中国神经再生研究(英文版) ›› 2024, Vol. 19 ›› Issue (12): 2573-2574.doi: 10.4103/NRR.NRR-D-23-01962

• 观点:退行性病与再生 • 上一篇    下一篇

神经发生中的微胶质细胞自噬:阿尔茨海默病的新参与者

  

  • 出版日期:2024-12-15 发布日期:2024-03-30

Microglial autophagy in neurogenesis: a new player in Alzheimer’s disease

Xin Tang, Aarti Nagayach, Chenran Wang*#br#   

  1. Department of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, USA
  • Online:2024-12-15 Published:2024-03-30
  • Contact: Chenran Wang, PhD, wang2cr@ucmail.uc.edu.
  • Supported by:
    The work was supported by NIHR01NS103981 and R01CA273586 to CW.

摘要: https://orcid.org/0000-0003-4181-2729 (Chenran Wang)

Abstract: While extensive studies have illuminated the impact of Alzheimer’s disease (AD) on neuronal survival, there is growing evidence that abnormal postnatal neurogenesis in early AD brains contributes to disease progression. Postnatal neurogenesis serves as a mechanism to replace dead or damaged neurons. New neurons generated from neural stem cells (NSCs) in the subgranular zone (SGZ) of the dentate gyrus integrate into the existing hippocampal circuit, which is essential for learning and memory and is one of the first regions affected in AD. Macroautophagy (referred to as autophagy) is a conserved self-degrading process for cytoplasm or organelles through the formation of autophagosomes and subsequent fusion with lysosomes. Autophagy is important to maintain protein homeostasis. Microglia are the brain-resident macrophages and their functions in the pathogenesis of AD are gaining attention. Since microglia are the first cell population responding to early changes in AD, it is pivotal to understand the interplay between microglia and other neural cells in AD.