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The role of microglial autophagy in Parkinson’s disease
Parkinson’s disease (PD) is the second most common neurodegenerative disease. Studies have shown that abnormal accumulation of α-synuclein (α-Syn) in the substantia nigra is a specific pathological characteristic of PD. Abnormal accumulation of α-Syn in PD induces the activation of microglia. Microg...
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/PMC9664157/ https://www.ncbi.nlm.nih.gov/pubmed/36389074 http://dx.doi.org/10.3389/fnagi.2022.1039780 |
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author | Zhu, Rui Luo, Yuyi Li, Shangang Wang, Zhengbo |
author_facet | Zhu, Rui Luo, Yuyi Li, Shangang Wang, Zhengbo |
author_sort | Zhu, Rui |
collection | PubMed |
description | Parkinson’s disease (PD) is the second most common neurodegenerative disease. Studies have shown that abnormal accumulation of α-synuclein (α-Syn) in the substantia nigra is a specific pathological characteristic of PD. Abnormal accumulation of α-Syn in PD induces the activation of microglia. Microglia, which are immune cells in the central nervous system, are involved in the function and regulation of inflammation in PD by autophagy. The role of microglial autophagy in the pathophysiology of PD has become a hot-pot issue. This review outlines the pathways of microglial autophagy, and explores the key factor of microglial autophagy in the mechanism of PD and the possibility of microglial autophagy as a potential therapeutic target for PD. |
format | Online Article Text |
id | pubmed-9664157 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-96641572022-11-15 The role of microglial autophagy in Parkinson’s disease Zhu, Rui Luo, Yuyi Li, Shangang Wang, Zhengbo Front Aging Neurosci Aging Neuroscience Parkinson’s disease (PD) is the second most common neurodegenerative disease. Studies have shown that abnormal accumulation of α-synuclein (α-Syn) in the substantia nigra is a specific pathological characteristic of PD. Abnormal accumulation of α-Syn in PD induces the activation of microglia. Microglia, which are immune cells in the central nervous system, are involved in the function and regulation of inflammation in PD by autophagy. The role of microglial autophagy in the pathophysiology of PD has become a hot-pot issue. This review outlines the pathways of microglial autophagy, and explores the key factor of microglial autophagy in the mechanism of PD and the possibility of microglial autophagy as a potential therapeutic target for PD. Frontiers Media S.A. 2022-11-01 /pmc/articles/PMC9664157/ /pubmed/36389074 http://dx.doi.org/10.3389/fnagi.2022.1039780 Text en Copyright © 2022 Zhu, Luo, Li and Wang. 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 Zhu, Rui Luo, Yuyi Li, Shangang Wang, Zhengbo The role of microglial autophagy in Parkinson’s disease |
title | The role of microglial autophagy in Parkinson’s disease |
title_full | The role of microglial autophagy in Parkinson’s disease |
title_fullStr | The role of microglial autophagy in Parkinson’s disease |
title_full_unstemmed | The role of microglial autophagy in Parkinson’s disease |
title_short | The role of microglial autophagy in Parkinson’s disease |
title_sort | role of microglial autophagy in parkinson’s disease |
topic | Aging Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9664157/ https://www.ncbi.nlm.nih.gov/pubmed/36389074 http://dx.doi.org/10.3389/fnagi.2022.1039780 |
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