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Mitochondrial dysfunction in neurological disorders: Exploring mitochondrial transplantation
Mitochondria are fundamental for metabolic homeostasis in all multicellular eukaryotes. In the nervous system, mitochondria-generated adenosine triphosphate (ATP) is required to establish appropriate electrochemical gradients and reliable synaptic transmission. Notably, several mitochondrial defects...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7683736/ https://www.ncbi.nlm.nih.gov/pubmed/33298971 http://dx.doi.org/10.1038/s41536-020-00107-x |
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author | Norat, Pedro Soldozy, Sauson Sokolowski, Jennifer D. Gorick, Catherine M. Kumar, Jeyan S. Chae, Youngrok Yağmurlu, Kaan Prada, Francesco Walker, Melanie Levitt, Michael R. Price, Richard J. Tvrdik, Petr Kalani, M. Yashar S. |
author_facet | Norat, Pedro Soldozy, Sauson Sokolowski, Jennifer D. Gorick, Catherine M. Kumar, Jeyan S. Chae, Youngrok Yağmurlu, Kaan Prada, Francesco Walker, Melanie Levitt, Michael R. Price, Richard J. Tvrdik, Petr Kalani, M. Yashar S. |
author_sort | Norat, Pedro |
collection | PubMed |
description | Mitochondria are fundamental for metabolic homeostasis in all multicellular eukaryotes. In the nervous system, mitochondria-generated adenosine triphosphate (ATP) is required to establish appropriate electrochemical gradients and reliable synaptic transmission. Notably, several mitochondrial defects have been identified in central nervous system disorders. Membrane leakage and electrolyte imbalances, pro-apoptotic pathway activation, and mitophagy are among the mechanisms implicated in the pathogenesis of neurodegenerative diseases, such as Alzheimer’s, Parkinson’s, and Huntington’s disease, as well as ischemic stroke. In this review, we summarize mitochondrial pathways that contribute to disease progression. Further, we discuss pathological states that damaged mitochondria impose on normal nervous system processes and explore new therapeutic approaches to mitochondrial diseases. |
format | Online Article Text |
id | pubmed-7683736 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-76837362020-12-03 Mitochondrial dysfunction in neurological disorders: Exploring mitochondrial transplantation Norat, Pedro Soldozy, Sauson Sokolowski, Jennifer D. Gorick, Catherine M. Kumar, Jeyan S. Chae, Youngrok Yağmurlu, Kaan Prada, Francesco Walker, Melanie Levitt, Michael R. Price, Richard J. Tvrdik, Petr Kalani, M. Yashar S. NPJ Regen Med Review Article Mitochondria are fundamental for metabolic homeostasis in all multicellular eukaryotes. In the nervous system, mitochondria-generated adenosine triphosphate (ATP) is required to establish appropriate electrochemical gradients and reliable synaptic transmission. Notably, several mitochondrial defects have been identified in central nervous system disorders. Membrane leakage and electrolyte imbalances, pro-apoptotic pathway activation, and mitophagy are among the mechanisms implicated in the pathogenesis of neurodegenerative diseases, such as Alzheimer’s, Parkinson’s, and Huntington’s disease, as well as ischemic stroke. In this review, we summarize mitochondrial pathways that contribute to disease progression. Further, we discuss pathological states that damaged mitochondria impose on normal nervous system processes and explore new therapeutic approaches to mitochondrial diseases. Nature Publishing Group UK 2020-11-23 /pmc/articles/PMC7683736/ /pubmed/33298971 http://dx.doi.org/10.1038/s41536-020-00107-x Text en © The Author(s) 2020, corrected publication 2021 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Review Article Norat, Pedro Soldozy, Sauson Sokolowski, Jennifer D. Gorick, Catherine M. Kumar, Jeyan S. Chae, Youngrok Yağmurlu, Kaan Prada, Francesco Walker, Melanie Levitt, Michael R. Price, Richard J. Tvrdik, Petr Kalani, M. Yashar S. Mitochondrial dysfunction in neurological disorders: Exploring mitochondrial transplantation |
title | Mitochondrial dysfunction in neurological disorders: Exploring mitochondrial transplantation |
title_full | Mitochondrial dysfunction in neurological disorders: Exploring mitochondrial transplantation |
title_fullStr | Mitochondrial dysfunction in neurological disorders: Exploring mitochondrial transplantation |
title_full_unstemmed | Mitochondrial dysfunction in neurological disorders: Exploring mitochondrial transplantation |
title_short | Mitochondrial dysfunction in neurological disorders: Exploring mitochondrial transplantation |
title_sort | mitochondrial dysfunction in neurological disorders: exploring mitochondrial transplantation |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7683736/ https://www.ncbi.nlm.nih.gov/pubmed/33298971 http://dx.doi.org/10.1038/s41536-020-00107-x |
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