与年龄相关的眼病中的加速生物衰老和遗传性:以人口为基础的队列和综合遗传分析
Yuelan Gao1, Yuyao Wang1, Yuzhou Zhang1
1Department of Ophthalmology and Visual Sciences, The Chinese University of Hong Kong, Hong Kong.
Investigative ophthalmology & visual science
|November 6, 2025
概括
加快的生物衰老增加了与年龄相关的眼病 (ARED) 的风险,特别是具有高遗传倾向的人. 这突出了改善视力健康预期寿命的干预措施的潜在目标.
科学领域:
- 眼科医生 眼科 眼科
- 遗传学 遗传学 是一个
- 老年学是指老年学的学科.
背景情况:
- 与年龄相关的眼睛疾病 (ARED) 是全球视力丧失的主要原因之一.
- 生物衰老加速 (BAA) 是系统衰老的标志物,但其与ARED和遗传因素的联系尚不清楚.
研究的目的:
- 研究BAA和遗传风险对ARED和失明的综合影响.
- 探索共享的遗传途径,并确定眼睛疾病的潜在抗衰老治疗点.
主要方法:
- 使用Klemera-Doubal方法 (KDM-BA) 和PhenoAge算法估计的生物年龄.
- 在297,375名英国生物库参与者中对BAA和ARED进行横截面和前性分析.
- 遗传类分析以确定共享的遗传影响.
主要成果:
- 较高的BAA与增加的ARED发病率和基线流行率相关.
- 加快的生物衰老在遗传敏感个体中放大了ARED风险,显示了附加性相互作用.
- 多omics分析显示了115个类变体和512个候选基因,包括APOE,APOC1,TOMM40,PVRL2和BCAM,在BAA和ARED之间共享.
- 在ARED患者中,BAA与视力健康预期寿命的减少有关.
结论:
- 加快的生物衰老是ARED的重要风险因素,特别是在具有高遗传易感性的人群中.
- 早期识别加速衰老的个体可能有助于降低ARED风险,提高视力健康的预期寿命.
- 像APOE,APOC1,TOMM40,PVRL2和BCAM这样的基因代表了眼部抗衰老策略的有希望的目标.
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