The pathogenic aβ43 is enriched in familial and sporadic Alzheimer disease
about
Calcium-Sensing Receptors of Human Neural Cells Play Crucial Roles in Alzheimer's DiseaseSuccessful therapies for Alzheimer's disease: why so many in animal models and none in humans?The conformational stability of nonfibrillar amyloid-β peptide oligomers critically depends on the C-terminal peptide length.The C-terminal threonine of Aβ43 nucleates toxic aggregation via structural and dynamical changes in monomers and protofibrils.Cerebrospinal Fluid Aβ43 Is Reduced in Early-Onset Compared to Late-Onset Alzheimer's Disease, But Has Similar Diagnostic Accuracy to Aβ42.Amyloid β Protein and Alzheimer's Disease: When Computer Simulations Complement Experimental Studies.Specific aromatic foldamers potently inhibit spontaneous and seeded Aβ42 and Aβ43 fibril assembly.Aβ43 is neurotoxic and primes aggregation of Aβ40 in vivo.Specific Triazine Herbicides Induce Amyloid-β42 Production.Cerebrospinal Fluid Levels of Amyloid Beta 1-43 in Patients with Amnestic Mild Cognitive Impairment or Early Alzheimer's Disease: A 2-Year Follow-Up Study.Cerebrospinal Fluid Levels of Amyloid Beta 1-43 Mirror 1-42 in Relation to Imaging Biomarkers of Alzheimer's Disease.Extracellular vesicles in Alzheimer's disease: friends or foes? Focus on aβ-vesicle interaction.Familial Presenilin Mutations and Sporadic Alzheimer's Disease Pathology: Is the Assumption of Biochemical Equivalence Justified?α-Mangostin decreases β-amyloid peptides production via modulation of amyloidogenic pathway.Comparison of neurotoxicity of different aggregated forms of Aβ40, Aβ42 and Aβ43 in cell cultures.Zinc and Copper Differentially Modulate Amyloid Precursor Protein Processing by γ-Secretase and Amyloid-β Peptide Production.T-cell epitope-dependent immune response in inbred (C57BL/6J, SJL/J, and C3H/HeN) and transgenic P301S and Tg2576 mice.C-Terminal Threonine Reduces Aβ43 Amyloidogenicity Compared with Aβ42.Protein folding, misfolding and aggregation: The importance of two-electron stabilizing interactions.Generation and deposition of Aβ43 by the virtually inactive presenilin-1 L435F mutant contradicts the presenilin loss-of-function hypothesis of Alzheimer's disease.Do astrocytes collaborate with neurons in spreading the "infectious" aβ and Tau drivers of Alzheimer's disease?Tau hyperphosphorylation induces oligomeric insulin accumulation and insulin resistance in neurons.NSAIDs as potential treatment option for preventing amyloid β toxicity in Alzheimer's disease: an investigation by docking, molecular dynamics, and DFT studies.Perforin Promotes Amyloid Beta Internalisation in Neurons.
P2860
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P2860
The pathogenic aβ43 is enriched in familial and sporadic Alzheimer disease
description
2013 nî lūn-bûn
@nan
2013 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2013 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2013年の論文
@ja
2013年論文
@yue
2013年論文
@zh-hant
2013年論文
@zh-hk
2013年論文
@zh-mo
2013年論文
@zh-tw
2013年论文
@wuu
name
The pathogenic aβ43 is enriched in familial and sporadic Alzheimer disease
@ast
The pathogenic aβ43 is enriched in familial and sporadic Alzheimer disease
@en
The pathogenic aβ43 is enriched in familial and sporadic Alzheimer disease
@nl
type
label
The pathogenic aβ43 is enriched in familial and sporadic Alzheimer disease
@ast
The pathogenic aβ43 is enriched in familial and sporadic Alzheimer disease
@en
The pathogenic aβ43 is enriched in familial and sporadic Alzheimer disease
@nl
prefLabel
The pathogenic aβ43 is enriched in familial and sporadic Alzheimer disease
@ast
The pathogenic aβ43 is enriched in familial and sporadic Alzheimer disease
@en
The pathogenic aβ43 is enriched in familial and sporadic Alzheimer disease
@nl
P2093
P2860
P1433
P1476
The pathogenic aβ43 is enriched in familial and sporadic Alzheimer disease
@en
P2093
Anna Sandebring
Hedvig Welander
Lars O Tjernberg
P2860
P304
P356
10.1371/JOURNAL.PONE.0055847
P407
P577
2013-02-11T00:00:00Z