Alcohol dependence (AD) is a chronic relapsing brain disorder with both environmental and genetic contributions to risk. It is estimated that 40–60% of the difference in risk among individuals is due to genetic variations (Edenberg & Foroud, 2013, 2014; Rietschel & Treutlein, 2013). However, few individual genes have been robustly associated with risk for AD. The largest meta-analysis to date of alcohol dependence in those of European and African Ancestry found only one gene associated with the disorder at genome-wide significance, ADH1B (Walters et al., 2018). Another metabolic gene, ALDH2, is associated with alcohol dependence in Asians (Edenberg and McClintick, 2018). Many of the variants for alcohol-related traits identified by GWAS are not in coding regions, and might be eQTLs or be in linkage disequilibrium (LD) with them (Gamazon et al., 2018). Transcriptome analyses may help prioritize genes within GWAS loci, identify the eQTLs and pathways affected by ethanol, and help understand mechanisms by which they act.
