Extending research on other neurological traits32,43, we show that individual genetic markers (sQTLs) and polygenic risk underlie alternative mRNA splicing associated with AUD. Similar to other research44, we found that sQTLs were enriched among DNaseI hypersensitivity sites, corroborating that loose chromatin regions are hotspots for alternative mRNA splicing regulation. Previous splicing studies used a single tissue type2,43–45. Our study suggests that future work should consider multiple tissues when possible—as the genetic links with splicing events may differ by brain region.
