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A genome-wide association study of alcohol-dependence symptom counts in extended pedigrees identifies C15orf53.

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Title: A genome-wide association study of alcohol-dependence symptom counts in extended pedigrees identifies C15orf53.
Authors: Wang, J-C, Foroud, T, Hinrichs, A L, Le, N X H, Bertelsen, S, Budde, J P, Harari, O, Koller, D L, Wetherill, L, Agrawal, A, Almasy, L, Brooks, A I, Bucholz, K, Dick, D, Hesselbrock, V, Johnson, E O, Kang, S, Kapoor, M, Kramer, J, Kuperman, S
Source: Molecular Psychiatry. Nov2013, Vol. 18 Issue 11, p1218-1224. 7p.
Subjects: Genealogy, Alcohol-induced disorders, Single nucleotide polymorphisms, Alcoholism, Phenotypes, Genetics
Abstract: Several studies have identified genes associated with alcohol-use disorders (AUDs), but the variation in each of these genes explains only a small portion of the genetic vulnerability. The goal of the present study was to perform a genome-wide association study (GWAS) in extended families from the Collaborative Study on the Genetics of Alcoholism to identify novel genes affecting risk for alcohol dependence (AD). To maximize the power of the extended family design, we used a quantitative endophenotype, measured in all individuals: number of alcohol-dependence symptoms endorsed (symptom count (SC)). Secondary analyses were performed to determine if the single nucleotide polymorphisms (SNPs) associated with SC were also associated with the dichotomous phenotype, DSM-IV AD. This family-based GWAS identified SNPs in C15orf53 that are strongly associated with DSM-IV alcohol-dependence symptom counts (P=4.5 × 10−8, inflation-corrected P=9.4 × 10−7). Results with DSM-IV AD in the regions of interest support our findings with SC, although the associations were less significant. Attempted replications of the most promising association results were conducted in two independent samples: nonoverlapping subjects from the Study of Addiction: Genes and Environment (SAGE) and the Australian Twin Family Study of AUDs (OZALC). Nominal association of C15orf53 with SC was observed in SAGE. The variant that showed strongest association with SC, rs12912251 and its highly correlated variants (D′=1, r2 0.95), have previously been associated with risk for bipolar disorder. [ABSTRACT FROM AUTHOR]
Copyright of Molecular Psychiatry is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: A genome-wide association study of alcohol-dependence symptom counts in extended pedigrees identifies C15orf53.
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  Data: <searchLink fieldCode="AR" term="%22Wang%2C+J-C%22">Wang, J-C</searchLink><br /><searchLink fieldCode="AR" term="%22Foroud%2C+T%22">Foroud, T</searchLink><br /><searchLink fieldCode="AR" term="%22Hinrichs%2C+A+L%22">Hinrichs, A L</searchLink><br /><searchLink fieldCode="AR" term="%22Le%2C+N+X+H%22">Le, N X H</searchLink><br /><searchLink fieldCode="AR" term="%22Bertelsen%2C+S%22">Bertelsen, S</searchLink><br /><searchLink fieldCode="AR" term="%22Budde%2C+J+P%22">Budde, J P</searchLink><br /><searchLink fieldCode="AR" term="%22Harari%2C+O%22">Harari, O</searchLink><br /><searchLink fieldCode="AR" term="%22Koller%2C+D+L%22">Koller, D L</searchLink><br /><searchLink fieldCode="AR" term="%22Wetherill%2C+L%22">Wetherill, L</searchLink><br /><searchLink fieldCode="AR" term="%22Agrawal%2C+A%22">Agrawal, A</searchLink><br /><searchLink fieldCode="AR" term="%22Almasy%2C+L%22">Almasy, L</searchLink><br /><searchLink fieldCode="AR" term="%22Brooks%2C+A+I%22">Brooks, A I</searchLink><br /><searchLink fieldCode="AR" term="%22Bucholz%2C+K%22">Bucholz, K</searchLink><br /><searchLink fieldCode="AR" term="%22Dick%2C+D%22">Dick, D</searchLink><br /><searchLink fieldCode="AR" term="%22Hesselbrock%2C+V%22">Hesselbrock, V</searchLink><br /><searchLink fieldCode="AR" term="%22Johnson%2C+E+O%22">Johnson, E O</searchLink><br /><searchLink fieldCode="AR" term="%22Kang%2C+S%22">Kang, S</searchLink><br /><searchLink fieldCode="AR" term="%22Kapoor%2C+M%22">Kapoor, M</searchLink><br /><searchLink fieldCode="AR" term="%22Kramer%2C+J%22">Kramer, J</searchLink><br /><searchLink fieldCode="AR" term="%22Kuperman%2C+S%22">Kuperman, S</searchLink>
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  Data: <searchLink fieldCode="JN" term="%22Molecular+Psychiatry%22">Molecular Psychiatry</searchLink>. Nov2013, Vol. 18 Issue 11, p1218-1224. 7p.
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  Data: Several studies have identified genes associated with alcohol-use disorders (AUDs), but the variation in each of these genes explains only a small portion of the genetic vulnerability. The goal of the present study was to perform a genome-wide association study (GWAS) in extended families from the Collaborative Study on the Genetics of Alcoholism to identify novel genes affecting risk for alcohol dependence (AD). To maximize the power of the extended family design, we used a quantitative endophenotype, measured in all individuals: number of alcohol-dependence symptoms endorsed (symptom count (SC)). Secondary analyses were performed to determine if the single nucleotide polymorphisms (SNPs) associated with SC were also associated with the dichotomous phenotype, DSM-IV AD. This family-based GWAS identified SNPs in C15orf53 that are strongly associated with DSM-IV alcohol-dependence symptom counts (P=4.5 × 10−8, inflation-corrected P=9.4 × 10−7). Results with DSM-IV AD in the regions of interest support our findings with SC, although the associations were less significant. Attempted replications of the most promising association results were conducted in two independent samples: nonoverlapping subjects from the Study of Addiction: Genes and Environment (SAGE) and the Australian Twin Family Study of AUDs (OZALC). Nominal association of C15orf53 with SC was observed in SAGE. The variant that showed strongest association with SC, rs12912251 and its highly correlated variants (D′=1, r2 0.95), have previously been associated with risk for bipolar disorder. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Molecular Psychiatry is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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