ALTERATIONS IN RESTING STATE FUNCTIONAL CONNECTIVITY ASSOCIATED WITH ALCOHOL USE SEVERITY AND IMPULSIVITY IN A COMMUNITY SAMPLE

Alcohol Use Disorder (AUD) is characterized by neurocognitive and behavioral impairments including the multidimensional construct of impulsivity. Increased impulsivity is both a risk factor for, and a consequence of problematic alcohol use. Individuals with AUD exhibit alterations in neural circuitry when compared to those who do not have AUD. These circuit-level changes in AUD may underlie the difficulties that these individuals experience with heightened impulsivity. The present study uses data-driven resting state functional connectivity (rsFC) methodology to examine the differences in intrinsic functional networks between individuals with AUD and those who are social drinkers (SD). Participants in this secondary data analysis were non-treatment seeking young adult alcohol drinkers (n = 53; with n = 23 who met criteria for an AUD). Group independent component analysis (gICA) was used to test AUD and SD group differences in within- and between-network rsFC, as well as associations between impulsivity constructs and these hypothesized alterations in rsFC. Although we expected to see hypoconnectivity in the AUD group, particularly among the default mode, executive control, reward, and salience networks, we found no statistically significant group differences on any measure of rsFC. Furthermore, we found no associations between impulsivity constructs and rsFC in this sample. In order to explore these null findings, we visualized small-to-moderate effect size differences in spatial map intensity between the groups and found evidence for relatively reduced rsFC in frontal (orbitofrontal cortex, medial prefrontal, right frontal, anterior default mode), precuneus, and visual networks in AUD compared to SD. These effect sizes were small, representing statistically non-significant group differences in within-network rsFC, but they were in the expected direction of AUD hypoconnectivity. Given the statistically null findings, various explanations are presented and future directions are proposed to further advance our understanding of the associations between behavioral traits and neurobiological mechanisms that may contribute to risk for AUD among young adult drinkers