Mitochondrial dysfunction in Alzheimer's disease - a proteomics perspective.
Alzheimer’s disease
Mitochondrial dysfunction
Proteomics
Journal
Expert review of proteomics
ISSN: 1744-8387
Titre abrégé: Expert Rev Proteomics
Pays: England
ID NLM: 101223548
Informations de publication
Date de publication:
04 2021
04 2021
Historique:
pubmed:
21
4
2021
medline:
3
2
2022
entrez:
20
4
2021
Statut:
ppublish
Résumé
Mitochondrial dysfunction is involved in Alzheimer's disease (AD) pathogenesis. Mitochondria have their own genetic material; however, most of their proteins (∼99%) are synthesized as precursors on cytosolic ribosomes, and then imported into the mitochondria. Therefore, exploring proteome changes in these organelles can yield valuable information and shed light on the molecular mechanisms underlying mitochondrial dysfunction in AD. Here, we review AD-associated mitochondrial changes including the effects of amyloid beta and tau protein accumulation on the mitochondrial proteome. We also discuss the relationship of ApoE genetic polymorphism with mitochondrial changes, and present a meta-analysis of various differentially expressed proteins in the mitochondria in AD.
Identifiants
pubmed: 33874826
doi: 10.1080/14789450.2021.1918550
doi:
Substances chimiques
Amyloid beta-Peptides
0
Proteome
0
Types de publication
Journal Article
Meta-Analysis
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM