生物标志物 生物标志物
James Groves1, Hamilton Se-Hwee Oh2, Amelia Farinas2,3
1Dementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, United Kingdom.
Alzheimer's & dementia : the journal of the Alzheimer's Association
|December 24, 2025
概括
在个体中加速大脑衰老.
科学领域:
- 神经科学和衰老研究研究
- 蛋白质组学和生物标志物发现发现
背景情况:
- 老龄化是阿尔茨海默病 (AD) 的主要危险因素,但潜在的分子机制仍然不清楚.
- 这项研究调查了同样年龄的队列中蛋白质性大脑衰老轨迹,以了解与AD病理学的联系.
研究的目的:
- 为了追踪整个生命的第七个十年的蛋白质大脑衰老轨迹.
- 将这些衰老轨迹与阿尔茨海默病 (AD) 生物标志物联系起来.
- 确定影响大脑衰老和AD之间的关系的特定蛋白质.
主要方法:
- 利用SomaScan从1946年英国出生队列 (n=414) 的蛋白质组数据在两个时间点.
- 估计"大脑年龄差距" (BAG) 使用蛋白质时钟,并计算"BAG变化得分"以反映衰老轨迹.
- 评估了主要结果,包括粉样蛋白-PET阳性和血p-tau217,以及CSF生物标志物的次要结果.
主要成果:
- 观察到异质的大脑衰老轨迹,BAG变化得分从-21.3年到17.3年不等.
- 加快大脑衰老 (更高的BAG变化得分) 显著预测了粉样蛋白-PET阳性和升高的p-tau217水平 (血和脑液).
- 在调整APOE4状态和其他神经退行性标志物后,关联仍然很重要;确定了Aldolase C,NPTXR和LRRTM2等关键蛋白质.
结论:
- 异质的蛋白质性大脑衰老轨迹甚至存在于相同年龄的个体中.
- 加快大脑衰老是AD生物标志物积极性的重要预测因素,独立于遗传风险.
- 需要进一步的研究,以阐明已识别的蛋白质在将大脑衰老与AD病理学联系起来的作用.
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