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Mitophagy in Alzheimer’s Disease and Other Age-Related Neurodegenerative Diseases

Mitochondrial dysfunction is a central aspect of aging and neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and Huntington’s disease. Mitochondria are the main cellular energy powerhouses, supplying most of ATP by oxidative phosphorylatio...

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Detalles Bibliográficos
Autores principales: Cai, Qian, Jeong, Yu Young
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7017092/
https://www.ncbi.nlm.nih.gov/pubmed/31936292
http://dx.doi.org/10.3390/cells9010150
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author Cai, Qian
Jeong, Yu Young
author_facet Cai, Qian
Jeong, Yu Young
author_sort Cai, Qian
collection PubMed
description Mitochondrial dysfunction is a central aspect of aging and neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and Huntington’s disease. Mitochondria are the main cellular energy powerhouses, supplying most of ATP by oxidative phosphorylation, which is required to fuel essential neuronal functions. Efficient removal of aged and dysfunctional mitochondria through mitophagy, a cargo-selective autophagy, is crucial for mitochondrial maintenance and neuronal health. Mechanistic studies into mitophagy have highlighted an integrated and elaborate cellular network that can regulate mitochondrial turnover. In this review, we provide an updated overview of the recent discoveries and advancements on the mitophagy pathways and discuss the molecular mechanisms underlying mitophagy defects in Alzheimer’s disease and other age-related neurodegenerative diseases, as well as the therapeutic potential of mitophagy-enhancing strategies to combat these disorders.
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spelling pubmed-70170922020-02-28 Mitophagy in Alzheimer’s Disease and Other Age-Related Neurodegenerative Diseases Cai, Qian Jeong, Yu Young Cells Review Mitochondrial dysfunction is a central aspect of aging and neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and Huntington’s disease. Mitochondria are the main cellular energy powerhouses, supplying most of ATP by oxidative phosphorylation, which is required to fuel essential neuronal functions. Efficient removal of aged and dysfunctional mitochondria through mitophagy, a cargo-selective autophagy, is crucial for mitochondrial maintenance and neuronal health. Mechanistic studies into mitophagy have highlighted an integrated and elaborate cellular network that can regulate mitochondrial turnover. In this review, we provide an updated overview of the recent discoveries and advancements on the mitophagy pathways and discuss the molecular mechanisms underlying mitophagy defects in Alzheimer’s disease and other age-related neurodegenerative diseases, as well as the therapeutic potential of mitophagy-enhancing strategies to combat these disorders. MDPI 2020-01-08 /pmc/articles/PMC7017092/ /pubmed/31936292 http://dx.doi.org/10.3390/cells9010150 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Cai, Qian
Jeong, Yu Young
Mitophagy in Alzheimer’s Disease and Other Age-Related Neurodegenerative Diseases
title Mitophagy in Alzheimer’s Disease and Other Age-Related Neurodegenerative Diseases
title_full Mitophagy in Alzheimer’s Disease and Other Age-Related Neurodegenerative Diseases
title_fullStr Mitophagy in Alzheimer’s Disease and Other Age-Related Neurodegenerative Diseases
title_full_unstemmed Mitophagy in Alzheimer’s Disease and Other Age-Related Neurodegenerative Diseases
title_short Mitophagy in Alzheimer’s Disease and Other Age-Related Neurodegenerative Diseases
title_sort mitophagy in alzheimer’s disease and other age-related neurodegenerative diseases
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7017092/
https://www.ncbi.nlm.nih.gov/pubmed/31936292
http://dx.doi.org/10.3390/cells9010150
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