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Effat S. Emamian, M.D. (Young Investigator 2004) of Rockefeller University, aims to study whether lower levels of the protein AKT1 may be implicated in schizophrenia by studying the behavior of a mouse missing the gene. Dr. Emamian’s preliminary studies have shown that white blood cells and brains of schizophrenic patients not treated with medications have decreased levels of AKT1. Further, in a large sample of families with schizophrenia, a certain AKT1 gene variant associated with lower protein levels also is associated with schizophrenia. Dr. Emamian hypothesizes AKT1 signaling contributes to schizophrenia pathogenesis and certain types of the gene may predispose someone to the disease. AKT1 is involved in protein phosphorylation, a regulatory process used by the nervous system to regulate the specificity, efficacy and plasticity of synaptic transmission. The antipsychotic halperidol increases the regulatory phosphorylation of AKT1 in mice with the gene and may explain the drug’s effect in schizophrenic patients. Dr. Emamian will subject knockout mice to a battery of tests that simulate schizophrenia. Program Area: SCHIZOPHRENIA/PSYCHOTIC DISORDERS\Schizophrenia |
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