期刊
ALZHEIMERS & DEMENTIA
卷 16, 期 2, 页码 345-353出版社
WILEY
DOI: 10.1016/j.jalz.2019.09.086
关键词
Alcohol consumption; Alcohol dependence; Alzheimer's disease; Mendelian randomization
资金
- NHMRC [1002560]
- JPB Foundation
- National Institute onAlcohol Abuse and Alcoholism [U10AA08401]
- Inserm
- Medical Research Council [503480]
- Alzheimer's Research UK [503176]
- Wellcome Trust [082604/2/07/Z]
- Federal Ministry of Education and Research
- NIH
- NIA [R01AG033193, AG081220, U01 AG032984, U24AG021886, U01AG016976]
- NHLBI [R01HL105756]
- Icelandic Heart Association
- Erasmus Medical Center
- Erasmus University Rotterdam
- Alzheimer's Association [ADGC-10-196728]
- InstitutPasteur
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, gamma-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 gamma-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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