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New understanding of schizophrenia could lead to new treatment approaches

New research helps bridge an important gap in understanding schizophrenia, providing the best evidence to date that defects in the brain's white matter are a key contributor to the disease, which affects about 1 percent of people worldwide. The findings, to be published online by the Proceedings of the National Academy of Sciences during the week of April 23, also demonstrate how two of the dozen or more genes previously linked with schizophrenia may contribute to the disease.

Prior genetic studies had linked schizophrenia to the genes for neuregulin 1 (NRG1), a growth factor involved in brain development, and erbB4, a receptor on brain cells through which NRG1 exerts its action. But until now it hadn't been shown that alterations in these genes lead to psychiatric disorders. Working in a mouse model, researchers led by Gabriel Corfas, PhD, Kristine Roy, PhD, and Joshua Murtie, PhD, in the Children's Hospital Boston Neurobiology Program now demonstrate, for the first time, that alterations in NRG1-erbB signaling induce pathologic changes in the brain's white matter. They further show that these changes lead to alterations in biochemical signaling and to behaviors suggestive of mental illness.

"We show that causing a defect in white matter is sufficient to cause biochemical and behavioral changes resembling those seen in neuropsychiatric disorders," says Corfas, the study's senior author. "I think this will provide a new way of thinking about the causes of, and possibly, therapies for schizophrenia."

The findings could also have implications for bipolar disorder, which has also been linked with NRG1 and also involves white matter defects, he adds.

Working with mice, the researchers blocked NRG1-erbB signaling in oligodendrocytes the cells that form the fatty sheath, known as myelin, which insulates nerve fibers. These myelinated nerve fibers make up the brain's white matter. When NRG1-erbB signaling was blocked, the mice ha
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Contact: James Newton
james.newton@childrens.harvard.edu
617-355-6420
Children's Hospital Boston
23-Apr-2007


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