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The Role of Mitochondrial Dysfunction in the Progression of Alzheimer’s Disease
The current molecular understanding of Alzheimer’s disease (AD) has still not re-sulted in successful interventions. Mitochondrial dysfunction of the AD brain is currently emerging as a hallmark of this disease. One mitochondrial function often affected in AD is oxidative phosphorylation responsible...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Bentham Science Publishers
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6446443/ https://www.ncbi.nlm.nih.gov/pubmed/28618998 http://dx.doi.org/10.2174/0929867324666170616110111 |
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author | Desler, Claus Lillenes, Meryl S. Tønjum, Tone Rasmussen, Lene Juel |
author_facet | Desler, Claus Lillenes, Meryl S. Tønjum, Tone Rasmussen, Lene Juel |
author_sort | Desler, Claus |
collection | PubMed |
description | The current molecular understanding of Alzheimer’s disease (AD) has still not re-sulted in successful interventions. Mitochondrial dysfunction of the AD brain is currently emerging as a hallmark of this disease. One mitochondrial function often affected in AD is oxidative phosphorylation responsible for ATP production, but also for production of reactive oxygen species (ROS) and for the de novo synthesis of pyrimidines. This paper reviews the role of mitochondrial produced ROS and pyrimidines in the aetiology of AD and their pro-posed role in oxidative degeneration of macromolecules, synthesis of essential phospholipids and maintenance of mitochondrial viability in the AD brain. |
format | Online Article Text |
id | pubmed-6446443 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Bentham Science Publishers |
record_format | MEDLINE/PubMed |
spelling | pubmed-64464432019-04-23 The Role of Mitochondrial Dysfunction in the Progression of Alzheimer’s Disease Desler, Claus Lillenes, Meryl S. Tønjum, Tone Rasmussen, Lene Juel Curr Med Chem Article The current molecular understanding of Alzheimer’s disease (AD) has still not re-sulted in successful interventions. Mitochondrial dysfunction of the AD brain is currently emerging as a hallmark of this disease. One mitochondrial function often affected in AD is oxidative phosphorylation responsible for ATP production, but also for production of reactive oxygen species (ROS) and for the de novo synthesis of pyrimidines. This paper reviews the role of mitochondrial produced ROS and pyrimidines in the aetiology of AD and their pro-posed role in oxidative degeneration of macromolecules, synthesis of essential phospholipids and maintenance of mitochondrial viability in the AD brain. Bentham Science Publishers 2018-12 2018-12 /pmc/articles/PMC6446443/ /pubmed/28618998 http://dx.doi.org/10.2174/0929867324666170616110111 Text en © 2018 Bentham Science Publishers https://creativecommons.org/licenses/by-nc/4.0/legalcode This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) (https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited. |
spellingShingle | Article Desler, Claus Lillenes, Meryl S. Tønjum, Tone Rasmussen, Lene Juel The Role of Mitochondrial Dysfunction in the Progression of Alzheimer’s Disease |
title | The Role of Mitochondrial Dysfunction in the Progression of Alzheimer’s Disease |
title_full | The Role of Mitochondrial Dysfunction in the Progression of Alzheimer’s Disease |
title_fullStr | The Role of Mitochondrial Dysfunction in the Progression of Alzheimer’s Disease |
title_full_unstemmed | The Role of Mitochondrial Dysfunction in the Progression of Alzheimer’s Disease |
title_short | The Role of Mitochondrial Dysfunction in the Progression of Alzheimer’s Disease |
title_sort | role of mitochondrial dysfunction in the progression of alzheimer’s disease |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6446443/ https://www.ncbi.nlm.nih.gov/pubmed/28618998 http://dx.doi.org/10.2174/0929867324666170616110111 |
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