High molecular weight amyloid β
Alzheimer Disease
/ metabolism
Amyloid beta-Peptides
/ chemistry
Calcium
/ metabolism
Cell Line, Tumor
Cell Membrane
/ drug effects
Electrophysiology
Hippocampus
/ drug effects
Humans
Lipid Peroxidation
/ drug effects
Membrane Fluidity
Microscopy, Atomic Force
Molecular Weight
Patch-Clamp Techniques
Reactive Oxygen Species
/ metabolism
Alzheimer disease
amyloid β-protein
membrane disruption
Journal
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
ISSN: 1530-6860
Titre abrégé: FASEB J
Pays: United States
ID NLM: 8804484
Informations de publication
Date de publication:
08 2019
08 2019
Historique:
pubmed:
16
5
2019
medline:
2
6
2020
entrez:
16
5
2019
Statut:
ppublish
Résumé
Amyloid β-protein (Aβ) molecules tend to aggregate and subsequently form low MW (LMW) oligomers, high MW (HMW) aggregates such as protofibrils, and ultimately fibrils. These Aβ species can generally form amyloid plaques implicated in the neurodegeneration of Alzheimer disease (AD), but therapies designed to reduce plaque load have not demonstrated clinical efficacy. Recent evidence implicates amyloid oligomers in AD neuropathology, but the precise mechanisms are uncertain. We examined the mechanisms of neuronal dysfunction from HMW-Aβ
Identifiants
pubmed: 31084283
doi: 10.1096/fj.201900604R
doi:
Substances chimiques
Amyloid beta-Peptides
0
Reactive Oxygen Species
0
Calcium
SY7Q814VUP
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM