Neural correlates associated with a family history of alcohol use disorder: A narrative review of recent findings.

Abstract

A family history of alcohol use disorder (AUD) is associated with a significantly increased risk of developing AUD in one's lifetime. The previously reviewed literature suggests there are structural and functional neurobiological markers associated with familial AUD, but to our knowledge, no recent review has synthesized the latest findings across neuroimaging studies in this at-risk population. For this narrative review, we conducted keyword searches in electronic databases to find cross-sectional and longitudinal studies (2015-present) that used magnetic resonance imaging (MRI), diffusion tensor imaging, task-based functional MRI (fMRI), and/or resting state functional connectivity MRI. These studies were used to identify gray matter, white matter, and brain activity markers of risk and resilience in family history positive (FHP) individuals with a family history of AUD. FHP individuals have greater early adolescent thinning of executive functioning (frontal lobe) regions; however, some studies have reported null effects or greater gray matter volume and thickness relative to family history negative (FHN) peers without familial AUD. FHP individuals also have white matter microstructure alterations, such as reduced integrity of fronto-striatal pathways. Recent fMRI studies have found greater inhibitory control activity in FHP individuals, while reward-related findings are mixed. A growing interest in identifying intrinsic connectivity differences between FHP and FHN individuals has emerged in recent years. Familial AUD is related to both structural and functional brain alterations. Research should continue to focus on (1) longitudinal analyses with larger samples, (2) assessment of personal substance use and prenatal exposure to alcohol, (3) the effects of comorbid familial psychopathology, (4) examination of sex-specific markers of risk and resilience, (5) neural predictors of alcohol use initiation, and (6) brain-behavior relationships. These efforts would aid the design of neurobiologically informed prevention and intervention efforts focused on this at-risk population.