A Glimmer of Hope: Maintain Mitochondrial Homeostasis to Mitigate Alzheimer's Disease.
Alzheimer’s disease
NAD+
mitochondria dysfunction
mitophagy
Journal
Aging and disease
ISSN: 2152-5250
Titre abrégé: Aging Dis
Pays: United States
ID NLM: 101540533
Informations de publication
Date de publication:
Oct 2020
Oct 2020
Historique:
received:
19
10
2019
accepted:
05
01
2020
entrez:
5
10
2020
pubmed:
6
10
2020
medline:
6
10
2020
Statut:
epublish
Résumé
Mitochondria are classically known to be cellular energy producers. Given the high-energy demanding nature of neurons in the brain, it is essential that the mitochondrial pool remains healthy and provides a continuous and efficient supply of energy. However, mitochondrial dysfunction is inevitable in aging and neurodegenerative diseases. In Alzheimer's disease (AD), neurons experience unbalanced homeostasis like damaged mitochondrial biogenesis and defective mitophagy, with the latter promoting the disease-defining amyloid β (Aβ) and p-Tau pathologies impaired mitophagy contributes to inflammation and the aggregation of Aβ and p-Tau-containing neurotoxic proteins. Interventions that restore defective mitophagy may, therefore, alleviate AD symptoms, pointing out the possibility of a novel therapy. This review aims to illustrate mitochondrial biology with a focus on mitophagy and propose strategies to treat AD while maintaining mitochondrial homeostasis.
Identifiants
pubmed: 33014536
doi: 10.14336/AD.2020.0105
pii: ad-11-5-1260
pmc: PMC7505280
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
1260-1275Informations de copyright
copyright: © 2020 Li et al.
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