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少突胶质细胞在阿尔茨海默病中是罪魁祸首还是受害者?

Are Oligodendrocytes the Culprits or Victims in Alzheimer's Disease.

作者信息

Rapaka D, Saniotis A, Henneberg M, Bitra V R

机构信息

Veera R Bitra, School of Pharmacy, Faculty of Health Sciences, University of Botswana, Gaborone, Botswana. Email:

出版信息

Physiol Res. 2025 Apr 30;74(2):219-231.

PMID:40432437
Abstract

Oligodendrocytes are vital for the functioning of the nervous system. Oligodendrocyte-created myelin sheaths work as dynamic partners which play a substantial role in the myelination of axons. In addition to its well-known functions of providing insulation and enhancing conduction velocity, myelination controls axons' maturity, longevity, and regenerative ability via trophic support and signalling molecules. Myelination also regulates ion concentration and offers neuroprotection. Myelin is generated via complex procedures including cell differentiation, specialised lipids, and protein synthesis. Understanding the physiology of myelin sheath formation is required to understand various neurological disorders associated with myelin sheath damage. This review focuses on our growing understanding of the intricate actions and changes in oligodendrocytes during the course of evolution and in Alzheimer's disease.

摘要

少突胶质细胞对神经系统的功能至关重要。少突胶质细胞产生的髓鞘作为动态伙伴,在轴突髓鞘形成中发挥着重要作用。除了其众所周知的提供绝缘和提高传导速度的功能外,髓鞘形成还通过营养支持和信号分子控制轴突的成熟、寿命和再生能力。髓鞘形成还调节离子浓度并提供神经保护。髓鞘是通过包括细胞分化、特殊脂质和蛋白质合成在内的复杂过程产生的。了解髓鞘形成的生理学对于理解与髓鞘损伤相关的各种神经系统疾病是必要的。本综述重点关注我们对少突胶质细胞在进化过程和阿尔茨海默病过程中复杂作用和变化的日益深入的理解。

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本文引用的文献

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Tau trajectory in Alzheimer's disease: Evidence from the connectome-based computational models.阿尔茨海默病中的tau蛋白轨迹:基于连接组的计算模型的证据
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Alzheimer's Disease and Its Possible Evolutionary Origin: Hypothesis.阿尔茨海默病及其可能的进化起源:假说。
Cells. 2023 Jun 13;12(12):1618. doi: 10.3390/cells12121618.
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Myelin dysfunction drives amyloid-β deposition in models of Alzheimer's disease.髓鞘功能障碍导致阿尔茨海默病模型中的淀粉样β沉积。
Nature. 2023 Jun;618(7964):349-357. doi: 10.1038/s41586-023-06120-6. Epub 2023 May 31.
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Myelin in Alzheimer's disease: culprit or bystander?阿尔茨海默病中的髓鞘:罪魁祸首还是旁观者?
Acta Neuropathol Commun. 2023 Mar 31;11(1):56. doi: 10.1186/s40478-023-01554-5.
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Early microglial response, myelin deterioration and lethality in mice deficient for very long chain ceramide synthesis in oligodendrocytes.少突胶质细胞中非常长链神经酰胺合成缺陷小鼠的早期小胶质细胞反应、髓鞘恶化和致死性。
Glia. 2023 Apr;71(4):1120-1141. doi: 10.1002/glia.24329. Epub 2022 Dec 30.
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The Structure and Function of Glial Networks: Beyond the Neuronal Connections.胶质细胞网络的结构与功能:超越神经元连接。
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Cells. 2022 Oct 29;11(21):3421. doi: 10.3390/cells11213421.
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Decreased Oligodendrocyte Number in Hippocampal Subfield CA4 in Schizophrenia: A Replication Study.精神分裂症中海马亚区 CA4 少突胶质细胞数量减少:一项复制研究。
Cells. 2022 Oct 15;11(20):3242. doi: 10.3390/cells11203242.
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Aging compromises oligodendrocyte precursor cell maturation and efficient remyelination in the monkey brain.衰老会影响猴子大脑中少突胶质前体细胞的成熟和有效的髓鞘再生。
Geroscience. 2023 Feb;45(1):249-264. doi: 10.1007/s11357-022-00621-4. Epub 2022 Aug 5.
10
Development of myelinating glia: An overview.成髓鞘胶质细胞的发育:概述。
Glia. 2022 Dec;70(12):2237-2259. doi: 10.1002/glia.24238. Epub 2022 Jul 4.