Abstract：
Oligodendrocyte precursor cells (OPCs) comprise 5-8 % of the adult glial cell population and stand out as the most proliferative cell type in the central nervous system (CNS). OPCs are responsible for generating oligodendrocytes (OLs), the myelinating cells of the CNS. However, OPC functions decline as we age, resulting in impaired differentiation and inadequate remyelination. This review explores the cellular and molecular changes associated with OPC aging, and their impact on OPC differentiation and functionality. Furthermore, it examines the impact of OPC aging within the context of multiple sclerosis and Alzheimer\'s disease, both neurodegenerative conditions wherein aged OPCs exacerbate disease progression by impeding remyelination. Moreover, various pharmacological interventions targeting pathways related to senescence and differentiation are discussed as potential strategies to rejuvenate aged OPCs. Enhancing our understanding of OPC aging mechanisms holds promise for developing new therapies to improve remyelination and repair in age-related neurodegenerative disorders.
摘要：
少突胶质细胞前体细胞（OPCs）占成年神经胶质细胞群的5-8％，是中枢神经系统（CNS）中最增殖的细胞类型。OPCs负责产生少突胶质细胞（OLs），中枢神经系统的髓鞘细胞。然而,OPC功能随着年龄的增长而下降，导致分化受损和髓鞘再生不足。这篇综述探讨了与OPC衰老相关的细胞和分子变化，以及它们对OPC差异化和功能性的影响。此外，它研究了在多发性硬化症和阿尔茨海默病的背景下OPC衰老的影响，这两种神经退行性疾病，其中老化的OPCs通过阻碍髓鞘再生而加剧疾病进展。此外，讨论了针对衰老和分化相关途径的各种药理学干预措施，作为恢复衰老OPCs的潜在策略。增强我们对OPC衰老机制的理解有望开发新的疗法来改善与年龄相关的神经退行性疾病的髓鞘再生和修复。
