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The role of cofilin in age-related neuroinflammation

Aging brain becomes susceptible to neurodegenerative diseases due to the shifting of microglia and astrocyte phenotypes to an active “pro-inflammatory” state, causing chronic low-grade neuroinflammation. Despite the fact that the role of neuroinflammation during aging has been extensively studied in...

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Detalles Bibliográficos
Autores principales: Alsegiani, Amsha S., Shah, Zahoor A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer - Medknow 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059588/
https://www.ncbi.nlm.nih.gov/pubmed/31997804
http://dx.doi.org/10.4103/1673-5374.274330
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author Alsegiani, Amsha S.
Shah, Zahoor A.
author_facet Alsegiani, Amsha S.
Shah, Zahoor A.
author_sort Alsegiani, Amsha S.
collection PubMed
description Aging brain becomes susceptible to neurodegenerative diseases due to the shifting of microglia and astrocyte phenotypes to an active “pro-inflammatory” state, causing chronic low-grade neuroinflammation. Despite the fact that the role of neuroinflammation during aging has been extensively studied in recent years, the underlying causes remain unclear. The identification of relevant proteins and understanding their potential roles in neuroinflammation can help explain their potential of becoming biomarkers in the aging brain and as drug targets for prevention and treatment. This will eventually reduce the chances of developing neurodegenerative diseases and promote healthier lives in the elderly. In this review, we have summarized the morphological and cellular changes in the aging brain, the effects of age-related neuroinflammation, and the potential role of cofilin-1 during neuroinflammation. We also discuss other factors contributing to brain aging and neuroinflammation.
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spelling pubmed-70595882020-03-16 The role of cofilin in age-related neuroinflammation Alsegiani, Amsha S. Shah, Zahoor A. Neural Regen Res Review Aging brain becomes susceptible to neurodegenerative diseases due to the shifting of microglia and astrocyte phenotypes to an active “pro-inflammatory” state, causing chronic low-grade neuroinflammation. Despite the fact that the role of neuroinflammation during aging has been extensively studied in recent years, the underlying causes remain unclear. The identification of relevant proteins and understanding their potential roles in neuroinflammation can help explain their potential of becoming biomarkers in the aging brain and as drug targets for prevention and treatment. This will eventually reduce the chances of developing neurodegenerative diseases and promote healthier lives in the elderly. In this review, we have summarized the morphological and cellular changes in the aging brain, the effects of age-related neuroinflammation, and the potential role of cofilin-1 during neuroinflammation. We also discuss other factors contributing to brain aging and neuroinflammation. Wolters Kluwer - Medknow 2020-01-28 /pmc/articles/PMC7059588/ /pubmed/31997804 http://dx.doi.org/10.4103/1673-5374.274330 Text en Copyright: © Neural Regeneration Research http://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
Alsegiani, Amsha S.
Shah, Zahoor A.
The role of cofilin in age-related neuroinflammation
title The role of cofilin in age-related neuroinflammation
title_full The role of cofilin in age-related neuroinflammation
title_fullStr The role of cofilin in age-related neuroinflammation
title_full_unstemmed The role of cofilin in age-related neuroinflammation
title_short The role of cofilin in age-related neuroinflammation
title_sort role of cofilin in age-related neuroinflammation
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059588/
https://www.ncbi.nlm.nih.gov/pubmed/31997804
http://dx.doi.org/10.4103/1673-5374.274330
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