Lodewijk A. Sandkuijl: Deceased 12/04/02.
Brief Research Communication
Genetic mapping using haplotype and model-free linkage analysis supports previous evidence for a locus predisposing to severe bipolar disorder at 5q31-33†
Article first published online: 25 AUG 2003
Copyright © 2003 Wiley-Liss, Inc.
American Journal of Medical Genetics Part B: Neuropsychiatric Genetics
Volume 125B, Issue 1, pages 83–86, 15 February 2004
How to Cite
Hong, K. S., McInnes, L. A., Service, S. K., Song, T., Lucas, J., Silva, S., Fournier, E., León, P., Molina, J., Reus, V. I., Sandkuijl, L. A. and Freimer, N. B. (2004), Genetic mapping using haplotype and model-free linkage analysis supports previous evidence for a locus predisposing to severe bipolar disorder at 5q31-33. Am. J. Med. Genet., 125B: 83–86. doi: 10.1002/ajmg.b.20091
- Issue published online: 27 JAN 2004
- Article first published online: 25 AUG 2003
- Manuscript Accepted: 2 JUN 2003
- Manuscript Received: 19 FEB 2003
- The National Institutes of Health, (NIH) (to L.A.M.). Grant Number: MH-01748
- The National Institutes of Health, (NIH) (to N.B.F.). Grant Numbers: MH-00916, MH-49499
- The Vice Rectory of Research of the University of Costa Rica
- allele sharing methods;
- linkage analysis;
- population isolates
We report further evidence for our previous suggestion [Garner et al., 2001: Am J Hum Genet 68:1061–1064] of a locus on 5q predisposing to bipolar I disorder (BP-I) in an extended Costa Rican pedigree. We genotyped additional microsatellite markers in this region and applied a multi-point non-parametric linkage analysis (SimWalk2). Significant identity-by-descent allele sharing among affected relatives was observed for all of the 20 markers tested in a segment of approximately 15 cM. Most affected individuals shared a single haplotype over this region; breaks within this haplotype may suggest a more restricted candidate location for a BP-I gene. These results support the suggestion that a locus at 5q31-33, together with a previously reported locus at 18q22-23, may provide the major genetic risk for BP-I in this family. © 2003 Wiley-Liss, Inc.