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 <5×10-6) and independent (r2 < 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.

中文翻译：

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单纯疱疹病毒和阿尔茨海默病：孟德尔随机化研究

本研究使用 2 样本孟德尔随机化评估了任何单纯疱疹病毒 (HSV) 感染是否是晚发性阿尔茨海默病 (AD) 的遗传有效目标。我们将针对任何 HSV 感染（n = 450,581）的强（p 值 <5×10-6）和独立（r2 < 0.05）遗传变异应用于认知功能的全基因组关联研究（n = 300,486）和迟发性AD (n = 455,258) 以获得估计值。任何 HSV 感染的遗传预测对数比值与认知功能无关（每种 HSV 感染的平均差异为 0.0004，95% 置信区间 (CI) -0.001 至 0.001）或迟发性 AD（比值比 (OR) 0.999, 95 % CI 0.998-1.001)。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性 AD 干预的遗传有效目标，