期刊
MOLECULAR PSYCHIATRY
卷 21, 期 10, 页码 1391-1399出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/mp.2015.197
关键词
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资金
- NIH grant [R01MH87646]
- Japan Society for the Promotion of Science [21-8373]
- IMH Schizophrenia Genetics Initiative U01s [MH046276, MH46289, MH46318]
- MGS Part 1 (MGS1)
- Research Institute for Diseases in the Elderly (RIDE2) [014-93-015]
- Netherlands Genomics Initiative (NGI)/Netherlands Consortium for Healthy Ageing (NCHA) [050-060-810]
- Vidi [017.106.370]
- Erasmus Medical Center, Rotterdam
- Netherlands Organization for the Health Research and Development (ZonMw)
- Ministry of Education, Culture and Science
- Ministry for Health, Welfare and Sports
- Federal Ministry of Education and Research [01ZZ9603, 01ZZ0103, 01ZZ040, 03ZIK012]
- Ministry of Cultural Affairs
- Social Ministry of the Federal State of Mecklenburg-West Pomerania
- Siemens Healthcare, Erlangen, Germany
- Federal State of Mecklenburg-West Pomerania
- Grants-in-Aid for Scientific Research [25461723, 26461712] Funding Source: KAKEN
Anxiety disorders (ADs), namely generalized AD, panic disorder and phobias, are common, etiologically complex conditions with a partially genetic basis. Despite differing on diagnostic definitions based on clinical presentation, ADs likely represent various expressions of an underlying common diathesis of abnormal regulation of basic threat-response systems. We conducted genome-wide association analyses in nine samples of European ancestry from seven large, independent studies. To identify genetic variants contributing to genetic susceptibility shared across interview-generated DSM-based ADs, we applied two phenotypic approaches: (1) comparisons between categorical AD cases and supernormal controls, and (2) quantitative phenotypic factor scores (FS) derived from a multivariate analysis combining information across the clinical phenotypes. We used logistic and linear regression, respectively, to analyze the association between these phenotypes and genome-wide single nucleotide polymorphisms. Meta-analysis for each phenotype combined results across the nine samples for over 18 000 unrelated individuals. Each meta-analysis identified a different genome-wide significant region, with the following markers showing the strongest association: for case-control contrasts, rs1709393 located in an uncharacterized non-coding RNA locus on chromosomal band 3q12.3 (P = 1.65 x 10(-8)); for FS, rs1067327 within CAMKMT encoding the calmodulin-lysine N-methyltransferase on chromosomal band 2p21 (P = 2.86 x 10(-9)). Independent replication and further exploration of these findings are needed to more fully understand the role of these variants in risk and expression of ADs.
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