In conclusion, we provide a detailed picture of the vast transcriptional and epigenetic differences between individuals with and without AUD in many different cell types within the caudate nucleus that illuminates biological mechanisms underlying these differences and identifies potential driver genes causing these differences. Our work adds novel insights into the etiology associated with AUD, pointing to key pathways and regulatory genes, and underscores the potential of large-scale multiomic datasets to provide novel insights into brain regions and diseases.
