Here, we integrated deep RNA-seq and SNP genotyping data from four different brain regions of 30 subjects with AUD and 30 social/non-drinking control subjects to detect genes whose ASE differs. The brain regions were: (i) the basolateral nucleus of the amygdala (BLA), which plays crucial roles in stimulus value coding and alcohol withdrawal-induced increase in anxiety [9]; (ii) the central nucleus of amygdala (CE), which mediates alcohol-related behaviors and alcohol dependency [10]; (iii) the nucleus accumbens (NAC), in which alcohol promotes dopamine release [11]; and (iv) the superior frontal cortex (SFC), which is implicated in cognitive control and experiences neuronal cell loss after long-term alcohol abuse [12]. We then used a high-throughput reporter assay called PASSPORT-seq (parallel assessment of polymorphisms in miRNA target-sites by sequencing) [13] to systematically screen all the SNPs in the 3′UTR regions of the genes that demonstrated differential ASE between AUD and control subjects, in any of the four brain regions, to determine which variants altered RNA levels in cells of neural origin. We identified 25 functional SNPs that altered gene expression in the same direction
