaling and synaptic function.Presenilin-1 regulates induction of hypoxia inducible factor-1α: altered activation by a mutation associated with familial Alzheimer's diseaseCrystal structure of the γ-secretase component nicastrin.Identification of novel γ-secretase-associated proteins in detergent-resistant membranes from brain.Alzheimer presenilin-1 mutations dramatically reduce trimming of long amyloid β-peptides (Aβ) by γ-secretase to increase 42-to-40-residue Aβ.The pathogenic aβ43 is enriched in familial and sporadic Alzheimer diseaseGenetics of Alzheimer diseaseDetection of bacterial antigens and Alzheimer's disease-like pathology in the central nervous system of BALB/c mice following intranasal infection with a laboratory isolate of Chlamydia pneumoniae.Induced pluripotent stem cells from familial Alzheimer's disease patients differentiate into mature neurons with amyloidogenic propertiesAmyloid accumulation is a late event in sporadic Alzheimer's disease-like pathology in nontransgenic rats.Dissociation between the processivity and total activity of γ-secretase: implications for the mechanism of Alzheimer's disease-causing presenilin mutations.Drug development for Alzheimer's disease: recent progressPutting presenilins centre stage. Introduction to the Talking Point on the role of presenilin mutations in Alzheimer disease.Alzheimer's disease: pathological mechanisms and recent insights.Role of common and rare APP DNA sequence variants in Alzheimer diseaseThe mechanism of γ-Secretase dysfunction in familial Alzheimer disease.Protein post-translational modifications and misfolding: new concepts in heart failure.Alzheimer's disease in a dish: promises and challenges of human stem cell models.Oxidative stress and lipid peroxidation are upstream of amyloid pathology.Presenilin transgenic mice as models of Alzheimer's disease.Presenilin 1 interacts with acetylcholinesterase and alters its enzymatic activity and glycosylation.Presenilin-1 adopts pathogenic conformation in normal aging and in sporadic Alzheimer's disease.Interactome analyses of mature γ-secretase complexes reveal distinct molecular environments of presenilin (PS) paralogs and preferential binding of signal peptide peptidase to PS2.Looking for novel ways to treat the hallmarks of Alzheimer's disease.
P2860
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P2860
When loss is gain: reduced presenilin proteolytic function leads to increased Abeta42/Abeta40. Talking Point on the role of presenilin mutations in Alzheimer disease
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2007 nî lūn-bûn
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2007 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2007 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2007年の論文
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2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
name
When loss is gain: reduced pre ...... mutations in Alzheimer disease
@ast
When loss is gain: reduced pre ...... mutations in Alzheimer disease
@en
When loss is gain: reduced pre ...... mutations in Alzheimer disease
@nl
type
label
When loss is gain: reduced pre ...... mutations in Alzheimer disease
@ast
When loss is gain: reduced pre ...... mutations in Alzheimer disease
@en
When loss is gain: reduced pre ...... mutations in Alzheimer disease
@nl
prefLabel
When loss is gain: reduced pre ...... mutations in Alzheimer disease
@ast
When loss is gain: reduced pre ...... mutations in Alzheimer disease
@en
When loss is gain: reduced pre ...... mutations in Alzheimer disease
@nl
P2860
P3181
P356
P1433
P1476
When loss is gain: reduced pre ...... mutations in Alzheimer disease
@en
P2093
Michael S Wolfe
P2860
P304
P3181
P356
10.1038/SJ.EMBOR.7400896
P407
P577
2007-02-01T00:00:00Z