Kwok Man Ki, Schooling Catherine Mary
School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, China.
School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, China; City University of New York Graduate School of Public Health and Health Policy, New York, United States.
Neurobiol Aging. 2021 Mar;99:101.e11-101.e13. doi: 10.1016/j.neurobiolaging.2020.09.025. Epub 2020 Oct 9.
This study assessed if any herpes simplex virus (HSV) infection was a genetically valid target for late-onset Alzheimer's disease (AD) using 2-sample Mendelian randomization. We applied strong (p-value <5×10) and independent (r < 0.05) genetic variants for any HSV infection (n = 450,581) to genome wide association studies of cognitive function (n = 300,486), and late-onset AD (n = 455,258) to obtain estimates. Genetically predicted log odds of any HSV infection was not associated with cognitive function (mean difference 0.0004 per any HSV infection, 95% confidence interval (CI) -0.001 to 0.001), or late-onset AD (odds ratio (OR) 0.999, 95% CI 0.998-1.001). Different genetic variant selections produced similar results. Any HSV infection does not appear to be a genetically valid target of intervention in late-onset AD, suggesting a rethink of the relevance of any HSV infection to late-onset AD.
本研究使用两样本孟德尔随机化方法评估单纯疱疹病毒（HSV）感染是否为晚发型阿尔茨海默病（AD）的有效遗传靶点。我们将针对任何HSV感染的强关联（p值<5×10）且独立（r<0.05）的遗传变异（n = 450,581）应用于认知功能（n = 300,486）和晚发型AD（n = 455,258）的全基因组关联研究以获得估计值。遗传预测的任何HSV感染的对数优势比与认知功能（每例HSV感染的平均差异为0.0004，95%置信区间（CI）为-0.001至0.001）或晚发型AD（优势比（OR）为0.999，95%CI为0.998 - 1.001）均无关联。不同的遗传变异选择产生了相似的结果。任何HSV感染似乎都不是晚发型AD的有效遗传干预靶点，这提示需重新思考任何HSV感染与晚发型AD的相关性。
