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Mouse model of schizophrenia could speed identification of new antipsychotic drugs

Howard Hughes Medical Institute researchers have produced a genetically altered mouse that exhibits behavioral abnormalities that are strikingly similar to those observed in humans with schizophrenia.

The scientists report that they have already used insights from studying the mouse to identify a genetic variant associated with schizophrenia in humans.

According to the researchers, the findings could well mean that they have identified a molecular signaling pathway involved in the origin of schizophrenia, which affects about one percent of the population. If so, the search for drugs affecting that pathway could yield a new class of antipsychotic drugs that more precisely and effectively treat the disorder.

The researchers, led by Howard Hughes Medical Institute investigator Susumu Tonegawa at the Massachusetts Institute of Technology, published their findings June 30, 2003, in two articles in the early edition of the Proceedings of the National Academy of Sciences (PNAS). Tonegawa collaborated on the studies with researchers from Duke University Medical Center, The Rockefeller University and the Columbia University College of Physicians and Surgeons.

In their latest studies, Tonegawa and his colleagues built on their earlier research on a genetically engineered mouse, which had been specifically altered to knock out the gene for the enzyme calcineurin only in the animal's forebrain. Calcineurin is an enzymatic switch that plays regulatory roles in both the immune system and the brain. Until a brain-specific knockout mouse was developed in Tonegawa's laboratory, it had not been possible to pinpoint the enzyme's function in the brain. In earlier studies, Tonegawa and his colleagues found that the mutant mouse showed severe, specific deficits in a type of short-term memory called working memory.

Although schizophrenics show similar memory deficits, sai
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Contact: Avice Meehan
meehana@hhmi.org
301-215-8855
Howard Hughes Medical Institute
30-Jun-2003


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