paperKB
coga / coga-kb
Help
Sign in

Chunk #19 — RESULTS — Stratified models of heritability and genetic (co)variance

Source
Neurogenetic and multi-omic sources of overlap among sensation seeking, alcohol consumption, and alcohol use disorder.
Embedded
yes

Text

Twenty‐two, 46, and 24 functional annotations were significantly enriched for sensation seeking, alcohol consumption, and AUD, respectively, following FDR correction (Table S6). Across all three traits, significant enrichment was observed for gene expression in the frontal cortex; the H3K4me1 transcriptional enhancer in the dlPFC, inferior temporal lobe, and middle hippocampus; the H3K27ac promoter in the dlPFC and inferior temporal lobe; and the H3K9ac promoter in the inferior temporal lobe and anterior caudate. Unique enrichment of sensation seeking and alcohol consumption and their covariance, but not for AUD, was observed for H3K4me1 in the anterior caudate. Unique significant enrichment for sensation seeking and alcohol consumption, but not for their covariance or AUD, was also observed for H3K4me1 in the substantia nigra, H3K27ac in the cingulate cortex, and H3K9ac in the angular gyrus. No significant overlap in enrichment for sensation seeking and AUD was observed that did not also include alcohol consumption. However, there was common enrichment of gene expression in the anterior cingulate and cerebellum, H3K27ac in the anterior caudate, and the H3K4me3 transcriptional activator in the cingulate gyrus for alcohol consumption and AUD, which was not observed for sensation seeking.