A family history of alcohol use disorders is a well-established risk factor for the development of adolescent alcohol abuse and dependence. Studies have linked a positive family history (FHP) of AUD to neurocognitive and electrophysiological abnormalities in non-abusing adolescents, suggesting that youth at risk for developing subsequent AUD may carry neural markers for predisposition. Increased vulnerability for AUD may depend upon the nature of these cognitive features. Using structural equation modeling (SEM) to contrast models of brain activation in response to a spatial working memory task, this study proposes that a subtle neurodevelopmental lag, as characterized by protracted development of the neural substrate of spatial working memory, may distinguish FHP (n=27) from FH negative (FHN) (n=38) youth. Functional connectivity analyses may help elucidate a pattern of altered systems employed in complex cognitive tasks in FHP youth. Importantly, cognitive abnormalities, traditionally ascribed to heavy drinking, may be moderated by family history effects. Increased understanding of these neurocognitive components may aid in uncovering factors that contribute to heightened risk for alcohol dependence. [unreadable] [unreadable] [unreadable]