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Schizophrenia related portal that aims to solve the mystery of genetic predisposition to psychosis, develop new methods for early diagnosis and prevention, and discover new treatments that will cure people suffering from it. Our objectives are to fully characterize: # neurobiological mechanisms related to susceptibility genes for schizophrenia and related clinical disorders; # genetic variation in aspects of cognition and emotionality associated with schizophrenia; and # small molecular targets for novel therapies. A unique feature of this Program is that its diverse scientific resources will be focused on a highly specific scientific agenda, that is to acquire the critical biological information about the susceptibility genes associated with schizophrenia and related illnesses. Our mission and goal, to understand the basic mechanisms of serious mental illness, has again guided us into new areas of research and to new insights. We have found evidence of new genes implicated in the cause of schizophrenia and involved in brain functions related to cognition and emotion and we have begun to explore how genes interact with each other and with the environment to individualize risk for these conditions. We are working now with over 20 genes related to schizophrenia. One of the key developments in our research over the past year has been the emergence of some targets for the development of novel therapeutics. We have discovered a new schizophrenia susceptibility gene, KCNH2, which represents the first clear target for the development of novel treatments. Just in this past year, for example, we published the first extensive statistical analysis of how schizophrenia genes may vary in their risk effects based on different genetic background (Nicodemus et al Hum Gen 2006), the first studies of schizophrenia genes interacting in effecting gene expression in brain (Lipska et al Hum Mol Genetics 2006a, Lipska et al Hum Mol Gen 2006 b); the first evidence that the mechanism of genetic association of NRG1 with schizophrenia involves a novel isoform of the gene in human brain (Law et al PNAS 2006), and the first evidence that MAOA may be linked to mood and impulse control because it effects critical mood regulatory neural networks (Meyer-Lindenberg et al PNAS 2006).
Proper citation: Genes Cognition and Psychosis Program (RRID:SCR_006292) Copy
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