To date, there have been relatively few genetic studies examining beta EEG and only one finding that has been replicated. In addition, no previous gene identification study of beta EEG had been conducted in a population of AA. As the ultimate goal of this research is providing prevention and/or interventions for all individuals, it is crucial that AA populations are included in this work, especially because African-Americans are at greater risk for drinking-related consequences. This study found association between an intergenic signal on 3q26 and fast beta EEG in a sample of related individuals of AA. The most significant SNP is an eQTL for BCHE, a gene previously implicated in disinhibitory disorders and expressed in the thalamus, a brain region central to beta EEG and AUD. Further, fast beta EEG genome-wide associated variants (rs7428372 and rs13093097) were associated with AD both in the discovery sample and an independent sample. Converging data provide support for the role of genetic variants within 3q26 in neural hyperexcitability and disorders characterized by impulsivity. In addition, this study demonstrates the utility of the endophenotype approach13;
