Journal
AMERICAN JOURNAL OF HUMAN GENETICS
Volume 73, Issue 1, Pages 107-114Publisher
CELL PRESS
DOI: 10.1086/376562
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Funding
- NHGRI NIH HHS [N01HG65403, N01 HG 65403] Funding Source: Medline
- NIAAA NIH HHS [AA 13358, AA 00285, F32 AA013358] Funding Source: Medline
- NIMH NIH HHS [R01 MH059545, R01 MH059567, MH 60068, R01 MH060068, R01 MH 59545, MH 59567] Funding Source: Medline
- PHS HHS [R01 59553] Funding Source: Medline
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We conducted genomewide linkage analyses on 1,152 individuals from 250 families segregating for bipolar disorder and related affective illnesses. These pedigrees were ascertained at 10 sites in the United States, through a proband with bipolar I affective disorder and a sibling with bipolar I or schizoaffective disorder, bipolar type. Uniform methods of ascertainment and assessment were used at all sites. A 9-cM screen was performed by use of 391 markers, with an average heterozygosity of 0.76. Multipoint, nonparametric linkage analyses were conducted in affected relative pairs. Additionally, simulation analyses were performed to determine genomewide significance levels for this study. Three hierarchical models of affection were analyzed. Significant evidence for linkage (genomewide P < .10) was found on chromosome 17q, with a peak maximum LOD score of 3.63, at the marker D17S928, and on chromosome 6q, with a peak maximum LOD score of 3.61, near the marker D6S1021. These loci met both standard and simulation-based criteria for genomewide significance. Suggestive evidence of linkage was observed in three other regions (genomewide P <.10), on chromosomes 2p, 3q, and 8q. This study, which is based on the largest linkage sample for bipolar disorder analyzed to date, indicates that several genes contribute to bipolar disorder.
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