|
|||||
|
|
Genome screening for linkage disequilibrium in a Costa Rican sample of patients with bipolar‐I disorder: A follow‐up study on chromosome 18 |
|
| Authors: | Michael A. Escamilla L. Alison McInnes Susan K. Service Mitzi Spesny Victor I. Reus Julio Molina Alvaro Gallegos Eduardo Fournier Steven Batki Thomas Neylan Carol Matthews Sophia Vinogradov Erin Roche David J. Tyler Norito Shimayoshi Roxana Mendez Rolando Ramirez Margarita Ramirez Carmen Araya Xinia Araya Pedro E. Leon Lodewijk A. Sandkuijl Nelson B. Freimer M.D. |
| Affiliation: | 1. Neurogenetics Laboratory, University of California at San Francisco, San Francisco, California;2. Center for Neurobiology and Psychiatry, University of California at San Francisco, San Francisco, California;3. Department of Psychiatry, University of California at San Francisco, San Francisco, California;4. Michael A. Escamilla and L. Alison McInnes contributed equally to this work.;5. Cell and Molecular Biology Research Center and Escuela de Medicina, Universidad de Costa Rica, San Jose, Costa Rica;6. Hospital Calderon Guardia, San José, Costa Rica;7. Alvaro Gallegos is deceased.;8. Department of Clinical Genetics, Erasmus University, Rotterdam, The Netherlands;9. Department of Human Genetics, Leiden University, Leiden, The Netherlands;10. Department of Human Genetics, University of Utrecht, Utrecht, The Netherlands |
| Abstract: | Linkage disequilibrium (LD) methods offer great promise for mapping complex traits, but have thus far been applied sparingly. In this paper we describe an LD mapping study of severe bipolar disorder (BP‐I) in the genetically isolated population of the Central Valley of Costa Rica. This study provides the first complete screen of a chromosome for a complex trait using LD mapping and presents the first application of a new LD mapping statistic (ancestral haplotype reconstruction (AHR)) that evaluates haplotype sharing among affected individuals. The results of this chromosome‐wide analysis are instructive for genome‐wide LD mapping in isolated populations. Furthermore, the analysis continues to support a possible BP‐I locus on 18pter, suggested by previous analyses in this population. Evidence for a possible BP‐I locus on 18q12.2 is also described. © 2001 Wiley‐Liss, Inc. |
| Keywords: | complex phenotype population isolate association mapping |