Finally, while BOLD fMRI assessment of reward- and threat-related brain function may help subtype individuals into distinct categories of AUD risk, it is likely impractical to implement neuroimaging in a general clinical setting, especially in large groups of people. Genetic assays in contrast have become increasingly accessible in recent years and may offer a faster and more affordable way to identify at-risk individuals, while also offering valuable insight into the molecular basis of some of the observed inter-individual variability. Efforts to map reward- and threat-related brain function onto common genetic variation have been ongoing.62 Recent work from our group has highlighted promising novel strategies to increase the amount of variability accounted for by readily assayed molecular indices of these neural risk phenotypes. Specifically, we have demonstrated that a biologically-informed multilocus genetic profile reflecting the cumulative impact of five polymorphisms on dopamine signaling predicts approximately 11% of the inter-individual variability in reward-related VS reactivity.63 In addition, we recently provided evidence that epigenetic modifications impacting serotonin signaling predict a similar amount of variability in threat-related amygdala reactivity.64 Combining and refining these two
