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Mechanisms of Mitochondrial Malfunction in Alzheimer's Disease: New Therapeutic Hope
Mitochondria play a critical role in neuron viability or death as it regulates energy metabolism and cell death pathways. They are essential for cellular energy metabolism, reactive oxygen species production, apoptosis, Ca(++) homeostasis, aging, and regeneration. Mitophagy and mitochondrial dynamic...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9124149/ https://www.ncbi.nlm.nih.gov/pubmed/35607703 http://dx.doi.org/10.1155/2022/4759963 |
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author | Nabi, Showkat Ul Khan, Andleeb Siddiqui, Ehraz Mehmood Rehman, Muneeb U. Alshahrani, Saeed Arafah, Azher Mehan, Sidharth Alsaffar, Rana M. Alexiou, Athanasios Shen, Bairong |
author_facet | Nabi, Showkat Ul Khan, Andleeb Siddiqui, Ehraz Mehmood Rehman, Muneeb U. Alshahrani, Saeed Arafah, Azher Mehan, Sidharth Alsaffar, Rana M. Alexiou, Athanasios Shen, Bairong |
author_sort | Nabi, Showkat Ul |
collection | PubMed |
description | Mitochondria play a critical role in neuron viability or death as it regulates energy metabolism and cell death pathways. They are essential for cellular energy metabolism, reactive oxygen species production, apoptosis, Ca(++) homeostasis, aging, and regeneration. Mitophagy and mitochondrial dynamics are thus essential processes in the quality control of mitochondria. Improvements in several fundamental features of mitochondrial biology in susceptible neurons of AD brains and the putative underlying mechanisms of such changes have made significant progress. AD's etiology has been reported by mitochondrial malfunction and oxidative damage. According to several recent articles, a continual fusion and fission balance of mitochondria is vital in their normal function maintenance. As a result, the shape and function of mitochondria are inextricably linked. This study examines evidence suggesting that mitochondrial dysfunction plays a significant early impact on AD pathology. Furthermore, the dynamics and roles of mitochondria are discussed with the link between mitochondrial malfunction and autophagy in AD has also been explored. In addition, recent research on mitochondrial dynamics and mitophagy in AD is also discussed in this review. It also goes into how these flaws affect mitochondrial quality control. Furthermore, advanced therapy techniques and lifestyle adjustments that lead to improved management of the dynamics have been demonstrated, hence improving the conditions that contribute to mitochondrial dysfunction in AD. |
format | Online Article Text |
id | pubmed-9124149 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-91241492022-05-22 Mechanisms of Mitochondrial Malfunction in Alzheimer's Disease: New Therapeutic Hope Nabi, Showkat Ul Khan, Andleeb Siddiqui, Ehraz Mehmood Rehman, Muneeb U. Alshahrani, Saeed Arafah, Azher Mehan, Sidharth Alsaffar, Rana M. Alexiou, Athanasios Shen, Bairong Oxid Med Cell Longev Review Article Mitochondria play a critical role in neuron viability or death as it regulates energy metabolism and cell death pathways. They are essential for cellular energy metabolism, reactive oxygen species production, apoptosis, Ca(++) homeostasis, aging, and regeneration. Mitophagy and mitochondrial dynamics are thus essential processes in the quality control of mitochondria. Improvements in several fundamental features of mitochondrial biology in susceptible neurons of AD brains and the putative underlying mechanisms of such changes have made significant progress. AD's etiology has been reported by mitochondrial malfunction and oxidative damage. According to several recent articles, a continual fusion and fission balance of mitochondria is vital in their normal function maintenance. As a result, the shape and function of mitochondria are inextricably linked. This study examines evidence suggesting that mitochondrial dysfunction plays a significant early impact on AD pathology. Furthermore, the dynamics and roles of mitochondria are discussed with the link between mitochondrial malfunction and autophagy in AD has also been explored. In addition, recent research on mitochondrial dynamics and mitophagy in AD is also discussed in this review. It also goes into how these flaws affect mitochondrial quality control. Furthermore, advanced therapy techniques and lifestyle adjustments that lead to improved management of the dynamics have been demonstrated, hence improving the conditions that contribute to mitochondrial dysfunction in AD. Hindawi 2022-05-14 /pmc/articles/PMC9124149/ /pubmed/35607703 http://dx.doi.org/10.1155/2022/4759963 Text en Copyright © 2022 Showkat Ul Nabi et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Nabi, Showkat Ul Khan, Andleeb Siddiqui, Ehraz Mehmood Rehman, Muneeb U. Alshahrani, Saeed Arafah, Azher Mehan, Sidharth Alsaffar, Rana M. Alexiou, Athanasios Shen, Bairong Mechanisms of Mitochondrial Malfunction in Alzheimer's Disease: New Therapeutic Hope |
title | Mechanisms of Mitochondrial Malfunction in Alzheimer's Disease: New Therapeutic Hope |
title_full | Mechanisms of Mitochondrial Malfunction in Alzheimer's Disease: New Therapeutic Hope |
title_fullStr | Mechanisms of Mitochondrial Malfunction in Alzheimer's Disease: New Therapeutic Hope |
title_full_unstemmed | Mechanisms of Mitochondrial Malfunction in Alzheimer's Disease: New Therapeutic Hope |
title_short | Mechanisms of Mitochondrial Malfunction in Alzheimer's Disease: New Therapeutic Hope |
title_sort | mechanisms of mitochondrial malfunction in alzheimer's disease: new therapeutic hope |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9124149/ https://www.ncbi.nlm.nih.gov/pubmed/35607703 http://dx.doi.org/10.1155/2022/4759963 |
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