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Analysis of shared underlying mechanism in neurodegenerative disease
In this review, the relationship between bioenergetics, mitochondrial dysfunction, and inflammation will be and how they contribute to neurodegeneration, specifically in Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS) will be reviewed. Long-term changes in...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9745190/ https://www.ncbi.nlm.nih.gov/pubmed/36523957 http://dx.doi.org/10.3389/fnagi.2022.1006089 |
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author | Butler, Rickeem Bradford, David Rodgers, Kathleen E. |
author_facet | Butler, Rickeem Bradford, David Rodgers, Kathleen E. |
author_sort | Butler, Rickeem |
collection | PubMed |
description | In this review, the relationship between bioenergetics, mitochondrial dysfunction, and inflammation will be and how they contribute to neurodegeneration, specifically in Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS) will be reviewed. Long-term changes in mitochondrial function, autophagy dysfunction, and immune activation are commonalities shared across these age-related disorders. Genetic risk factors for these diseases support an autophagy-immune connection in the underlying pathophysiology. Critical areas of deeper evaluation in these bioenergetic processes may lead to potential therapeutics with efficacy across multiple neurodegenerative diseases. |
format | Online Article Text |
id | pubmed-9745190 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-97451902022-12-14 Analysis of shared underlying mechanism in neurodegenerative disease Butler, Rickeem Bradford, David Rodgers, Kathleen E. Front Aging Neurosci Aging Neuroscience In this review, the relationship between bioenergetics, mitochondrial dysfunction, and inflammation will be and how they contribute to neurodegeneration, specifically in Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS) will be reviewed. Long-term changes in mitochondrial function, autophagy dysfunction, and immune activation are commonalities shared across these age-related disorders. Genetic risk factors for these diseases support an autophagy-immune connection in the underlying pathophysiology. Critical areas of deeper evaluation in these bioenergetic processes may lead to potential therapeutics with efficacy across multiple neurodegenerative diseases. Frontiers Media S.A. 2022-11-29 /pmc/articles/PMC9745190/ /pubmed/36523957 http://dx.doi.org/10.3389/fnagi.2022.1006089 Text en Copyright © 2022 Butler, Bradford and Rodgers. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Aging Neuroscience Butler, Rickeem Bradford, David Rodgers, Kathleen E. Analysis of shared underlying mechanism in neurodegenerative disease |
title | Analysis of shared underlying mechanism in neurodegenerative disease |
title_full | Analysis of shared underlying mechanism in neurodegenerative disease |
title_fullStr | Analysis of shared underlying mechanism in neurodegenerative disease |
title_full_unstemmed | Analysis of shared underlying mechanism in neurodegenerative disease |
title_short | Analysis of shared underlying mechanism in neurodegenerative disease |
title_sort | analysis of shared underlying mechanism in neurodegenerative disease |
topic | Aging Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9745190/ https://www.ncbi.nlm.nih.gov/pubmed/36523957 http://dx.doi.org/10.3389/fnagi.2022.1006089 |
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