We further investigated the role of alternative splicing for the genetic basis of AUD. Using LDscore regression we observed that heritable influences explained 7.81% of the individual differences in AUD. Our partitioned heritability analyses revealed that SNPs in and around differentially spliced genes accounted for 30% of the genetic risk for AUD (OR = 1.349, se = 0.064, p = 6.46e−7; see Fig. 5), but not for our negative control trait (Joint disorders, p = 0.161).
