Navigating oligodendrocyte precursor cell aging in brain health

被引:5
|
作者
Leenders, Freddy [1 ,2 ]
Koole, Lisa [1 ,2 ]
Slaets, Helena [3 ,4 ]
Tiane, Assia [1 ,2 ,3 ]
van den Hove, Daniel [1 ]
Vanmierlo, Tim [1 ,2 ,3 ]
机构
[1] Maastricht Univ, Mental Hlth & Neurosci Res Inst, Dept Psychiat & Neuropsychol, Div Translat Neurosci, Maastricht, Netherlands
[2] Hasselt Univ, Biomed Res Inst, Fac Med & Life Sci, Dept Neurosci, Diepenbeek, Belgium
[3] Univ MS Ctr UMSC Hasselt, Pelt, Belgium
[4] Hasselt Univ, Biomed Res Inst, Dept Immunol & Infect, Neuroimmune Connect & Repair Lab, Diepenbeek, Belgium
关键词
Oligodendrocyte precursor cell; Aging; Myelination; Multiple sclerosis; Alzheimer's disease; PROGENITOR CELLS; ALZHEIMERS-DISEASE; REMYELINATION; MICROGLIA; SENESCENCE; GENERATION; DIFFERENTIATION; REGENERATION; MYELINATION; INEFFICIENT;
D O I
10.1016/j.mad.2024.111959
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页数:11
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