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衰老大脑中的少突胶质细胞。

Oligodendrocytes in the aging brain.

作者信息

Sams Eleanor Catherine

机构信息

Blizard Institute, Barts and The London School of Medicine and Dentistry Centre for Neuroscience, Surgery and Trauma, Blizard Institute, 4 Newark Street, Whitechapel E1 2AT, London.

出版信息

Neuronal Signal. 2021 Jul 6;5(3):NS20210008. doi: 10.1042/NS20210008. eCollection 2021 Sep.

DOI:10.1042/NS20210008
PMID:34290887
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8264650/
Abstract

More than half of the human brain volume is made up of white matter: regions where axons are coated in myelin, which primarily functions to increase the conduction speed of axon potentials. White matter volume significantly decreases with age, correlating with cognitive decline. Much research in the field of non-pathological brain aging mechanisms has taken a neuron-centric approach, with relatively little attention paid to other neural cells. This review discusses white matter changes, with focus on oligodendrocyte lineage cells and their ability to produce and maintain myelin to support normal brain homoeostasis. Improved understanding of intrinsic cellular changes, general senescence mechanisms, intercellular interactions and alterations in extracellular environment which occur with aging and impact oligodendrocyte cells is paramount. This may lead to strategies to support oligodendrocytes in aging, for example by supporting myelin synthesis, protecting against oxidative stress and promoting the rejuvenation of the intrinsic regenerative potential of progenitor cells. Ultimately, this will enable the protection of white matter integrity thus protecting cognitive function into the later years of life.

摘要

超过一半的人类脑容量由白质组成

轴突被髓鞘包裹的区域,其主要功能是提高轴突电位的传导速度。白质体积会随着年龄的增长而显著减少,这与认知能力下降相关。在非病理性脑衰老机制领域的许多研究都采用了以神经元为中心的方法,而对其他神经细胞的关注相对较少。本综述讨论了白质变化,重点关注少突胶质细胞谱系细胞及其产生和维持髓鞘以支持正常脑稳态的能力。深入了解随着衰老而发生并影响少突胶质细胞的内在细胞变化、一般衰老机制、细胞间相互作用和细胞外环境改变至关重要。这可能会带来支持衰老过程中少突胶质细胞的策略,例如通过支持髓鞘合成、抵御氧化应激以及促进祖细胞内在再生潜能的恢复。最终,这将能够保护白质完整性,从而在生命后期保护认知功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/934d/8264650/8e6616034fcb/ns-05-ns20210008-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/934d/8264650/218138de8af0/ns-05-ns20210008-g1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/934d/8264650/886cdef1fafb/ns-05-ns20210008-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/934d/8264650/f5a8be576722/ns-05-ns20210008-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/934d/8264650/8e6616034fcb/ns-05-ns20210008-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/934d/8264650/218138de8af0/ns-05-ns20210008-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/934d/8264650/f74f312e4057/ns-05-ns20210008-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/934d/8264650/886cdef1fafb/ns-05-ns20210008-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/934d/8264650/f5a8be576722/ns-05-ns20210008-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/934d/8264650/8e6616034fcb/ns-05-ns20210008-g5.jpg

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