Although previous studies have reported variation in beta EEG among individuals diagnosed with AD and related conditions, there have been relatively few studies examining genetic variants in relation to beta EEG and only one finding that has been replicated to date (GABRA2 (Porjesz et al. 2002b; Edenberg et al. 2004; Lydall et al. 2011; Ittiwut et al. 2012; Malone et al. 2014)). Subsequently, associations between GABRA2, AD (Edenberg et al. 2004; Lappalainen et al. 2005; Covault et al, 2004; Drgon et al., 2006; Fehr et al., 2006; Soyka et al. 2008; Enoch et al. 2006, 2010; Roh et al. 2011), drug dependence (Agrawal et al. 2006; Enoch et al. 2010; Ehlers & Gizer 2013), and externalizing behavior (Dick et al., 2013; Salvatore et al., 2015; Trucco et al., 2016; Wang et al., 2016) have been observed, indicating the potential of genetic studies of beta EEG to facilitate discovery of genes underlying disinhibitory behavior. However, the number of replicable genetic variants uncovered by this approach has been limited (Iacono et al., 2016), necessitating large scale genetic association studies of beta EEG utilizing the best-practices of genetic epidemiology.
