sequencing (ATAC-seq32)) analysis from these same caudate samples, allowing us to both identify uncommon cell types and unique cell states, and measure small differences in both gene expression and chromatin accessibility in the same nuclei. We profiled the biological pathways underlying these differences, and AUD-associated differences in transcription factor activity and cell-cell communication in major glial cell types (Supplementary Fig. 1). This study provides a comprehensive profile of AUD-related differences in the caudate nucleus, identifies potential mechanisms contributing to AUD and several directions for further exploration, and highlights the broader utility of large-scale multiomic studies for identifying regulatory mechanisms, which can be applied to other neurological and psychiatric conditions.
