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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.

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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