Alessandro Bertolino, M.D., Ph.D., of the University of Bari, is studying epigenetic risk for schizophrenia. Epigenetics refers to environmentally-induced events that alter gene activity. Having demonstrated that methylation of the gene COMT (Catechol-O-methyltransferase) affects the functioning of dopamine, a brain chemical involved in schizophrenia, the Bertolino lab plans to now evaluate DNA methylation interaction with genes controlling dopamine pathways.
Peng Jin, Ph.D., of Emory University, proposes to expand testing his hypothesis that malfunction of a genetic regulator of neurodevelopment called microRNA-137 (miR-137) contributes to the development of schizophrenia. Postmortem brain-tissue studies suggest that miR-137 is down-regulated in schizophrenia. To explore its activity in a living organism, Dr. Jin and colleagues have bred mice with a disabled miR-137 gene.
Carsten Korth, M.D. Ph.D., of the University of Dsseldorf, is examining the interaction of DISC1, a key risk gene for schizophrenia, and dopamine, a chemical neurotransmitter of messages between nerve cells. The Korth lab has identified a novel function of DISC1 in modulating the dopamine transporter, the molecule critical to reuptake of released dopamine following neural communication. The lab will now conduct animal studies to characterize DISC1 and dopamine transporter interaction.
Antonieta Lavin, Ph.D., of the Medical University of South Carolina, will explore the underlying mechanisms of the decreases in release of the brain chemical glutamate and the role of the protein dysbindin in relation to the cognitive deficits associated with schizophrenia. Brain tissues from schizophrenia patients show
|Contact: Sally Corbett|
Brain & Behavior Research Foundation