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Mitochondrial Dysfunction and Multiple Sclerosis

In recent years, several studies have examined the potential associations between mitochondrial dysfunction and neurodegenerative diseases such as multiple sclerosis (MS), Parkinson’s disease and Alzheimer’s disease. In MS, neurological disability results from inflammation, demyelination, and ultima...

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Detalles Bibliográficos
Autores principales: de Barcelos, Isabella Peixoto, Troxell, Regina M., Graves, Jennifer S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6627385/
https://www.ncbi.nlm.nih.gov/pubmed/31083577
http://dx.doi.org/10.3390/biology8020037
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author de Barcelos, Isabella Peixoto
Troxell, Regina M.
Graves, Jennifer S.
author_facet de Barcelos, Isabella Peixoto
Troxell, Regina M.
Graves, Jennifer S.
author_sort de Barcelos, Isabella Peixoto
collection PubMed
description In recent years, several studies have examined the potential associations between mitochondrial dysfunction and neurodegenerative diseases such as multiple sclerosis (MS), Parkinson’s disease and Alzheimer’s disease. In MS, neurological disability results from inflammation, demyelination, and ultimately, axonal damage within the central nervous system. The sustained inflammatory phase of the disease leads to ion channel changes and chronic oxidative stress. Several independent investigations have demonstrated mitochondrial respiratory chain deficiency in MS, as well as abnormalities in mitochondrial transport. These processes create an energy imbalance and contribute to a parallel process of progressive neurodegeneration and irreversible disability. The potential roles of mitochondria in neurodegeneration are reviewed. An overview of mitochondrial diseases that may overlap with MS are also discussed, as well as possible therapeutic targets for the treatment of MS and other neurodegenerative conditions.
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spelling pubmed-66273852019-07-23 Mitochondrial Dysfunction and Multiple Sclerosis de Barcelos, Isabella Peixoto Troxell, Regina M. Graves, Jennifer S. Biology (Basel) Review In recent years, several studies have examined the potential associations between mitochondrial dysfunction and neurodegenerative diseases such as multiple sclerosis (MS), Parkinson’s disease and Alzheimer’s disease. In MS, neurological disability results from inflammation, demyelination, and ultimately, axonal damage within the central nervous system. The sustained inflammatory phase of the disease leads to ion channel changes and chronic oxidative stress. Several independent investigations have demonstrated mitochondrial respiratory chain deficiency in MS, as well as abnormalities in mitochondrial transport. These processes create an energy imbalance and contribute to a parallel process of progressive neurodegeneration and irreversible disability. The potential roles of mitochondria in neurodegeneration are reviewed. An overview of mitochondrial diseases that may overlap with MS are also discussed, as well as possible therapeutic targets for the treatment of MS and other neurodegenerative conditions. MDPI 2019-05-11 /pmc/articles/PMC6627385/ /pubmed/31083577 http://dx.doi.org/10.3390/biology8020037 Text en © 2019 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
de Barcelos, Isabella Peixoto
Troxell, Regina M.
Graves, Jennifer S.
Mitochondrial Dysfunction and Multiple Sclerosis
title Mitochondrial Dysfunction and Multiple Sclerosis
title_full Mitochondrial Dysfunction and Multiple Sclerosis
title_fullStr Mitochondrial Dysfunction and Multiple Sclerosis
title_full_unstemmed Mitochondrial Dysfunction and Multiple Sclerosis
title_short Mitochondrial Dysfunction and Multiple Sclerosis
title_sort mitochondrial dysfunction and multiple sclerosis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6627385/
https://www.ncbi.nlm.nih.gov/pubmed/31083577
http://dx.doi.org/10.3390/biology8020037
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