Targeting mitophagy in Alzheimer's disease

Document Type

Journal Article

Publication Title

Journal of Alzheimer's Disease

Volume

78

Issue

4

First Page

1273

Last Page

1297

PubMed ID

33285629

Publisher

IOS Press

School

School of Medical and Health Sciences

RAS ID

35385

Comments

Jayatunga, D. P. W., Hone, E., Bharadwaj, P., Garg, M., Verdile, G., Guillemin, G. J., & Martins, R. N. (2020). Targeting mitophagy in Alzheimer’s disease. Journal of Alzheimer's Disease, 78(4), 1273-1297. https://doi.org/10.3233/JAD-191258

Abstract

© 2020 - IOS Press and the authors. All rights reserved. Mitochondria perform many essential cellular functions including energy production, calcium homeostasis, transduction of metabolic and stress signals, and mediating cell survival and death. Maintaining viable populations of mitochondria is therefore critical for normal cell function. The selective disposal of damaged mitochondria, by a pathway known as mitophagy, plays a key role in preserving mitochondrial integrity and quality. Mitophagy reduces the formation of reactive oxygen species and is considered as a protective cellular process. Mitochondrial dysfunction and deficits of mitophagy have important roles in aging and especially in neurodegenerative disorders such as Alzheimer's disease (AD). Targeting mitophagy pathways has been suggested to have potential therapeutic effects against AD. In this review, we aim to briefly discuss the emerging concepts on mitophagy, molecular regulation of the mitophagy process, current mitophagy detection methods, and mitophagy dysfunction in AD. Finally, we will also briefly examine the stimulation of mitophagy as an approach for attenuating neurodegeneration in AD.

DOI

10.3233/JAD-191258

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