for genes which represent plausible candidates based on earlier work. In all, we conducted several levels of analyses to examine enrichment of signals and produced statistically significant results at the gene-level, and a few at experiment-wide level, for signals affecting our AD factor score, gene-level replication of previous candidates and enrichment of pathways. We are at an early stage in the process of identifying individual risk loci in the human genome for AD using GWAS methods and our results need to be examined in independent samples to test whether they represent true positive findings. We hope that this paper makes a contribution towards the effort of identifying etiological genes and gene pathways underlying alcohol use disorders.
