Journal
GENES BRAIN AND BEHAVIOR
Volume 13, Issue 2, Pages 195-201Publisher
WILEY
DOI: 10.1111/gbb.12095
Keywords
Anxiety disorder; bipolar disorder; catenin 2; genetic association; humans; major depression; rats; schizophrenia
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Funding
- Netherlands Organization for Scientific Research (NWO)
- MagW/ZonMW grants [Middelgroot-911-09-032, Spinozapremie 56-464-14192]
- Netherlands Organization for Health Research and Development [ZonMW 10-000-1002]
- Center for Medical Systems Biology (CSMB, NWO Genomics)
- ZonMW [912-10-020]
- NBIC/BioAssist/RK [2008.024]
- Biobanking and Biomolecular Resources Research Infrastructure (BBMRI- NL) [184.021.007]
- VU University's Institute for Health and Care Research (EMGO+)
- Neuroscience Campus Amsterdam (NCA)
- European Science Council (ERC) [230374]
- Genetic Association Information Network (GAIN) of the Foundation for the National Institutes of Health
- Rutgers University Cell and DNA Repository [NIMH U24 MH068457-06]
- Avera Institute, Sioux Falls, South Dakota (USA)
- National Institutes of Health [NIH R01 HD042157-01A1, MH081802, 1RC2 MH089951, 1RC2 MH089995]
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The rat genome sequencing and mapping consortium found evidence for an association between the catenin-2 gene (CTNND2) and anxious behaviour. We replicated these results in humans by carrying out a genetic association test in patients with panic disorder, social phobia, generalized anxiety disorder and/or agoraphobia (N=1714) and controls (N=4125). We further explored the association between CTNND2 and other psychiatric disorders based on publicly available genome-wide association results. A gene-based test showed that single nucleotide polymorphisms (SNPs) in CTNND2 have a significantly increased signal (P<1e(-5)) and decreased P-values. Single nucleotide polymorphism rs1012176 showed the strongest association with any anxiety disorder (odds ratio: 0.8128, SE=0.063, P=0.00099), but this effect was not significant after correction for multiple testing. In available genome-wide association results from the Psychiatric Genomics Consortium we found that SNPs in CTNND2 collectively showed an increased signal for schizophrenia (P<1e(-5)) and major depressive disorder (P<1e(-5)), but not for bipolar disorder. These signals remained significant after correction for potential confounders. The association between CTNND2 and anxiety was not strong enough to be picked up in the current generation of human genome-wide analyses, indicating the usefulness of and need for animal genetic studies to identify candidate genes for further study in human samples.
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