Genome-wide linkage analysis using genetic variance components of alcohol dependency-associated censored and continuous traits

We used variance-components analysis to investigate the additive genetic ef fects regulating some of the phenotypes included in the GAW11 data set. Var iance-components models were fitted using Gibbs sampling methods in BUGS v 0.6. Linkage analyses for both multivariate normal (MvN) traits and right c ensored survival times (age-of-onset) were based upon standard Haseman-Elst on identity-by-descent sib-pair methods applied directly to traits showing evidence of substantial additive genetic determination (residualized for an y important covariates) and to the estimated a: residuals for those traits. Harm avoidance behavior (TPQ subscale) showed evidence of linkage to marke rs on chromosomes 1, 13, and 18. P300 levels at the Fp1 site showed evidenc e of linkage to markers on chromosomes 2, 3, 9, 12, 17, 19, and 20. Platele t 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 li nkage 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 l inkage to markers on chromosomes 7 and 14. These results are consistent wit h a complex, multifactorial susceptibility to alcohol dependency. (C) 1999 Wiley-Liss, Inc.