Alcohol use disorder is a complex and multifactorial disorder, making the understanding of pathways from genetic predispositions to phenotypic expression of AUD a huge challenge. It was initially theorized that alcohol‐related measures of brain function such as neurophysiological markers, described as “endophenotypes” or “intermediate phenotypes,” may reflect simpler genetic processes and be more proximal to the genes involved in the predisposition to AUD. 19 , 20 , 21 However, regarding AUD, research has found that brain‐based phenotypes are also complex, multi‐factorial traits that reflect the contribution of many genetic variants of small effect from across the genome. Nonetheless, measures of brain function associated with AUD, such as neurophysiological markers of risk, continue to be extremely useful in delineating underlying mechanisms (e.g., attention, impulsivity) associated with liability for complex conditions such as AUD. Over multiple decades, COGA has led the field in characterizing genetic variation associated with brain functioning and has advanced understanding of how genomic risk affects the development and course of AUD.
