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Updated: May 21, 2025

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失眠会加速老年人的表观遗传钟

Nadia Alejandra Rivero-Segura¹, Julian Daniel Rodriguez Cuartas¹, Paola Garcia-delaTorre²

¹Dirección de Investigación, Instituto Nacional de Geriatría (INGER), 10200, Mexico City, Mexico.

|March 18, 2025

概括

失眠加速了生物衰老,增加了GrimAGE和SkinBloodClock的年龄. 这种睡眠障碍还导致DNA低甲基化,影响蛋白质稳定和氧化应激通路.

科学领域:

表观遗传学和老年学
睡眠医学睡眠医学

背景情况:

失眠是一种普遍存在的睡眠障碍,与认知,精神和身体健康问题有关,包括加速衰老和与年龄有关的疾病.
基于DNA甲基化模式的表观遗传钟估计生物年龄和疾病风险,对它们与失眠的联系的研究有限.
衰老涉及DNA甲基化的显著变化,这些变化被用于表观遗传钟来评估生物年龄和健康风险.

研究的目的:

在老年人中使用Illumina EPICv.2阵列调查失眠和表观遗传衰老之间的关联.
评估失眠与各种表观遗传年龄估计之间的关系,包括HorvathAGE,HannumAGE,PhenoAGE,SkinBloodClock,GrimAGE,DunedinPACE和DNA甲基化端粒长度 (DNAmTL).

主要方法:

使用Illumina EPICv.2阵列对63名老年人进行表观遗传学分析 (33名失眠患者,30名对照人).
在失眠和没有失眠的个体之间计算和比较多个表观遗传年龄估计器.
全表观基因组关联研究 (EWAS) 以确定差异甲基化位置和丰富通路.

主要成果:

失眠的个体表现出加速的GrimAGE和SkinBloodClock,以及减少的DNAmTL.
EWAS揭示了失眠患者的全球低甲基化模式.
丰富分析表明,受影响的途径与蛋白质稳定和氧化应激有关.

结论:

失眠与表观遗传衰老加速有关,特别是GrimAGE和SkinBloodClock,并可能导致端粒缩短.
失眠引起的DNA甲基化变化会影响至关重要的细胞过程,包括蛋白质稳定和氧化应激反应.
这些发现强调了失眠,加速衰老和疾病风险增加之间的潜在分子联系.

关键词:

通过DNA甲基化.欧洲经济联盟 (EWAS) 的成员.氧化应激是一种氧化应激.蛋白质稳定性蛋白质稳定性睡眠障碍睡眠障碍是一种睡眠障碍.

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