Nature Neuroscience 8, 1500 - 1502 (2005)
Published online: 23 October 2005; | doi:10.1038/nn1572
COMT genotype predicts longitudinal cognitive decline and psychosis in 22q11.2 deletion syndromeDoron Gothelf1, 2, Stephan Eliez3, Tracy Thompson1, Christine Hinard4, Lauren Penniman1, Carl Feinstein1, Hower Kwon5, Shuting Jin1, Booil Jo1, Stylianos E Antonarakis6, Michael A Morris4
& Allan L Reiss11
Center for Interdisciplinary Brain Sciences Research, Stanford University School of Medicine, 401 Quarry Road, Stanford, California 94305–5795, USA. 2
Sackler Faculty of Medicine, Tel Aviv University, Ramat Aviv, Israel. 3
Department of Psychiatry, University of Geneva School of Medicine, 41 Ch. des Crêts-de-Champel, CH-1206 Geneva, Switzerland. 4
Medical Genetics Service, University Hospitals, 1 Rue Michel Servet, 1211 Geneva, Switzerland. 5
Department of Psychiatry and Behavioral Sciences, University of Washington, Box 359911, Seattle, Washington 98104, USA. 6
Department of Genetic Medicine and Development, University Medical School, Centre Medicale Universitaire, 1 Rue Michel Servet, 1211 Geneva, Switzerland.
Correspondence should be addressed to Allan L Reiss reiss@stanford.edu Although schizophrenia is strongly hereditary, there are limited data regarding biological risk factors and pathophysiological processes. In this longitudinal study of adolescents with 22q11.2 deletion syndrome, we identified the catechol-O-methyltransferase low-activity allele (COMT
L) as a risk factor for decline in prefrontal cortical volume and cognition, as well as for the consequent development of psychotic symptoms during adolescence. The 22q11.2 deletion syndrome is a promising model for identifying biomarkers related to the development of schizophrenia.
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