小鼠大脑少突胶质前体细胞的衰老和衰老命运。

IF 4.1 Q2 GERIATRICS & GERONTOLOGY npj aging Pub Date : 2024-10-22 DOI:10.1038/s41514-024-00176-y
Paul T Gomez, Chase M Carver, Sonia L Rodriguez, Liguo Wang, Xu Zhang, Marissa J Schafer
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引用次数: 0

摘要

少突胶质前体细胞(OPCs)与年龄有关的变化会导致白质功能障碍。在老年小鼠中,我们假设髓鞘致密的边缘 OPCs 与海马 OPCs 相比,具有龛特异性。衰老的边缘 OPCs 数量更少、体积更大,并定位在邻近的小胶质细胞中。我们发现了年龄增加的 p16/Cdkn2a 表达的 OPCs,这些 OPCs 富含衰老相关通路,而且海马和边缘体之间存在不同的衰老特征。老年脑OPC群体在微环境特性和对衰老定向干预的反应方面存在差异。
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Aging and senescent fates of oligodendrocyte precursor cells in the mouse brain.

Age-related changes in oligodendrocyte precursor cells (OPCs) contribute to white matter dysfunction. In aged mice, we hypothesized that myelin-dense fimbria OPCs possess niche-specific properties, compared to hippocampal OPCs. Aged fimbria OPCs were fewer, larger, and localized to neighboring microglia. We identified age-increased p16/Cdkn2a-expressing OPCs enriched for senescence-related pathways and distinct senescence signatures between hippocampus and fimbria. Aged brain OPC populations differ in microenvironment properties and responses to senescence-directed intervention.

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