% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Hansen:17372,
      author       = {Hansen, T. and Ingason, A. and Djurovic, S. and Melle, I.
                      and Fenger, M. and Gustafsson, O. and Jakobsen, K.D. and
                      Ramussen, H.B. and Tosato, S. and Rietschel, M. and Frank,
                      J. and Owen, M. and Bonetto, C. and Suvisaari, J. and
                      Thygesen, J.H. and Petursson, H. and Lönnqvist, J. and
                      Sigurdsson, E. and Giegling, I. and Craddock, N. and
                      O'Donovan, M.C. and Ruggeri, M. and Cichon, S. and Ophoff,
                      R.A. and Pietiläinen, O. and Peltonen, L. and Nöthen, M.M.
                      and Rujescu, D. and St. Clair, D. and Collier, D.A. and
                      Andreassen, O.A. and Werge, T.},
      title        = {{A}t-risk variant in {TCF}7{L}2 for type {II} diabetes
                      increases risk of schizophrenia},
      journal      = {Biological psychiatry},
      volume       = {70},
      issn         = {0006-3223},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {PreJuSER-17372},
      pages        = {59 - 63},
      year         = {2011},
      note         = {We thank Hreinn Stefansson (DeCODE Genetics) for making the
                      Icelandic data available and commenting the manuscript.
                      Sadly, Leena Peltonen passed away after this study was
                      ended. We acknowledge the expert assistance of numerous
                      mental health professionals in the various clinical
                      departments. This work was sponsored by European Union
                      grants LSHM-CT-2006-037761 (Project SGENE,
                      http://www.sgene.eu) and PIAP-GA-2008-218251 (Project
                      PsychGene, http://www.psych-gene.eu). The work was also
                      supported by grants to Thomas Werge from the Copenhagen
                      Hospital Corporation Research Fund and the Danish National
                      Psychiatric Research Foundation, the Danish Agency for
                      Science, Technology and Innovation (Centre for
                      Pharmacogenomics), and the Danish Medical Research Council.
                      The Research Council of Norway supported the study (Grant
                      Nos. 167153/v50 and 163070/V50) together with Norwegian
                      South-Eastern Health Authority (Grant No. 123-2004) and
                      University of Oslo and Oslo University Hospital. Eli Lilly,
                      Inc., funded parts of the genotyping of the Norwegian
                      sample.},
      abstract     = {Schizophrenia is associated with increased risk of type II
                      diabetes and metabolic disorders. However, it is unclear
                      whether this comorbidity reflects shared genetic risk
                      factors, at-risk lifestyle, or side effects of antipsychotic
                      medication.Eleven known risk variants of type II diabetes
                      were genotyped in patients with schizophrenia in a sample of
                      410 Danish patients, each matched with two healthy control
                      subjects on sex, birth year, and month. Replication was
                      carried out in a large multinational European sample of 4089
                      patients with schizophrenia and 17,597 controls (SGENE+)
                      using Mantel-Haenszel test.One type II diabetes at-risk
                      allele located in TCF7L2, rs7903146 [T], was associated with
                      schizophrenia in the discovery sample (p = .0052) and in the
                      replication with an odds ratio of 1.07 $(95\%$ confidence
                      interval 1.01-1.14, p = .033).The association reported here
                      with a well-known diabetes variant suggests that the
                      observed comorbidity is partially caused by genetic risk
                      variants. This study also demonstrates how genetic studies
                      can successfully examine an epidemiologically derived
                      hypothesis of comorbidity.},
      keywords     = {Alleles / Case-Control Studies / Diabetes Mellitus, Type 2:
                      genetics / Female / Genetic Association Studies: methods /
                      Genetic Predisposition to Disease: genetics / Genotype /
                      Humans / Male / Polymorphism, Single Nucleotide /
                      Schizophrenia: genetics / Transcription Factor 7-Like 2
                      Protein: genetics / TCF7L2 protein, human (NLM Chemicals) /
                      Transcription Factor 7-Like 2 Protein (NLM Chemicals) / J
                      (WoSType)},
      cin          = {INM-1},
      ddc          = {570},
      cid          = {I:(DE-Juel1)INM-1-20090406},
      pnm          = {Funktion und Dysfunktion des Nervensystems (FUEK409) /
                      89571 - Connectivity and Activity (POF2-89571) / PSYCHGENE -
                      Copy Number Variation and Endophenotypes in Psychiatric
                      Disorders (218251)},
      pid          = {G:(DE-Juel1)FUEK409 / G:(DE-HGF)POF2-89571 /
                      G:(EU-Grant)218251},
      shelfmark    = {Neurosciences / Psychiatry},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:21414605},
      UT           = {WOS:000291559300012},
      doi          = {10.1016/j.biopsych.2011.01.031},
      url          = {https://juser.fz-juelich.de/record/17372},
}