Charting a Course to Schizophrenia’s Core: Research Uncovers Potential for New Treatment Mechanisms

May 12, 2010

Studies being conducted in the laboratory of senior scientist Joseph Coyle, MD, are among the longest-standing, federally funded research initiatives at McLean. For more than a decade, Coyle has been examining the underlying causes of schizophrenia with support from a $19-million National Institutes of Health grant. Recently, he has achieved what he calls “excellent traction” with some breakthrough results.

Coyle and his colleagues in the Mailman Research Center’s Laboratory of Psychiatric and Molecular Neuroscience have developed an animal model that could provide a genetic explanation for why abnormal neurons that control glutamate, a neurotransmitter, are present in the brains of individuals with schizophrenia. This model will help Coyle test for interventions that could reverse this abnormality, leading to better treatment of schizophrenia’s core pathology.

Joseph Coyle, MD
Joseph Coyle, MD

“Many of the drugs used to treat schizophrenia focus on dopamine, another neurotransmitter, which accounts for the psychosis seen in the disease. But psychosis is a symptom, not a cause. We believe that focusing on glutamate pathways in the cortex of the brain addresses the core pathology,” Coyle says.

The pharmaceutical industry seems to agree. New schizophrenia drugs that target glutamate are currently being tested by several companies, with promising results. “It’s encouraging to see new medications that focus on glutamate instead of dopamine,” says Coyle. “These drugs are looking at the exact same pathways we describe in our research.”

Basic research, such as Coyle’s, is instrumental in the quest to find improved treatments for schizophrenia and other forms of psychiatric illness. “An important part of basic research is being able to hand off our findings to drug companies that have the resources to develop breakthrough medications,” he says.

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