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<p>Oligodendrocyte precursor cells (OPCs) shape brain function through many non-canonical regulatory mechanisms beyond myelination. Here we show that OPCs form contacts with their processes on neuronal somata in a neuronal activity-dependent manner. These contacts facilitate exocytosis of neuronal lysosomes. A reduction in the number or branching of OPCs reduces these contacts, which is associated with lysosome accumulation and altered metabolism in neurons and more senescent neurons with age. A similar reduction in OPC branching and neuronal lysosome accumulation is seen in an early-stage mouse model of Alzheimer’s disease. Our findings have implications for the prevention of age-related pathologies and the treatment of neurodegenerative diseases.</p>

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Oligodendrocyte precursor cells facilitate neuronal lysosome release

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年1月30日

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  • Li-Pao Fang,
  • Ching-Hsin Lin,
  • Yasser Medlej,
  • Renping Zhao,
  • Hsin-Fang Chang,
  • Qilin Guo,
  • Zhonghao Wu,
  • Yixun Su,
  • Na Zhao,
  • Davide Gobbo,
  • Amanda Wyatt,
  • Vanessa Wahl,
  • Frederic Fiore,
  • Szu-Min Tu,
  • Ulrich Boehm,
  • Wenhui Huang,
  • Shan Bian,
  • Amit Agarwal,
  • Marcel A. Lauterbach,
  • Chenju Yi,
  • Jianqin Niu,
  • Anja Scheller,
  • Frank Kirchhoff,
  • Xianshu Bai

摘要

Oligodendrocyte precursor cells (OPCs) shape brain function through many non-canonical regulatory mechanisms beyond myelination. Here we show that OPCs form contacts with their processes on neuronal somata in a neuronal activity-dependent manner. These contacts facilitate exocytosis of neuronal lysosomes. A reduction in the number or branching of OPCs reduces these contacts, which is associated with lysosome accumulation and altered metabolism in neurons and more senescent neurons with age. A similar reduction in OPC branching and neuronal lysosome accumulation is seen in an early-stage mouse model of Alzheimer’s disease. Our findings have implications for the prevention of age-related pathologies and the treatment of neurodegenerative diseases.