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Exercise suppresses neuroinflammation for alleviating Alzheimer’s disease
Alzheimer’s disease (AD) is a chronic neurodegenerative disease, with the characteristics of neurofibrillary tangle (NFT) and senile plaque (SP) formation. Although great progresses have been made in clinical trials based on relevant hypotheses, these studies are also accompanied by the emergence of...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10026496/ https://www.ncbi.nlm.nih.gov/pubmed/36935511 http://dx.doi.org/10.1186/s12974-023-02753-6 |
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author | Wang, Minghui Zhang, Hu Liang, Jiling Huang, Jielun Chen, Ning |
author_facet | Wang, Minghui Zhang, Hu Liang, Jiling Huang, Jielun Chen, Ning |
author_sort | Wang, Minghui |
collection | PubMed |
description | Alzheimer’s disease (AD) is a chronic neurodegenerative disease, with the characteristics of neurofibrillary tangle (NFT) and senile plaque (SP) formation. Although great progresses have been made in clinical trials based on relevant hypotheses, these studies are also accompanied by the emergence of toxic and side effects, and it is an urgent task to explore the underlying mechanisms for the benefits to prevent and treat AD. Herein, based on animal experiments and a few clinical trials, neuroinflammation in AD is characterized by long-term activation of pro-inflammatory microglia and the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasomes. Damaged signals from the periphery and within the brain continuously activate microglia, thus resulting in a constant source of inflammatory responses. The long-term chronic inflammatory response also exacerbates endoplasmic reticulum oxidative stress in microglia, which triggers microglia-dependent immune responses, ultimately leading to the occurrence and deterioration of AD. In this review, we systematically summarized and sorted out that exercise ameliorates AD by directly and indirectly regulating immune response of the central nervous system and promoting hippocampal neurogenesis to provide a new direction for exploring the neuroinflammation activity in AD. |
format | Online Article Text |
id | pubmed-10026496 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-100264962023-03-21 Exercise suppresses neuroinflammation for alleviating Alzheimer’s disease Wang, Minghui Zhang, Hu Liang, Jiling Huang, Jielun Chen, Ning J Neuroinflammation Review Alzheimer’s disease (AD) is a chronic neurodegenerative disease, with the characteristics of neurofibrillary tangle (NFT) and senile plaque (SP) formation. Although great progresses have been made in clinical trials based on relevant hypotheses, these studies are also accompanied by the emergence of toxic and side effects, and it is an urgent task to explore the underlying mechanisms for the benefits to prevent and treat AD. Herein, based on animal experiments and a few clinical trials, neuroinflammation in AD is characterized by long-term activation of pro-inflammatory microglia and the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasomes. Damaged signals from the periphery and within the brain continuously activate microglia, thus resulting in a constant source of inflammatory responses. The long-term chronic inflammatory response also exacerbates endoplasmic reticulum oxidative stress in microglia, which triggers microglia-dependent immune responses, ultimately leading to the occurrence and deterioration of AD. In this review, we systematically summarized and sorted out that exercise ameliorates AD by directly and indirectly regulating immune response of the central nervous system and promoting hippocampal neurogenesis to provide a new direction for exploring the neuroinflammation activity in AD. BioMed Central 2023-03-19 /pmc/articles/PMC10026496/ /pubmed/36935511 http://dx.doi.org/10.1186/s12974-023-02753-6 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Review Wang, Minghui Zhang, Hu Liang, Jiling Huang, Jielun Chen, Ning Exercise suppresses neuroinflammation for alleviating Alzheimer’s disease |
title | Exercise suppresses neuroinflammation for alleviating Alzheimer’s disease |
title_full | Exercise suppresses neuroinflammation for alleviating Alzheimer’s disease |
title_fullStr | Exercise suppresses neuroinflammation for alleviating Alzheimer’s disease |
title_full_unstemmed | Exercise suppresses neuroinflammation for alleviating Alzheimer’s disease |
title_short | Exercise suppresses neuroinflammation for alleviating Alzheimer’s disease |
title_sort | exercise suppresses neuroinflammation for alleviating alzheimer’s disease |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10026496/ https://www.ncbi.nlm.nih.gov/pubmed/36935511 http://dx.doi.org/10.1186/s12974-023-02753-6 |
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