Mitochondrial Disruption by Amyloid Beta 42 Identified by Proteomics and Pathway Mapping.


Journal

Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052

Informations de publication

Date de publication:
10 09 2021
Historique:
received: 23 07 2021
revised: 23 08 2021
accepted: 31 08 2021
entrez: 28 9 2021
pubmed: 29 9 2021
medline: 17 11 2021
Statut: epublish

Résumé

Alzheimer's disease (AD) is marked by chronic neurodegeneration associated with the occurrence of plaques containing amyloid β (Aβ) proteins in various parts of the human brain. An increase in several Aβ fragments is well documented in patients with AD and anti-amyloid targeting is an emerging area of therapy. Soluble Aβ can bind to various cell surface and intracellular molecules with the pathogenic Aβ

Identifiants

pubmed: 34572029
pii: cells10092380
doi: 10.3390/cells10092380
pmc: PMC8468661
pii:
doi:

Substances chimiques

Amyloid beta-Peptides 0
Peptide Fragments 0
Proteome 0
amyloid beta-protein (1-42) 0

Banques de données

figshare
['10.6084/m9.figshare.15157257']

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Références

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Auteurs

Patricia Sinclair (P)

Interdisciplinary Program in Neuroscience, School of Systems Biology, George Mason University, Fairfax, VA 22030, USA.

Ancha Baranova (A)

School of Systems Biology, George Mason University, Manassas VA 20110, USA.

Nadine Kabbani (N)

School of Systems Biology, George Mason University, Manassas VA 20110, USA.

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Classifications MeSH