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Genome‐wide linkage analysis using genetic variance components of alcohol dependency‐associated censored and continuous traits
Author(s) -
Palmer Lyle J.,
Tiller Katrina J.,
Burton Paul R.
Publication year - 1999
Publication title -
genetic epidemiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.301
H-Index - 98
eISSN - 1098-2272
pISSN - 0741-0395
DOI - 10.1002/gepi.1370170748
Subject(s) - linkage (software) , genetics , biology , genetic linkage , quantitative trait locus , covariate , statistics , gene , mathematics
We used variance‐components analysis to investigate the additive genetic effects regulating some of the phenotypes included in the GAW11 data set. Variance‐components models were fitted using Gibbs sampling methods in BUGS v 0.6. Linkage analyses for both multivariate normal (MvN) traits and right censored survival times (age‐of‐onset) were based upon standard Haseman‐Elston identity‐by‐descent sib‐pair methods applied directly to traits showing evidence of substantial additive genetic determination (residualized for any important covariates) and to the estimated σ 2 ∧ residuals for those traits. Harm avoidance behavior (TPQ subscale) showed evidence of linkage to markers on chromosomes 1, 13, and 18. P300 levels at the Fp1 site showed evidence of linkage to markers on chromosomes 2, 3, 9, 12, 17, 19, and 20. Platelet monoamine oxidase B (MAOB) levels showed evidence of linkage to D4S1651. The age‐of‐onset for ALDX1 in those over 30 years old showed evidence of linkage to markers on chromosomes 1, 6, 14, and 15. The age‐of‐onset for the more strictly defined ALDX2 in those over 30 years old showed evidence of linkage to markers on chromosomes 7 and 14. These results are consistent with a complex, multifactorial susceptibility to alcohol dependency.