Glutamate may be trigger for schizophrenia

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A new study from investigators at Columbia University Medical Center (CUMC) states that an excess of the brain neurotransmitter glutamate may cause a transition to psychosis in people who are at risk for schizophrenia.

The findings may point to a potential diagnostic tool for identifying people at risk for schizophrenia and suggest a possible glutamate-limiting treatment strategy for preventing or slowing the progress of schizophrenia and other psychotic disorders.

Trigger may be detected before the disease is diagnosable

“Previous studies of schizophrenia have shown that hypermetabolism and atrophy of the hippocampus are among the most prominent changes in the patient’s brain,” said senior author Scott Small, MD, Boris and Rose Katz Professor of neurology at CUMC. “The most recent findings had suggested that these changes occur very early in the disease, which may point to a brain process that could be detected even before the disease begins.”

Documented changes in the brain as psychosis developed

Columbia researchers used neuroimaging tools in patients and in mouse models. They followed a group of young people at risk for developing schizophrenia to see how their brain activity changed as the disease developed.

They discovered that for the people who acquired psychosis, first glutamate activity increased in the hippocampus, then hippocampus metabolism increased, and finally the hippocampus began to atrophy. They confirmed these changes in the mouse model.

Targeting glutamate may decrease chances of development

“Targeting glutamate may be more useful in high-risk people or in those with early signs of the disorder,” explained Jeffrey A. Lieberman, MD, renowned expert in the field of schizophrenia and president-elect of the American Psychiatric Association. “Early intervention may prevent the debilitating effect of schizophrenia, increasing recovery in one of humankind’s most costly mental disorders.”

Source: MedicalNewsToday, Neuron

 
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