| Autor: |
Martin Hautzinger, Manuel Mattheisen, Srdjan Djurovic, Jennifer Vollmer, Marian L. Hamshere, Michael Alexander, Alexander S. Tiganov, Maria Grigoroiu-Serbanescu, Johanna Sasse, Markus J. Schwarz, Scott D. Gordon, Michael Bauer, Lilia I. Abramova, René Breuer, H.-Erich Wichmann, Susanne Lucae, Susanne Moebus, Britta Haenisch, Carmen C. Diaconu, Grant W. Montgomery, Johannes Schumacher, Kari Stefansson, Jean-Pierre Kahn, Nicholas G. Martin, Wolfgang Maier, Piotr M. Czerski, Michael Steffens, Frank Bellivier, Ole A. Andreassen, Mark Lathrop, Joanna Hauser, Bertram Müller-Myhsok, Stéphane Jamain, Thomas F. Wienker, Omar Gustafsson, Hreinn Stefansson, Nicholas John Craddock, Lejla Kapur-Pojskić, Peter Tessmann, Chantal Henry, Fermín Mayoral, Michael Conlon O'Donovan, Jutta Kammerer-Ciernioch, Fabio Rivas, Liliana Oruc, Markus M. Nöthen, Alexander Chuchalin, Andreas Zimmer, Moritz Weingarten, Stefan Schreiber, Engilbert Sigurdsson, Sven Cichon, Adam Wright, Bruno Etain, Marcella Rietschel, Peter Propping, Franziska Degenhardt, Simon Heath, Thomas G. Schulze, Christine Schmäl, Galina Pantelejeva, Michael John Owen, Helmut Vedder, Christian Meesters, Andreas Reif, Gulja Babadjanova, Philip B. Mitchell, Jana Strohmaier, Thomas W. Mühleisen, Peter R. Schofield, Stefan Herms, Marion Leboyer, Stacy Steinberg, Sarah E. Medland, Lutz Priebe, Xavier Miró |
| Jazyk: |
angličtina |
| Předmět: |
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| Zdroj: |
The American Journal of Human Genetics. (3):372-381 |
| ISSN: |
0002-9297 |
| DOI: |
10.1016/j.ajhg.2011.01.017 |
| Popis: |
We conducted a genome-wide association study (GWAS) and a follow-up study of bipolar disorder (BD), a common neuropsychiatric disorder. In the GWAS, we investigated 499,494 autosomal and 12,484 X-chromosomal SNPs in 682 patients with BD and in 1300 controls. In the first follow-up step, we tested the most significant 48 SNPs in 1729 patients with BD and in 2313 controls. Eight SNPs showed nominally significant association with BD and were introduced to a meta-analysis of the GWAS and the first follow-up samples. Genetic variation in the neurocan gene (NCAN) showed genome-wide significant association with BD in 2411 patients and 3613 controls (rs1064395, p = 3.02 × 10(-8); odds ratio = 1.31). In a second follow-up step, we replicated this finding in independent samples of BD, totaling 6030 patients and 31,749 controls (p = 2.74 × 10(-4); odds ratio = 1.12). The combined analysis of all study samples yielded a p value of 2.14 × 10(-9) (odds ratio = 1.17). Our results provide evidence that rs1064395 is a common risk factor for BD. NCAN encodes neurocan, an extracellular matrix glycoprotein, which is thought to be involved in cell adhesion and migration. We found that expression in mice is localized within cortical and hippocampal areas. These areas are involved in cognition and emotion regulation and have previously been implicated in BD by neuropsychological, neuroimaging, and postmortem studies. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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