在WRAP中,生活方式,遗传风险,血pTau217和发生的认知障碍
Rachel L Studer1, Karly A Cody2,3, Julie E Oomens2
1Wisconsin Alzheimer's Institute, School of Medicine and Public Health, University of Wisconsin - Madison, Madison, Wisconsin, USA.
概括
在中年时更健康的生活方式降低了认知障碍的风险,无论遗传倾向 (apolipoprotein E ε4) 或生物标志物 (pTau217). 这突显了生活方式选择在痴呆症预防中的力量.
科学领域:
- 神经科学和衰老研究研究
- 公共卫生和预防医学
- 在神经退行症中发现生物标志物
背景情况:
- 中年生活方式因素越来越被认为对长期大脑健康至关重要.
- 在预测认知衰退方面,生活方式,阿波利波蛋白E (APOE) ε4等位基因和血pTau217之间的相互作用仍然不完全理解.
- 研究这些因素对于制定有效的痴呆症预防策略至关重要.
研究的目的:
- 检查中年生活方式的痴呆风险和发生认知障碍 (ICI) 的风险之间的关联.
- 为了确定这种关联是否因阿波利波蛋白E (APOE) ε4等位基因或血pTau217水平的存在而改变.
- 为减少痴呆风险提供生活方式干预措施的证据.
主要方法:
- 利用了来自威斯康星州阿尔茨海默病预防登记处 (WRAP) 1088名认知正常参与者的数据.
- 将参与者分类为基于生活方式的痴呆症风险三级 (低,中等,高).
- 采用考克斯回归模型来评估ICI风险,平均随访时间为8.2年,根据APOE ε4状态和pTau217水平进行调整.
主要成果:
- 与最健康的三分之一相比,中度和高生活方式痴呆风险三分之一的个体表现出显著更高的ICI风险.
- 这些关联在APOE ε4载体和非载体中保持一致.
- 同样,较高的基于生活方式的痴呆症风险与所有测量的血pTau217水平的ICI风险增加有关.
结论:
- 中年时更健康的生活方式独立地与发生认知障碍的风险降低有关.
- 无论是APOE ε4载体还是血pTau217水平都没有显著改变健康生活方式的保护作用.
- 这些发现强调了促进健康生活方式在各种遗传和生物标志物个人资料中预防痴呆的重要性.
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