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Role of neuroinflammation in neurodegeneration development

Studies in neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease and Amyotrophic lateral sclerosis, Huntington’s disease, and so on, have suggested that inflammation is not only a result of neurodegeneration but also a crucial player in this process. Protein aggregates which...

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Autores principales: Zhang, Weifeng, Xiao, Dan, Mao, Qinwen, Xia, Haibin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10336149/
https://www.ncbi.nlm.nih.gov/pubmed/37433768
http://dx.doi.org/10.1038/s41392-023-01486-5
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author Zhang, Weifeng
Xiao, Dan
Mao, Qinwen
Xia, Haibin
author_facet Zhang, Weifeng
Xiao, Dan
Mao, Qinwen
Xia, Haibin
author_sort Zhang, Weifeng
collection PubMed
description Studies in neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease and Amyotrophic lateral sclerosis, Huntington’s disease, and so on, have suggested that inflammation is not only a result of neurodegeneration but also a crucial player in this process. Protein aggregates which are very common pathological phenomenon in neurodegeneration can induce neuroinflammation which further aggravates protein aggregation and neurodegeneration. Actually, inflammation even happens earlier than protein aggregation. Neuroinflammation induced by genetic variations in CNS cells or by peripheral immune cells may induce protein deposition in some susceptible population. Numerous signaling pathways and a range of CNS cells have been suggested to be involved in the pathogenesis of neurodegeneration, although they are still far from being completely understood. Due to the limited success of traditional treatment methods, blocking or enhancing inflammatory signaling pathways involved in neurodegeneration are considered to be promising strategies for the therapy of neurodegenerative diseases, and many of them have got exciting results in animal models or clinical trials. Some of them, although very few, have been approved by FDA for clinical usage. Here we comprehensively review the factors affecting neuroinflammation and the major inflammatory signaling pathways involved in the pathogenicity of neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and Amyotrophic lateral sclerosis. We also summarize the current strategies, both in animal models and in the clinic, for the treatment of neurodegenerative diseases.
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spelling pubmed-103361492023-07-13 Role of neuroinflammation in neurodegeneration development Zhang, Weifeng Xiao, Dan Mao, Qinwen Xia, Haibin Signal Transduct Target Ther Review Article Studies in neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease and Amyotrophic lateral sclerosis, Huntington’s disease, and so on, have suggested that inflammation is not only a result of neurodegeneration but also a crucial player in this process. Protein aggregates which are very common pathological phenomenon in neurodegeneration can induce neuroinflammation which further aggravates protein aggregation and neurodegeneration. Actually, inflammation even happens earlier than protein aggregation. Neuroinflammation induced by genetic variations in CNS cells or by peripheral immune cells may induce protein deposition in some susceptible population. Numerous signaling pathways and a range of CNS cells have been suggested to be involved in the pathogenesis of neurodegeneration, although they are still far from being completely understood. Due to the limited success of traditional treatment methods, blocking or enhancing inflammatory signaling pathways involved in neurodegeneration are considered to be promising strategies for the therapy of neurodegenerative diseases, and many of them have got exciting results in animal models or clinical trials. Some of them, although very few, have been approved by FDA for clinical usage. Here we comprehensively review the factors affecting neuroinflammation and the major inflammatory signaling pathways involved in the pathogenicity of neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and Amyotrophic lateral sclerosis. We also summarize the current strategies, both in animal models and in the clinic, for the treatment of neurodegenerative diseases. Nature Publishing Group UK 2023-07-12 /pmc/articles/PMC10336149/ /pubmed/37433768 http://dx.doi.org/10.1038/s41392-023-01486-5 Text en © The Author(s) 2023 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
Zhang, Weifeng
Xiao, Dan
Mao, Qinwen
Xia, Haibin
Role of neuroinflammation in neurodegeneration development
title Role of neuroinflammation in neurodegeneration development
title_full Role of neuroinflammation in neurodegeneration development
title_fullStr Role of neuroinflammation in neurodegeneration development
title_full_unstemmed Role of neuroinflammation in neurodegeneration development
title_short Role of neuroinflammation in neurodegeneration development
title_sort role of neuroinflammation in neurodegeneration development
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10336149/
https://www.ncbi.nlm.nih.gov/pubmed/37433768
http://dx.doi.org/10.1038/s41392-023-01486-5
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