解剖学报 ›› 2024, Vol. 55 ›› Issue (4): 379-385.doi: 10.16098/j.issn.0529-1356.2024.04.001

• 脑科学进展综述 •    下一篇

髓鞘动态变化及其在阿尔茨海默病认知功能障碍中的作用

陈婧菲1* 肖岚2*   

  1. 1.陆军军医大学基础医学院组织胚胎学教研室,脑发育与认知重庆市重点实验室,重庆 400038;  2.陆军军医大学新桥医院神经外科,重庆 400037
  • 收稿日期:2024-03-04 修回日期:2024-04-22 出版日期:2024-08-06 发布日期:2024-08-06
  • 通讯作者: 陈婧菲 肖岚 E-mail:xiaolan35@qq.com
  • 基金资助:
    科技创新2030-脑科学与类脑研究重点项目;国家自然科学基金;全国博士后创新人才支持计划

Myelin dynamics and its role in cognitive dysfunction in Alzheimer’s disease

Chen Jing-fei 1*  XIAO Lan2*   

  1. 1.Department of Histology and Embryology, Brain and Intelligence Research Key Laboratory of Chongqing Education Commission, Army Medical University, Chongqing 400038, China; 2.Department of Neurosurgery,Xinqiao Hospital, Army Medical University, Chongqing 400037, China
  • Received:2024-03-04 Revised:2024-04-22 Online:2024-08-06 Published:2024-08-06
  • Contact: CHEN Jing-fei XIAO Lan E-mail:xiaolan35@qq.com

摘要:

少突胶质细胞是中枢神经系统 (CNS) 的髓鞘形成细胞。每个少突胶质细胞伸出的突起能够包裹轴突形成多个髓鞘,以保证动作电位沿着轴突高效、快速的传导。近年的研究显示,尽管成人大脑中大部分髓鞘处于稳定状态,但实际上髓鞘的变化相当活跃。一方面,少突胶质细胞前体细胞持续分化形成新的髓鞘;另一方面,小部分已形成的髓鞘随着时间的推移发生退化。髓鞘的动态变化被认为是成年大脑神经可塑性的一种方式,其目的是通过髓鞘的重塑,调节神经环路的功能以满足适应新环境或习得新技能的需要。在阿尔茨海默病 (AD) 大脑中,髓鞘的退化可导致新生髓鞘代偿性增加,但仍不足以弥补脱失的髓鞘,而促进新生髓鞘的形成可望成为改善 AD 相关认知功能障碍的新策略。

关键词: 少突胶质细胞, 髓鞘动态变化, 认知功能 

Abstract:

Oligodendrocytes are myelin-forming cells of the central nervous system (CNS). The processes extending from each oligodendrocyte are capable of wrapping axon to form multiple myelin sheaths to ensure efficient and rapid conduction of action potentials along the axon. Recent studies have shown that myelin changes are quite active although most of the myelin sheaths in the adult brain are in a stable state. On the one hand, oligodendrocyte precursor cells continue to differentiate to form new myelin sheaths; on the other hand, a small portion of the formed myelin sheaths degenerate over time. Dynamic changes in myelin sheaths are thought to be a form of neural plasticity in the adult brain, which aims to regulate the function of neural circuits for adapting of new environments or acquiring new skills. In the brains with Alzheimer's disease (AD), myelin degeneration can lead to a compensatory increase in myelin regeneration, but it is still insufficient to compensate for the loss of myelin, and the promotion of new myelin formation is expected to be a new strategy to improve AD-related cognitive dysfunction.

Key words:  Oligodendrocyte, Myelin dynamics, Cognitive function

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