Identification of loci associated with schizophrenia by genome-wide association and follow-up

Michael C. O'Donovan, Nicholas Craddock, Nadine Norton, Hywel Williams, Timothy Peirce, Valentina Moskvina, Ivan Nikolov, Marian Hamshere, Liam Carroll, Lyudmila Georgieva, Sarah Dwyer, Peter Holmans, Jonathan L. Marchini, Chris C.A. Spencer, Bryan Howie, Hin Tak Leung, Annette M. Hartmann, Hans Jürgen Möller, Derek W. Morris, Yong Yong ShiGuo Yin Feng, Per Hoffmann, Peter Propping, Catalina Vasilescu, Wolfgang Maier, Marcella Rietschel, Stanley Zammit, Johannes Schumacher, Emma M. Quinn, Thomas G. Schulze, Nigel M. Williams, Ina Giegling, Nakao Iwata, Masashi Ikeda, Ariel Darvasi, Sagiv Shifman, Lin He, Jubao Duan, Alan R. Sanders, Douglas F. Levinson, Pablo V. Gejman, Nancy G. Buccola, Bryan J. Mowry, Robert Freedman, Farooq Amin, Donald W. Black, Jeremy M. Silverman, William F. Byerley, C. Robert Cloninger, Sven Cichon, Markus M. Nöthen, Michael Gill, Aiden Corvin, Dan Rujescu, George Kirov, Michael J. Owen

Research output: Contribution to journalArticlepeer-review

935 Scopus citations


We carried out a genome-wide association study of schizophrenia (479 cases, 2,937 controls) and tested loci with P < 10-5 in up to 16,726 additional subjects. Of 12 loci followed up, 3 had strong independent support (P < 5 × 10-4), and the overall pattern of replication was unlikely to occur by chance (P = 9 × 10-8). Meta-analysis provided strongest evidence for association around ZNF804A (P = 1.61 × 10-7) and this strengthened when the affected phenotype included bipolar disorder (P = 9.96 × 10-9).

Original languageAmerican English
Pages (from-to)1053-1055
Number of pages3
JournalNature Genetics
Issue number9
StatePublished - Sep 2008

Bibliographical note

Funding Information:
The UK research was supported by grants from the MRC and the Wellcome Trust. We are grateful to the Wellcome Trust Case Control Consortium for access to control genotypes (and to the individuals acknowledged in that respect in ref. 4) and their contribution to the genome-wide study, and to the Welsh e-Science Centre at Cardiff University for access to computing resources for some of this work. In Dublin, the research was supported by Science Foundation Ireland, the Health Research Board (Ireland) and the Wellcome Trust. We are grateful to J. Waddington for sample recruitment. Irish controls were supplied by J. McPartlin and the Trinity College Biobank. In Bonn and Mannheim, the work was supported by the National Genomic Network of the ‘Bundesministerium für Bildung und Forschung’ (BMBF) and the Alfried Krupp von Bohlen und Halbach-Stiftung. We also thank the Department of Psychiatry, LMU Munich for clinical characterization of the Munich subjects and the processing of the samples. Recruitment in Munich was partially supported by GlaxoSmithKline. The Ashkenazi samples are part of the Hebrew University Genetic Resource.


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