to the classification suggests that alcohol-induced memory issues, at least in part, are associated with genomic liability. In general, family studies, twin studies, and GWAS have all demonstrated the heritability of AUD [153,154,155] and the utility of PRS to identify and quantify the risk of developing AUD and related outcomes [65,67,156]. Recently, Lai et al. [67] reported that individuals with AUD had higher PRS than controls and the PRS magnitude increased as the number of DSM-5 diagnostic criteria increased. Furthermore, PRS for alcohol dependence was found to be associated with neural connectivity [36,157] and cognitive functions, such as verbal fluency, vocabulary, digit-symbol coding, and logical memory [158], as well as brain structure [159]. Unfortunately, PRS factors related to neurocognitive phenotypes, which could have improved the predictive model, were not included in the study due to a lack of neurocognitive GWAS on AA populations when calculating PRS-CSx for the study sample. Further studies using neurocognitive PRS in multi-ethnic samples are needed to ascertain and quantify the genomic contribution of alcohol-induced memory problems for predictive purposes.
