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Common Gene Mutation Lowers Risk for Bipolar Disorder

Study found missing section protected against psychiatric illness

By Amanda Gardner
HealthDay Reporter


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MONDAY, Sept. 29 (HealthDay News) -- New research suggests that a missing section of DNA in a certain gene may hold the key to whether a person does or does not develop bipolar disorder.

"[Our] findings show that a natural, common mutation in the GRIK4 gene protects against bipolar disorder," said Ben Pickard, lead author of a study in this week's issue of the Proceedings of the National Academy of Sciences and a member of the department of medical genetics at the University of Edinburgh in Scotland. "If a natural mutation can result in protection, then this may offer clues as to how future drug treatments might be directed. . . Another benefit from this work is that in the future, when we possess a greater knowledge of psychiatric illness mutations, we may be able to predict which individuals are at risk of illness before they develop it or tailor appropriate medicine to subsets of patients."

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"These findings are important, because they link an important brain receptor to bipolar disorder, which may help researchers devise new drug treatments targeting kainate and related receptors, added Keith A. Young, an associate professor of psychiatry and behavioral science at the Texas A&M Health Science Center College of Medicine and co-director of the Central Texas Veterans Health Care System Neuropsychiatry Research Program.

According to Young, the GRIK4 gene provides the genetic coding for the glutamate neurotransmitter receptor known as the KA1 kainate receptor. These kainate receptors are considered "excitatory," because they generally make neurons more prone to firing signaling messages. The glutamate transmitter has been linked to different psychiatric disorders.

"Excitatory receptors neurons have long been thought to being involved in psychotic disorders, since drugs that attach to some glutamate receptors can mimic symptoms of psychosis, such as hallucinations," Young explained.

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Copyright © 2008 ScoutNews, LLC. All rights reserved.
Last updated 9/29/2008

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SOURCES: Ben Pickard, Ph.D., department of medical genetics, University of Edinburgh, Scotland; Keith A. Young, Ph.D., associate professor, psychiatry and behavioral science, Texas A&M Health Science Center College of Medicine, and co-director, Central Texas Veterans Health Care System Neuropsychiatry Research Program; Sept. 29-Oct. 3, 2008, Proceedings of the National Academy of Sciences


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