estimates provided by twin and family studies, there have been relatively few large (i.e., adequately powered) genetic studies of beta EEG (Iacono et al., 2016), and to date only one finding has replicated. An early analysis found linkage between beta EEG and a region of chromosome 4 (Porjesz et al., 2002) harboring variants in the gene that encodes the GABA α2 receptor subunit (GABRA2), which were subsequently associated with both beta EEG and AD (Edenberg et al., 2004). More recently, a study of 586 individuals of European ancestry (EA) with DSM-IV AD, and 603 ancestrally matched individuals without AD, replicated the association between beta activity and several GABRA2 variants (Lydall et al., 2011). To date, only two genome-wide association studies (GWAS) of beta EEG have been conducted (Hodgkinson et al., 2010; Malone et al., 2014). In a study of 322 Native-American individuals, there were no genome-wide significant associations reported for beta EEG (Hodgkinson et al., 2010). We note that there were genome-wide significant findings for other EEG parameters; an association was observed among theta power (and AD) and several variants in SGIP1 (Hodgkinson et al., 2010). A recent GWAS of several EEG measures (including monopolar beta EEG, assessed at the
