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The effects and potential of microglial polarization and crosstalk with other cells of the central nervous system in the treatment of Alzheimer’s disease
Microglia are resident immune cells in the central nervous system. During the pathogenesis of Alzheimer’s disease, stimulatory factors continuously act on the microglia causing abnormal activation and unbalanced phenotypic changes; these events have become a significant and promising area of researc...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Wolters Kluwer - Medknow
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9827789/ https://www.ncbi.nlm.nih.gov/pubmed/36254973 http://dx.doi.org/10.4103/1673-5374.355747 |
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author | Wu, Yi-Ge Song, Li-Juan Yin, Li-Jun Yin, Jun-Jun Wang, Qing Yu, Jie-Zhong Xiao, Bao-Guo Ma, Cun-Gen |
author_facet | Wu, Yi-Ge Song, Li-Juan Yin, Li-Jun Yin, Jun-Jun Wang, Qing Yu, Jie-Zhong Xiao, Bao-Guo Ma, Cun-Gen |
author_sort | Wu, Yi-Ge |
collection | PubMed |
description | Microglia are resident immune cells in the central nervous system. During the pathogenesis of Alzheimer’s disease, stimulatory factors continuously act on the microglia causing abnormal activation and unbalanced phenotypic changes; these events have become a significant and promising area of research. In this review, we summarize the effects of microglial polarization and crosstalk with other cells in the central nervous system in the treatment of Alzheimer’s disease. Our literature search found that phenotypic changes occur continuously in Alzheimer’s disease and that microglia exhibit extensive crosstalk with astrocytes, oligodendrocytes, neurons, and penetrated peripheral innate immune cells via specific signaling pathways and cytokines. Collectively, unlike previous efforts to modulate microglial phenotypes at a single level, targeting the phenotypes of microglia and the crosstalk with other cells in the central nervous system may be more effective in reducing inflammation in the central nervous system in Alzheimer’s disease. This would establish a theoretical basis for reducing neuronal death from central nervous system inflammation and provide an appropriate environment to promote neuronal regeneration in the treatment of Alzheimer’s disease. |
format | Online Article Text |
id | pubmed-9827789 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Wolters Kluwer - Medknow |
record_format | MEDLINE/PubMed |
spelling | pubmed-98277892023-01-10 The effects and potential of microglial polarization and crosstalk with other cells of the central nervous system in the treatment of Alzheimer’s disease Wu, Yi-Ge Song, Li-Juan Yin, Li-Jun Yin, Jun-Jun Wang, Qing Yu, Jie-Zhong Xiao, Bao-Guo Ma, Cun-Gen Neural Regen Res Review Microglia are resident immune cells in the central nervous system. During the pathogenesis of Alzheimer’s disease, stimulatory factors continuously act on the microglia causing abnormal activation and unbalanced phenotypic changes; these events have become a significant and promising area of research. In this review, we summarize the effects of microglial polarization and crosstalk with other cells in the central nervous system in the treatment of Alzheimer’s disease. Our literature search found that phenotypic changes occur continuously in Alzheimer’s disease and that microglia exhibit extensive crosstalk with astrocytes, oligodendrocytes, neurons, and penetrated peripheral innate immune cells via specific signaling pathways and cytokines. Collectively, unlike previous efforts to modulate microglial phenotypes at a single level, targeting the phenotypes of microglia and the crosstalk with other cells in the central nervous system may be more effective in reducing inflammation in the central nervous system in Alzheimer’s disease. This would establish a theoretical basis for reducing neuronal death from central nervous system inflammation and provide an appropriate environment to promote neuronal regeneration in the treatment of Alzheimer’s disease. Wolters Kluwer - Medknow 2022-10-10 /pmc/articles/PMC9827789/ /pubmed/36254973 http://dx.doi.org/10.4103/1673-5374.355747 Text en Copyright: © Neural Regeneration Research https://creativecommons.org/licenses/by-nc-sa/4.0/This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms. |
spellingShingle | Review Wu, Yi-Ge Song, Li-Juan Yin, Li-Jun Yin, Jun-Jun Wang, Qing Yu, Jie-Zhong Xiao, Bao-Guo Ma, Cun-Gen The effects and potential of microglial polarization and crosstalk with other cells of the central nervous system in the treatment of Alzheimer’s disease |
title | The effects and potential of microglial polarization and crosstalk with other cells of the central nervous system in the treatment of Alzheimer’s disease |
title_full | The effects and potential of microglial polarization and crosstalk with other cells of the central nervous system in the treatment of Alzheimer’s disease |
title_fullStr | The effects and potential of microglial polarization and crosstalk with other cells of the central nervous system in the treatment of Alzheimer’s disease |
title_full_unstemmed | The effects and potential of microglial polarization and crosstalk with other cells of the central nervous system in the treatment of Alzheimer’s disease |
title_short | The effects and potential of microglial polarization and crosstalk with other cells of the central nervous system in the treatment of Alzheimer’s disease |
title_sort | effects and potential of microglial polarization and crosstalk with other cells of the central nervous system in the treatment of alzheimer’s disease |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9827789/ https://www.ncbi.nlm.nih.gov/pubmed/36254973 http://dx.doi.org/10.4103/1673-5374.355747 |
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