在A4/LEARN研究中的BrainAge多遗传风险评分和血生物标志物之间的关系
Jorge Garcia Condado1,2,3, Mabel Seto3, Madison Cuppels3
1Computational Neuroimaging Lab, BioBizkaia Health Research Institute, Barakaldo, Spain.
medRxiv : the preprint server for health sciences
|July 17, 2025
概括
对加速大脑衰老的遗传倾向与老年女性的pTau217水平较高有关,这表明性别特异性遗传影响早期阿尔茨海默病的病理学.
科学领域:
- 神经科学是一个神经科学.
- 遗传学 遗传学 是一个
- 生物标志物 生物标志物
背景情况:
- 阿尔茨海默病 (AD) 病理学可以使用血生物标志物检测.
- 遗传因素可能会影响大脑衰老和AD风险.
- 了解对加速大脑衰老的遗传倾向对于早期AD检测至关重要.
研究的目的:
- 调查加速大脑衰老的遗传风险与血AD生物标志物之间的关联.
- 探索这些关联中的年龄和性别特异性影响.
主要方法:
- 从A4/LEARN研究中对1994年认知正常参与者的分析.
- 对加速灰质损失的多基因风险评分 (PRS) 的计算.
- 对血pTau217,GFAP和NfL水平的测量.
- 统计建模用于测试与年龄和性别的关联和相互作用.
主要成果:
- BrainAge PRS显著缓解了年龄与pTau217的关联,较高的PRS与老年人中升高的pTau217有关.
- 这种关联在女性中是显著的,但在男性中没有.
- 在BrainAge PRS和GFAP或NfL水平之间没有发现显著的关联.
结论:
- 对加速大脑衰老的遗传倾向与在没有认知障碍的老年女性中增加的pTau217有关.
- 这些发现突出了大脑衰老和早期AD病理之间潜在的性别和年龄特定的遗传联系.
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