Association between schizophrenia and common variation in neurocan (NCAN), a genetic risk factor for bipolar disorder

Thomas W. Mühleisen, Manuel Mattheisen, Jana Strohmaier, Franziska Degenhardt, Lutz Priebe, C. Christoph Schultz, René Breuer, Sandra Meier, Per Hoffmann, Fernando Rivandeneira, Albert Hofman, André G. Uitterlinden, Susanne Moebus, Christian Gieger, Rebecca Emeny, Karl Heinz Ladwig, H. Erich Wichmann, Markus Schwarz, Jutta Kammerer-Ciernioch, Ralf G.M. SchlösserIgor Nenadic, Heinrich Sauer, Rainald Mössner, Wolfgang Maier, Dan Rujescu, Christoph Lange, Roel A. Ophoff, Thomas G. Schulze, Marcella Rietschel, Markus M. Nöthen, Sven Cichon

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69 Citations (Scopus)

Résumé

A recent study found genome-wide significant association between common variation in the gene neurocan (NCAN, rs1064395) and bipolar disorder (BD). In view of accumulating evidence that BD and schizophrenia partly share genetic risk factors, we tested this single-nucleotide polymorphism for association with schizophrenia in three independent patient-control samples of European ancestry, totaling 5061 patients and 9655 controls. The rs1064395 A-allele, which confers risk for BD, was significantly over-represented in schizophrenia patients compared to controls (p=2.28×10 -3; odds ratio=1.11). Follow-up in non-overlapping samples from the Schizophrenia Psychiatric GWAS Consortium (5537 patients, 8043 controls) provided further support for our finding (p=0.0239, odds ratio=1.07). Our data suggest that genetic variation in NCAN is a common risk factor for BD and schizophrenia.

Langue d'origineEnglish
Pages (de-à)69-73
Nombre de pages5
JournalSchizophrenia Research
Volume138
Numéro de publication1
DOI
Statut de publicationPublished - juin 2012
Publié à l'externeOui

Note bibliographique

Funding Information:
The HNR study was conducted with the support of the Heinz Nixdorf Foundation, part of the genetic analyses was financed by the Medical Faculty of the University Hospital of Essen. The KORA study was initiated and financed by the Helmholtz Zentrum München — National Research Center for Environmental Health which is funded by the BMBF and by the State of Bavaria. Part of KORA was financed by the NGFN (NGFN-2 and NGFNplus grant 01GS0823) and supported within the Munich Center of Health Sciences (MC Health) as part of LMUinnovativ. Genotyping of the Dutch samples from Utrecht was sponsored by NIMH funding, R01 MH078075. Funding support for the Molecular Genetics of Schizophrenia (MGS) sample was provided by the National Institute of Mental Health (R01 MH67257, R01 MH59588, R01 MH59571, R01 MH59565, R01 MH59587, R01 MH60870, R01 MH59566, R01 MH59586, R01 MH61675, R01 MH60879, R01 MH81800, U01 MH46276, U01 MH46289, U01 MH46318, U01 MH79469, and U01 MH79470) and the genotyping of the sample was provided through the Genetic Association Information Network (GAIN). The datasets used for the analyses described in this manuscript were obtained from the database of Genotypes and Phenotypes (dbGaP) found at http://www.ncbi.nlm.nih.gov/gap through dbGaP accession numbers phs000167.v1.p1 and phs000021.v3.p2. Samples and associated phenotype data for the MGS sample were provided by the MGS Collaboration (PI: Pablo V. Gejman, Evanston Northwestern Healthcare (ENH) and Northwestern University, Evanston, IL, USA). The above mentioned funding sources had no involvement in the study design, the analysis and interpretation of data, the writing of the report, or the decision to submit the paper for publication.

Funding Information:
This study was supported by the German Federal Ministry of Education and Research (BMBF), within the context of the German National Genome Research Network plus (NGFNplus), and the Integrated Genome Research Network (IG) MooDS (grant 01GS08144 to Sven Cichon and Markus M. Nöthen, grant 01GS08147 to Marcella Rietschel). Igor Nenadic was supported by a Junior Scientist Grant of the IZKF, Medical School, Jena University Hospital. Igor Nenadic, Heinrich Sauer, Markus M. Nöthen, and Sven Cichon were additionally supported through an EU grant (EUTwinsS network, RTN, FP6). Jana Strohmaier was supported by the German Research Foundation (GRK 793). Christoph Lange and Manuel Mattheisen were supported by grants U01 HL089856, R01 MH087590 and R01 MH081862.

ASJC Scopus Subject Areas

  • Psychiatry and Mental health
  • Biological Psychiatry

PubMed: MeSH publication types

  • Journal Article
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

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