Alyssa Wong

Alcohol use disorder is a clinically established disease characterized by severe alcohol abuse, compulsive use, and disruptive drinking patterns. This disorder is a profound public health concern and a leading cause of mortality. Genetic etiology of alcohol addiction is an active field of research. A genome-wide association study identified variants in two genes — SLC39A8 and HGFAC — that have an association with the phenotypic trait of increased alcohol consumption. Despite this association, no current research has studied the particular role of these genes in alcohol use. We investigated the influence of the genes SLC39A8 and HGFAC on acute alcohol behavior and consumption in a mouse model. To assess the sedative effects of alcohol, a loss of righting reflex (LORR) procedure was employed to study the influence of SLC39A8 on acute alcohol behavior. A two-bottle choice procedure was used to study the influence of HGFAC on voluntary alcohol consumption. SLC39A8 mice displayed decreased alcohol-induced sedative behavior in comparison to mice that harbored a deletion of the gene in the LORR procedure. In the two-bottle choice model, HGFAC mice consumed more alcohol than the gene knock-out mice. These results suggest a trend that SLC39A8 and HGFAC influence alcohol use, which helps address the role of genetics in a prevalent disorder. These advances represent an example of back translation of human genetics in alcohol addiction research, elucidating our understanding of the genetic makeup of alcohol use.