Alcoholism is a common, complex (non-Mendelian) disorder with contributions from both genetic and environmental influences and their interactions. As seen in this review, neuroelectrophysiological measures (e.g., P3, theta ERO, EEG beta) that differentiate between alcoholics and controls, and between HR offspring from densely affected alcoholic families and LR controls, serve as effective endophenotypes (intermediate phenotypes that correlate with diagnosis). These endophenotypes are under genetic control and are highly heritable, and have been successfully used in the search for genes associated with risk for AUDs and related disorders (Porjesz and Rangaswamy, 2007; Rangaswamy and Porjesz, 2008a, b). As the genomic technologies have evolved from linkage scans with microsatellites to candidate gene studies and genomewide association studies (GWAS) these studies have highlighted targets that have proved to be relevant to understanding the pathophysiology of AUDs.
