The collection of brain data in COGA was motivated by early studies that documented alterations in P300 brain activity in offspring of individuals with AUD, prior to the age of alcohol initiation. 34 COGA further reinforced the role of P300 ERPs and pioneered the use of ERO methods as a means to further deconstruct the P300 component in this context, with frontal theta EROs being particularly useful in our genetic and phenotypic studies. 35 , 36 The intersection of longitudinal data and family structure allowed us to evaluate both predispositional (i.e., differences in brain activity that precede and predict onset of AUD in those with familial risk) and neurotoxic (i.e., heavy alcohol intake modifications of brain activity) mechanisms operating at the brain‐behavior interface. 37 Further, incorporation of genomic data, not only allowed for GWAS of novel phenotypes such as neural synchrony 38 but also polygenic characterization of sex‐specific longitudinal trajectories of brain maturation. 39 The addition of social and environmental contributors, such as peer affiliations and trauma exposure 40 , 41 have contributed to gene–environment interplay analyses within this gene‐brain‐behavior framework. The accompanying review (3. Brain Function) covers the available brain function data and resulting findings in detail.
