Possible Epistatic Role of ADH7 in the Protection Against Alcoholism

M. V. Osier; R. B. Lu; A. J. Pakstis; J. R. Kidd; S. Y. Huang; Kenneth K. Kidd

Possible Epistatic Role of ADH7 in the Protection Against Alcoholism

M. V. Osier, R. B. Lu, A. J. Pakstis, J. R. Kidd, S. Y. Huang, Kenneth K. Kidd

Department of Psychiatry

Research output: Contribution to journal › Article › peer-review

33 Citations (Scopus)

Abstract

In recent studies of the role of the alcohol dehydrogenase genes (ADH) in alcoholism the ADH1B Arg47His polymorphism appears to affect risk via a protective effect associated with the ADH1B*47His. Here we present evidence for an additional effect from outside the Class I ADH genes, presumably from functional variation at the ADH7 gene. The protective effect is restricted to one of two haplotypes identical at ADH1B but differing at an intronic SNP at ADH7 suggesting epistasis or strong linkage disequilibrium (LD).

Original language	English
Pages (from-to)	19-22
Number of pages	4
Journal	American Journal of Medical Genetics - Neuropsychiatric Genetics
Volume	126 B
Issue number	1
Publication status	Published - 2004 Apr 1

All Science Journal Classification (ASJC) codes

Genetics(clinical)
Psychiatry and Mental health
Cellular and Molecular Neuroscience

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AU - Osier, M. V.

AU - Lu, R. B.

AU - Pakstis, A. J.

AU - Kidd, J. R.

AU - Huang, S. Y.

AU - Kidd, Kenneth K.

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N2 - In recent studies of the role of the alcohol dehydrogenase genes (ADH) in alcoholism the ADH1B Arg47His polymorphism appears to affect risk via a protective effect associated with the ADH1B*47His. Here we present evidence for an additional effect from outside the Class I ADH genes, presumably from functional variation at the ADH7 gene. The protective effect is restricted to one of two haplotypes identical at ADH1B but differing at an intronic SNP at ADH7 suggesting epistasis or strong linkage disequilibrium (LD).

AB - In recent studies of the role of the alcohol dehydrogenase genes (ADH) in alcoholism the ADH1B Arg47His polymorphism appears to affect risk via a protective effect associated with the ADH1B*47His. Here we present evidence for an additional effect from outside the Class I ADH genes, presumably from functional variation at the ADH7 gene. The protective effect is restricted to one of two haplotypes identical at ADH1B but differing at an intronic SNP at ADH7 suggesting epistasis or strong linkage disequilibrium (LD).

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