Niu Jianqin, Verkhratsky Alexei, Butt Arthur, Yi Chenju
Department of Histology and Embryology, Third Military Medical University, Chongqing, China.
Chongqing Key Laboratory of Neurobiology, Chongqing, China.
Adv Neurobiol. 2025;43:363-405. doi: 10.1007/978-3-031-87919-7_13.
The central nervous system is susceptible to gradual decline with age, affecting all types of glial cells in the process. Compared to other glial cells, the oligodendroglial lineage is highly vulnerable to ageing and undergoes significant characteristic changes that impact upon its structure and impair its physiological functions. Therefore, the ageing and degeneration of oligodendroglia become major risk factors for neurodegenerative diseases. During the age-related disease process, changes in oligodendroglia lead to a decline in their ability to regenerate myelin and respond to the aged microenvironment, which are closely linked to the pathogenesis of neurodegenerative diseases, facilitating the emergence of these diseases in older populations. In this chapter, we introduce the physiological changes of oligodendroglia during ageing and the related mechanisms and then summarise their pathophysiological contributions to age-related cognitive disorders. Finally, we discuss potential therapeutic strategies that target oligodendroglia for future research on neurodegenerative diseases.
中枢神经系统易随年龄增长而逐渐衰退，在此过程中会影响所有类型的神经胶质细胞。与其他神经胶质细胞相比，少突胶质细胞谱系极易老化，并会发生显著的特征性变化，这些变化会影响其结构并损害其生理功能。因此，少突胶质细胞的老化和退化成为神经退行性疾病的主要危险因素。在与年龄相关的疾病过程中，少突胶质细胞的变化导致其再生髓鞘的能力下降，并对老化的微环境产生反应，这与神经退行性疾病的发病机制密切相关，促使这些疾病在老年人群中出现。在本章中，我们介绍了少突胶质细胞在衰老过程中的生理变化及其相关机制，然后总结了它们对与年龄相关的认知障碍的病理生理贡献。最后，我们讨论了针对少突胶质细胞的潜在治疗策略，以供未来神经退行性疾病研究参考。
