在大脑健康中探索少突胶质前体细胞衰老。

Navigating oligodendrocyte precursor cell aging in brain health.

机构信息

Department Psychiatry and Neuropsychology, Division Translational Neuroscience, Mental Health and Neuroscience Research Institute, Maastricht University, Maastricht, the Netherlands; Department of Neuroscience, Biomedical Research Institute, Faculty of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium.

University MS Centre (UMSC) Hasselt, Pelt, Belgium; Neuro-Immune Connections and Repair Lab, Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium.

出版信息

Mech Ageing Dev. 2024 Aug;220:111959. doi: 10.1016/j.mad.2024.111959. Epub 2024 Jun 29.

DOI:10.1016/j.mad.2024.111959

PMID:38950628

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

少突胶质前体细胞（OPC）占成年神经胶质细胞的 5-8%，是中枢神经系统（CNS）中最具增殖能力的细胞类型。OPC 负责生成少突胶质细胞（OLs），即 CNS 的髓鞘形成细胞。然而，随着年龄的增长，OPC 的功能会下降，导致分化受损和髓鞘再生不足。本综述探讨了与 OPC 衰老相关的细胞和分子变化，以及它们对 OPC 分化和功能的影响。此外，还研究了 OPC 衰老在多发性硬化症和阿尔茨海默病中的影响，这两种神经退行性疾病中，衰老的 OPC 通过阻碍髓鞘再生而加剧疾病进展。此外，还讨论了针对衰老和分化相关途径的各种药理学干预措施，作为使衰老 OPC 年轻化的潜在策略。深入了解 OPC 衰老机制有望为改善与年龄相关的神经退行性疾病中的髓鞘再生和修复开发新的治疗方法。