The current investigation suggests that functional neuroimaging may be useful for identifying neurocognitive risk factors associated with familial density of AUD. Although we did not find evidence that BOLD response specifically during spatial working memory demands was related to FH, we observed that greater neural activity during rest and reduced activity during an active baseline condition were linked to denser FH. We theorize that this may indicate an imbalance between excitatory and inhibitory action during neural transmission determined by genetic variation in GABAergic mechanisms. Behaviorally, CNS disinhibition might translate into reduced ability to inhibit task irrelevant stimuli or an increased risk for impulsive behavior. Further understanding of the default network in relation to CNS disinhibition and behavioral inhibition may help inform prevention programming and identify youth at risk for substance problems. Longitudinal studies may establish a causal link between neurocognitive characteristics and the risk for developing AUD.
