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乡村医学 ›› 2025, Vol.2 ›› Issue (3) DOI: 10.12238/jrm.v2i3.13442

• 指南解读 • 上一篇     下一篇

神经元与神经胶质细胞相互作用在阿尔茨海默病中的研究进展

俞雅萌 , 严佳乐 , 王杉 ()   
  1. 1 . 西安医学院基础与转化医学研究所
  2. 2 . 西安医学院基础与转化医学研究所
  3. 3 . 西安医学院基础与转化医学研究所
  • 收稿日期:2025-03-01 03:42:44 发布日期:2025-06-06
  • 通讯作者: 王杉

  • 作者贡献:
  • 基金资助:
    陕西省科技计划项目(2022JQ-814)。

Research Progress on the Interaction between Neurons and Glial Cells in Alzheimer’s Disease

YU Yameng YAN Jiale WANG Shan ()   
  1. Institute of Basic and Translational Medicine, Xi’an Medical University
  2. Institute of Basic and Translational Medicine, Xi’an Medical University
  3. Institute of Basic and Translational Medicine, Xi’an Medical University
  • Received:2025-03-01 03:42:44 Online:2025-06-06
  • Contact: WANG Shan

摘要: 阿尔茨海默病(Alzheimer’s Disease, AD)是一种中枢神经系统退行性疾病,以进行性认知功能衰退和行为障碍为主要特征。其发病机制错综复杂,至今尚未完全阐明。传统观点主要将神经元病变视为 AD 病理过程的关键角色。然而,近年来日益增多的研究证据表明,AD 的病理机制并非单一神经元病变所能解释,而更可能是多种神经细胞类型协同作用的结果。本综述将重点探讨 AD 中小胶质细胞、星形胶质细胞、少突胶质细胞与神经元之间的相互作用机制,通过深入剖析神经元与神经胶质细胞之间的调控网络,旨在为揭示 AD 的发病机制提供更为全面的线索和视角。

关键词: 阿尔茨海默病;小胶质细胞;星形胶质细胞;少突胶质细胞;神经元;协同作用

Abstract

Alzheimer’s Disease (AD) is a neurodegenerative disorder of the central nervous system, primarily characterized by progressive cognitive decline and behavioral disturbances/disorders. The pathogenesis of AD remains complex and incompletely elucidated. The traditional view mainly regards neurons as the key players in the pathological process of AD. However, in recent years, increasing evidence has shown that the pathological mechanism of AD can not be explained by a single neuronal lesion, but is more likely to be the result of the synergistic effect of multiple nerve cell types.This review will focus on the interaction between microglia, astrocytes, oligodendrocytes and neurons in AD, and provide more comprehensive clues and perspectives for revealing the pathogenesis of AD by in-depth analysis of the regulatory network between neurons and glial cells.

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Conclusion

Key words: Alzheimer’s disease; Microglia; Astrocytes; Oligodendrocytes; Neurons; Synergy

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