A genome-wide association study implicates diacylglycerol kinase eta (DGKH) and several other genes in the etiology of bipolar disorder.
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| Title: | A genome-wide association study implicates diacylglycerol kinase eta (DGKH) and several other genes in the etiology of bipolar disorder. |
|---|---|
| Authors: | Baum, A. E., Akula, N., Cabanero, M., Cardona, I., Corona, W., Klemens, B., Schulze, T. G., Cichon, S., Rietschel, M., Nöthen, M. M., Georgi, A., Schumacher, J., Schwarz, M., Jamra, R. Abou, Höfels, S., Propping, P., Satagopan, J., Detera-Wadleigh, S. D., Hardy, J., McMahon, F. J. |
| Source: | Molecular Psychiatry. Feb2008, Vol. 13 Issue 2, p197-207. 11p. 2 Diagrams, 3 Charts, 2 Graphs. |
| Subjects: | Genetics, Bipolar disorder, Genetic polymorphisms, DNA, Diglycerides, Etiology of diseases, Pathological psychology, Genomes, DNA replication, Heredity |
| Abstract: | The genetic basis of bipolar disorder has long been thought to be complex, with the potential involvement of multiple genes, but methods to analyze populations with respect to this complexity have only recently become available. We have carried out a genome-wide association study of bipolar disorder by genotyping over 550 000 single-nucleotide polymorphisms (SNPs) in two independent case-control samples of European origin. The initial association screen was performed using pooled DNA, and selected SNPs were confirmed by individual genotyping. While DNA pooling reduces power to detect genetic associations, there is a substantial cost saving and gain in efficiency. A total of 88 SNPs, representing 80 different genes, met the prior criteria for replication in both samples. Effect sizes were modest: no single SNP of large effect was detected. Of 37 SNPs selected for individual genotyping, the strongest association signal was detected at a marker within the first intron of diacylglycerol kinase eta (DGKH; P=1.5 × 10−8, experiment-wide P<0.01, OR=1.59). This gene encodes DGKH, a key protein in the lithium-sensitive phosphatidyl inositol pathway. This first genome-wide association study of bipolar disorder shows that several genes, each of modest effect, reproducibly influence disease risk. Bipolar disorder may be a polygenic disease.Molecular Psychiatry (2008) 13, 197–207; doi:10.1038/sj.mp.4002012; published online 8 May 2007 [ABSTRACT FROM AUTHOR] |
| Copyright of Molecular Psychiatry is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) | |
| Database: | Psychology and Behavioral Sciences Collection |
| FullText | Links: – Type: pdflink Text: Availability: 0 |
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| Header | DbId: pbh DbLabel: Psychology and Behavioral Sciences Collection An: 28457055 AccessLevel: 6 PubType: Academic Journal PubTypeId: academicJournal PreciseRelevancyScore: 0 |
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Feb2008, Vol. 13 Issue 2, p197-207. 11p. 2 Diagrams, 3 Charts, 2 Graphs. – Name: Subject Label: Subjects Group: Su Data: <searchLink fieldCode="DE" term="%22Genetics%22">Genetics</searchLink><br /><searchLink fieldCode="DE" term="%22Bipolar+disorder%22">Bipolar disorder</searchLink><br /><searchLink fieldCode="DE" term="%22Genetic+polymorphisms%22">Genetic polymorphisms</searchLink><br /><searchLink fieldCode="DE" term="%22DNA%22">DNA</searchLink><br /><searchLink fieldCode="DE" term="%22Diglycerides%22">Diglycerides</searchLink><br /><searchLink fieldCode="DE" term="%22Etiology+of+diseases%22">Etiology of diseases</searchLink><br /><searchLink fieldCode="DE" term="%22Pathological+psychology%22">Pathological psychology</searchLink><br /><searchLink fieldCode="DE" term="%22Genomes%22">Genomes</searchLink><br /><searchLink fieldCode="DE" term="%22DNA+replication%22">DNA replication</searchLink><br /><searchLink