Abstract
Parent-of-origin effects have been implicated as mediators of genetic susceptibility for a number of complex disease phenotypes, including bipolar disorder. Specifically, evidence for linkage on chromosome 18 is modified when allelic parent-of-origin is accommodated in the analysis. Our goal was to characterize the susceptibility locus for bipolar I disorder on chromosome 18p11 and investigate this parent-of-origin hypothesis in an association context. This was achieved by genotyping single nucleotide polymorphisms (SNPs) at a high density (1 SNP/5 kb) along 13.6 megabases of the linkage region. To increase our ability to detect a susceptibility locus, we restricted the phenotype definition to include only bipolar I probands. We also restricted our study population to Ashkenazi Jewish individuals; this population has characteristics of a genetic isolate and may therefore facilitate detection of variants for complex disease. Three hundred and forty-four pedigrees (363 parent/child trios) where probands were affected with bipolar 1 disorder were genotyped. Transmission disequilibrium test analysis revealed no statistically significant association to SNPs or haplotypes within this region in this sample. However, when parent-of-origin of transmitted SNPs was taken into account, suggestive association was revealed for two separate loci.
Original language | English (US) |
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Pages (from-to) | 367-375 |
Number of pages | 9 |
Journal | Molecular psychiatry |
Volume | 12 |
Issue number | 4 |
DOIs | |
State | Published - Apr 30 2007 |
Keywords
- 18p11
- Bipolar disorder
- Genetic association
- Parent of origin
- Psychiatric genetics
- Transmission disequilibrium
ASJC Scopus subject areas
- Molecular Biology
- Cellular and Molecular Neuroscience
- Psychiatry and Mental health