Chunk #38 — HOW DO NEURAL SIGNATURES ASSOCIATED WITH AUD HELP ELUCIDATE THE ROLE OF BRAIN FUNCTION IN THE RISK AND CONSEQUENCES OF ALCOHOL USE AND AUD ACROSS THE LIFESPAN? — How does the social–environmental context (and interaction with genetic risk factors) impact brain functioning and ultimately impact risk for AUD?
frontal theta during response inhibition. Importantly, these effects remained significant after accounting for other traumatic exposures, parental history of AUD and participants' substance use, but not measures of impulsivity. Lagged frontal neurophysiological development during response inhibition may reflect delays in frontal lobe development, synaptic pruning and/or cortical maturation involving neural circuits. These same areas were associated with increased risk for internalizing psychopathology and symptoms of AUD in young adulthood. 66 These findings support the hypothesis that changes in neurocognitive development related to early sexual trauma exposure may increase risk for mental health and substance use problems in young adulthood. Building on this work, COGA 67 observed that female, but not male, participants who experienced a sexual assaultive trauma, and were from families more densely affected with AUD, had higher rates of PTSD symptoms. In addition, exposure to nonsexual assaultive trauma was associated with poorer neurocognitive performance (planning and problem‐solving skills on the Tower of London test) in young adulthood. Parenting has been found to impact offspring brain development, neurocognitive function, risk and resilience for AUD via both genetic and socio‐environmental factors. Using data from the COGA prospective cohort, COGA demonstrated that greater ‘closeness with father’ was associated with larger P300
