少突胶质细胞是阿尔茨海默病的罪魁祸首还是受害者?

IF 1.9 4区 医学 Q3 PHYSIOLOGY
Physiological research Pub Date : 2025-04-30
D Rapaka, A Saniotis, M Henneberg, V R Bitra
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引用次数: 0

摘要

少突胶质细胞对神经系统的功能至关重要。少突细胞产生的髓鞘作为动态伙伴在轴突的髓鞘形成中起着重要作用。除了提供绝缘和提高传导速度的众所周知的功能外,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。髓鞘形成还能调节离子浓度并提供神经保护。髓磷脂是通过复杂的过程产生的,包括细胞分化、特化脂质和蛋白质合成。了解髓鞘形成的生理学是理解与髓鞘损伤相关的各种神经系统疾病的必要条件。本文综述了我们对少突胶质细胞在进化过程和阿尔茨海默病中的复杂作用和变化的日益了解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Are Oligodendrocytes the Culprits or Victims in Alzheimer's Disease.

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.

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来源期刊
Physiological research
Physiological research 医学-生理学
CiteScore
4.00
自引率
4.80%
发文量
108
审稿时长
3 months
期刊介绍: Physiological Research is a peer reviewed Open Access journal that publishes articles on normal and pathological physiology, biochemistry, biophysics, and pharmacology. Authors can submit original, previously unpublished research articles, review articles, rapid or short communications. Instructions for Authors - Respect the instructions carefully when submitting your manuscript. Submitted manuscripts or revised manuscripts that do not follow these Instructions will not be included into the peer-review process. The articles are available in full versions as pdf files beginning with volume 40, 1991. The journal publishes the online Ahead of Print /Pre-Press version of the articles that are searchable in Medline and can be cited.
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