fieldCode="DE" term="%22Heredity%22">Heredity</searchLink> – Name: Abstract Label: Abstract Group: Ab Data: The genetic basis of bipolar disorder has long been thought to be complex, with the potential involvement of multiple genes, but methods to analyze populations with respect to this complexity have only recently become available. We have carried out a genome-wide association study of bipolar disorder by genotyping over 550 000 single-nucleotide polymorphisms (SNPs) in two independent case-control samples of European origin. The initial association screen was performed using pooled DNA, and selected SNPs were confirmed by individual genotyping. While DNA pooling reduces power to detect genetic associations, there is a substantial cost saving and gain in efficiency. A total of 88 SNPs, representing 80 different genes, met the prior criteria for replication in both samples. Effect sizes were modest: no single SNP of large effect was detected. Of 37 SNPs selected for individual genotyping, the strongest association signal was detected at a marker within the first intron of diacylglycerol kinase eta (DGKH; P=1.5 × 10−8, experiment-wide P<0.01, OR=1.59). This gene encodes DGKH, a key protein in the lithium-sensitive phosphatidyl inositol pathway. This first genome-wide association study of bipolar disorder shows that several genes, each of modest effect, reproducibly influence disease risk. Bipolar disorder may be a polygenic disease.Molecular Psychiatry (2008) 13, 197–207; doi:10.1038/sj.mp.4002012; published online 8 May 2007 [ABSTRACT FROM AUTHOR] – Name: AbstractSuppliedCopyright Label: Group: Ab Data: <i>Copyright of Molecular Psychiatry is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.) |
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| RecordInfo | BibRecord: BibEntity: Identifiers: – Type: doi Value: 10.1038/sj.mp.4002012 Languages: – Code: eng Text: English PhysicalDescription: Pagination: PageCount: 11 StartPage: 197 Subjects: – SubjectFull: Genetics Type: general – SubjectFull: Bipolar disorder Type: general – SubjectFull: Genetic polymorphisms Type: general – SubjectFull: DNA Type: general – SubjectFull: Diglycerides Type: general – SubjectFull: Etiology of diseases Type: general – SubjectFull: Pathological psychology Type: general – SubjectFull: Genomes Type: general – SubjectFull: DNA replication Type: general – SubjectFull: Heredity Type: general Titles: – TitleFull: A genome-wide association study implicates diacylglycerol kinase eta (DGKH) and several other genes in the etiology of bipolar disorder. Type: main BibRelationships: HasContributorRelationships: – PersonEntity: Name: NameFull: Baum, A. E. – PersonEntity: Name: NameFull: Akula, N. – PersonEntity: Name: NameFull: Cabanero, M. – PersonEntity: Name: NameFull: Cardona, I. – PersonEntity: Name: NameFull: Corona, W. – PersonEntity: Name: NameFull: Klemens, B. – PersonEntity: Name: NameFull: Schulze, T. G. – PersonEntity: Name: NameFull: Cichon, S. – PersonEntity: Name: NameFull: Rietschel, M. – PersonEntity: Name: NameFull: Nöthen, M. M. – PersonEntity: Name: NameFull: Georgi, A. – PersonEntity: Name: NameFull: Schumacher, J. – PersonEntity: Name: NameFull: Schwarz, M. – PersonEntity: Name: NameFull: Jamra, R. Abou – PersonEntity: Name: NameFull: Höfels, S. – PersonEntity: Name: NameFull: Propping, P. – PersonEntity: Name: NameFull: Satagopan, J. – PersonEntity: Name: NameFull: Detera-Wadleigh, S. D. – PersonEntity: Name: NameFull: Hardy, J. – PersonEntity: Name: NameFull: McMahon, F. J. IsPartOfRelationships: – BibEntity: Dates: – D: 01 M: 02 Text: Feb2008 Type: published Y: 2008 Identifiers: – Type: issn-print Value: 13594184 Numbering: – Type: volume Value: 13 – Type: issue Value: 2 Titles: – TitleFull: Molecular Psychiatry Type: main |
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