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 Research & Giving News Article  M. Margarita Behrens, Ph.D., a 2004 NARSAD Young Investigator at the University of California, San Diego (UCSD) School of Medicine, and colleagues, used ketamine to mimic features of schizophrenia in mice. They then analyzed neurons in a region of the mouse brain that corresponds to the prefrontal cortex in humans where profound changes occur in patients with schizophrenia. They found a substantial increase in the activity of NADPH oxidase. The link between NADPH oxidase and the dysfunction of certain neurons exposed to ketamine surprised the researchers. NADPH oxidase is normally found in white blood cells circulating outside the brain, where it helps kill bacterial and fungal infections by producing superoxide, a compound that can cause substantial damage to cells. As reported in the December 7 issue of Science, the team found that the ketamine-induced activation of the NADPH oxidase complex resulted in the loss of a specific type of inhibitory interneuron in the mice, which led to the impairment of brain circuitry involved in memory, attention and other key functions related to learning. In the human brain, loss of such functions sets up individuals for psychosis and deficits in information processing, resulting in symptoms such as hallucinations and delusions, as well as social withdrawal and cognitive problems, according to Behrens. “Our findings suggest that compounds that inhibit NADPH oxidase in the brain, without totally blocking its protective function of killing bacteria, could provide future therapies for schizophrenia or other diseases in humans that exhibit similar changes in neural circuitry,” said Behrens. This article was adapted by NARSAD with permission of the University of California, San Diego. |
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