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deCODE and SGENE Consortium Discover Deletions in the Human Genome Linked to Risk of Schizophrenia
Date:7/30/2008

0 schizophrenics and 33,000 control subjects. The deletions on chromosomes 1q21, 15q11 and 15q13 were suggestively associated with schizophrenia in this first phase, and then validated in 3,300 cases and 8,000 controls. The SGENE consortium is comprised of deCODE genetics, the National-University Hospital in Reykjavik, the University of Aberdeen, the Ravenscraig Hospital in Greenock, the Institute of Psychiatry at King's College London, the National Public Health Institute in Helsinki, the Ludwig Maximilians University and GlaxoSmithKline's Genetic Research Center in Munich. The SGENE affiliated groups taking part in the second phase of the project were the University of Copenhagen, the University of Oslo, the University of Heidelberg, the University of Bonn, the University Medical Center of Utrecht, Nijmegen Medical Center, the University of Verona, the Duke University Center for Population Genomics and Pharmacogenetics and the University of Sichuan, China.

deCODE and the SGENE consortium gratefully acknowledge the participation in this study of the thousands of patients, family members and control subjects from these eleven countries. This study was supported by the European Union through the SGENE consortium (http://www.SGENE.eu), by grants LSHM-CT-2006-037761 and PIAP-GA-2008-218251.

About deCODE

deCODE is a biopharmaceutical company applying its discoveries in human genetics to the development of diagnostics and drugs for common diseases. deCODE is a global leader in gene discovery -- our population approach and resources have enabled us to isolate key genes contributing to major public health challenges from cardiovascular disease to cancer, genes that are providing us with drug targets rooted in the basic biology of disease. Through its CLIA-registered laboratory, deCODE is offering a growing range of DNA-based tests for gauging risk and empowering prevention of common diseases, including de
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