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Effects of Redox Homeostasis and Mitochondrial Damage on Alzheimer’s Disease

Bioenergetic mitochondrial dysfunction is a common feature of several diseases, including Alzheimer’s disease (AD), where redox imbalance also plays an important role in terms of disease development. AD is an age-related disease and begins many years before the appearance of neurodegenerative sympto...

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Autores principales: Wu, Yi-Hsuan, Hsieh, Hsi-Lung
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10604635/
https://www.ncbi.nlm.nih.gov/pubmed/37891895
http://dx.doi.org/10.3390/antiox12101816
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author Wu, Yi-Hsuan
Hsieh, Hsi-Lung
author_facet Wu, Yi-Hsuan
Hsieh, Hsi-Lung
author_sort Wu, Yi-Hsuan
collection PubMed
description Bioenergetic mitochondrial dysfunction is a common feature of several diseases, including Alzheimer’s disease (AD), where redox imbalance also plays an important role in terms of disease development. AD is an age-related disease and begins many years before the appearance of neurodegenerative symptoms. Intracellular tau aggregation, extracellular β-amyloid (Aβ) deposition in the brain, and even the APOE4 genotype contribute to the process of AD by impairing redox homeostasis and mitochondrial dysfunction. This review summarizes the evidence for the redox imbalance and mitochondrial dysfunction in AD and demonstrates the current therapeutic strategies related to mitochondrial maintenance.
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spelling pubmed-106046352023-10-28 Effects of Redox Homeostasis and Mitochondrial Damage on Alzheimer’s Disease Wu, Yi-Hsuan Hsieh, Hsi-Lung Antioxidants (Basel) Review Bioenergetic mitochondrial dysfunction is a common feature of several diseases, including Alzheimer’s disease (AD), where redox imbalance also plays an important role in terms of disease development. AD is an age-related disease and begins many years before the appearance of neurodegenerative symptoms. Intracellular tau aggregation, extracellular β-amyloid (Aβ) deposition in the brain, and even the APOE4 genotype contribute to the process of AD by impairing redox homeostasis and mitochondrial dysfunction. This review summarizes the evidence for the redox imbalance and mitochondrial dysfunction in AD and demonstrates the current therapeutic strategies related to mitochondrial maintenance. MDPI 2023-09-30 /pmc/articles/PMC10604635/ /pubmed/37891895 http://dx.doi.org/10.3390/antiox12101816 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/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 (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Wu, Yi-Hsuan
Hsieh, Hsi-Lung
Effects of Redox Homeostasis and Mitochondrial Damage on Alzheimer’s Disease
title Effects of Redox Homeostasis and Mitochondrial Damage on Alzheimer’s Disease
title_full Effects of Redox Homeostasis and Mitochondrial Damage on Alzheimer’s Disease
title_fullStr Effects of Redox Homeostasis and Mitochondrial Damage on Alzheimer’s Disease
title_full_unstemmed Effects of Redox Homeostasis and Mitochondrial Damage on Alzheimer’s Disease
title_short Effects of Redox Homeostasis and Mitochondrial Damage on Alzheimer’s Disease
title_sort effects of redox homeostasis and mitochondrial damage on alzheimer’s disease
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10604635/
https://www.ncbi.nlm.nih.gov/pubmed/37891895
http://dx.doi.org/10.3390/antiox12101816
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