孟德尔随机化
酒
联想(心理学)
饮酒量
医学
遗传关联
疾病
阿尔茨海默病
全基因组关联研究
内科学
精神科
心理学
单核苷酸多态性
遗传学
生物
心理治疗师
基因
基因型
生物化学
遗传变异
作者
Shea J. Andrews,Alison Goate,Kaarin J. Anstey
标识
DOI:10.1016/j.jalz.2019.09.086
摘要
Abstract Introduction Observational studies have suggested that light‐to‐moderate alcohol consumption decreases the risk of Alzheimer's disease, but it is unclear if this association is causal. Methods Two‐sample Mendelian randomization (MR) analysis was used to examine whether alcohol consumption, alcohol dependence, or Alcohol Use Disorder Identification Test (AUDIT) scores were causally associated with the risk of Late‐Onset Alzheimer's disease (LOAD) or Alzheimer's disease age of onset survival (AAOS). Additionally, γ‐glutamyltransferase levels were included as a positive control. Results There was no evidence of a causal association between alcohol consumption, alcohol dependence, or AUDIT, and LOAD. Alcohol consumption was associated with an earlier AAOS and increased γ‐glutamyltransferase blood concentrations. Alcohol dependence was associated with a delayed AAOS. Discussion MR found robust evidence of a causal association between alcohol consumption and an earlier AAOS, but not alcohol intake and LOAD risk. The protective effect of alcohol dependence is potentially due to survivor bias.
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