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• W2892663739 abstract "Background Efforts to promote the cessation of harmful alcohol use are hindered by the affective and physiological components of alcohol withdrawal ( AW ), which can include life‐threatening seizures. Although previous studies of AW and relapse have highlighted the detrimental role of stress, little is known about genetic risk factors. Methods We conducted a genome‐wide association study of AW symptom count in uniformly assessed subjects with histories of serious AW , followed by additional genotyping in independent AW subjects. Results The top association signal for AW severity was in sortilin family neurotrophin receptor gene SORCS 2 on chromosome 4 (European American meta‐analysis n = 1,478, p = 4.3 × 10 −9 ). There were no genome‐wide significant findings in African Americans ( n = 1,231). Bioinformatic analyses were conducted using publicly available high‐throughput transcriptomic and epigenomic data sets, showing that in humans SORCS 2 is most highly expressed in the nervous system. The identified SORCS 2 risk haplotype is predicted to disrupt a stress hormone‐modulated regulatory element that has tissue‐specific activity in human hippocampus. We used human neural lineage cells to demonstrate in vitro a causal relationship between stress hormone levels and SORCS 2 expression, and show that SORCS 2 levels in culture are increased upon ethanol exposure and withdrawal. Conclusions Taken together, these findings indicate that the pathophysiology of withdrawal may involve the effects of stress hormones on neurotrophic factor signaling. Further investigation of these pathways could produce new approaches to managing the aversive consequences of abrupt alcohol cessation." @default.
• W2892663739 created "2018-10-05" @default.
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• W2892663739 date "2018-10-25" @default.
• W2892663739 modified "2023-10-15" @default.
• W2892663739 title "Risk Locus Identification Ties Alcohol Withdrawal Symptoms to <i>SORCS2</i>" @default.
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• W2892663739 doi "https://doi.org/10.1111/acer.13890" @default.
• W2892663739 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6317871" @default.
• W2892663739 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30252935" @default.
• W2892663739 hasPublicationYear "2018" @default.
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