Genetic linkage analysis of bipolar affective disorder in an Old Order Amish pedigree |
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| Authors: | Adam Law Charles W. Richard III Robert W. Cottingham Jr. G. Mark Lathrop David R. Cox Richard M. Myers |
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| Affiliation: | (1) Department of Physiology, University of California San Francisco, San Francisco, California, USA;(2) Department of Psychiatry, University of California San Francisco, San Francisco, California, USA;(3) Department of Biochemistry and Biophysics, University of California San Francisco, San Francisco, California, USA;(4) Centre d'Etude du Polymorphisme Humain, Paris, France;(5) Present address: Department of Biochemistry, Cell and Molecular Biology, Division of Biological Sciences, Cornell University, 14853 Ithaca, NY, USA;(6) Present address: Department of Cell Biology, Baylor College of Medicine, 77030 Houston, TX, USA;(7) Department of Physiology, University of California San Francisco, 513 Parnassus Avenue, box 0444, 94143 San Francisco, CA, USA |
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| Abstract: | ![]()
Summary We have used genetic linkage analysis in an effort to identify a gene responsible for bipolar affective disorder (BAD) in an Old Order Amish pedigree. The initial study of this pedigree showed strong evidence for linkage of the chromosome 11p15 markers HRAS1 and the insulin gene (INS) to BAD, whereas a second report found no evidence for linkage. We have independently determined the INS and HRAS1 genotypes from 81 individuals in this pedigree. A polymerase chain reaction (PCR) assay was used to score INS alleles that are difficult to distinguish from one another by conventional agarose gel electrophoresis. In addition, we used four separate diagnostic models to score individuals with psychiatric illness as either affected or unaffected. No evidence of significant linkage between BAD and the markers was found with either two-point or multipoint analysis regardless of which diagnostic model was used. However, exclusion of the region of chromosome 11 between INS and RAS1 as a possible location for the BAD gene in this family depended on the diagnostic model. Further genetic linkage studies with additional DNA markers that span the genome are necessary to determine the chromosomal location of the BAD gene in this family. |
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