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Flawed Gene May Lead to Cognitive Problems in Schizophrenia

July 26, 2013. New details about how a defective gene, the nicotinic α7 receptor, may lead to cognitive impairments in schizophrenia have emerged in a study published July 16, 2013, in the Proceedings of the National Academy of Sciences. Led by Min Wang at Yale University in New Haven, Connecticut, researchers examined how the nicotinic α7 receptor interacts with the neurons in the brain that are responsible for a certain kind of memory. To do this, they measured monkeys’ memory and the activity of their neurons after giving different drugs to turn the receptors on and off. They found that turning off the receptors made the neurons less active, while turning them on enhanced the neurons’ activity and improved the monkeys’ memory.

Previous studies have found that having a faulty copy of the nicotinic α7 receptor gene, which is thought to disable some of the brain’s receptors, elevates one’s risk of schizophrenia. The researchers’ findings that the receptors are important for memory suggest a possible reason why cognitive problems are also present in the illness. In addition, the study suggests how drugs that bolster nicotinic α7 receptors, currently in clinical trials, may improve cognition in schizophrenia. (For more details, see the related news story.)—Allison A. Curley.

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