Researchers Move Closer to Schizophrenia Origins
> 10/17/2007 11:32:09 AM

A defect in a the creation of a chemical messenger responsible for moderating anxiety and regulating the growth of the brain's prefrontal cortex may facilitate the development of schizophrenia, according to researchers at Baylor College of Medicine and the Universtity of Massachusetts.

GABA is a neurotransmitter present in nerve endings throughout the human brain. It effectively acts as a brake for the neurochemical reactions that lead to heightened levels of anxiety, and GABA shortages have been linked to schizophrenia, panic attacks and related conditions in the past, but this study allows for a greater understanding of the neurological processes involved in the equation: the GAD1 gene produces enzymes that form a crucial part of GABA, and the gene comes with the inherent ability to turn itself on and off when needed. In schizophrenic patients, a defective variation of that chemical on/off switch leads to lower levels of GABA and an inability for the brain to properly regulate anxiety responses.

Researchers were also able to better explain why schizophrenia medications like clozapine effectively reduce symptoms for many patients. In lab mice affected by this genetic abnormality, doses of clozapine worked to correct the process. With a better understanding of the mechanisms by which these medications work, more effective variations can be developed. Unrelated research regarding potential treatments for schizophrenia continues, meanwhile, with unfortunately mixed results. The promising atypical antipsychotic medication RGH-188, long mired in various stages of development, has proven mildly effective only in very small doses, hardly amounting to the revolutionary treatment many hoped for. Continuing trials will determine the substance's efficiency and ultimate applications. This does not diminish the excitement of the GABA finding, which could lead to new medications or further refinements of existing meds.

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