Kathi O. Baker, 404-727-9371, email@example.com
Janet Christenbury, 404-727-8599, firstname.lastname@example.org
|June 17, 2003|
WASHINGTON, D.C. A new study presented at a Journal of the American Medical Association media briefing at the National Press Club on June 17 has given neuroscientists one more link in the chain to more fully understand, and effectively target, the changes in the brain that are responsible for vulnerability to depression.
Lead author J. Douglas Bremner, MD, associate professor in the Department of Psychiatry and Behavioral Sciences at Emory University School of Medicine, director of the Emory Center for Positron Emission Tomography, and director of Mental Health research at the Atlanta Veterans Affairs Medical Center, together with the National Institute of Mental Health, Yale University, and the University of Louisville, published their findings in an article in the June 18 issue of the Journal of the American Medical Association.
With the development of brain imaging studies, data has led to some understanding of a common circuitry of brain regions that are felt to mediate symptoms of depression.
"It appears that alterations in brain function continue to persist, even after patients have been successfully treated for depression," says Dr. Bremner. "It is known from prior imaging studies that the risk of depressive recurrence increases with the number of episodes of depression experienced during the individual's lifetime. This suggests that changes in the brain underlie the development of vulnerability to depressive recurrence."
In this randomized study, eighteen participants underwent Positron Emission Tomography (PET) imaging of brain metabolism either during a depressive episode or in remission. All participants had a history of lifetime major depression and had been treated with norepinephrine reuptake inhibitors (NRIs).
Data were analyzed for brain metabolic rates. After controlling for baseline metabolism, patients with depressive symptoms showed decreased brain metabolism. Patients who successfully remained in remission showed the opposite response. Earlier imaging studies with patients who were taking selective serotonin reuptake inhibitors (SSRIs) showed similar results.
"In those patients with recurrent symptoms," says Bremner, "the return of depressive symptoms was associated with decreased metabolism in multiple cortical regions, with the greatest effects in orbitofrontal cortex, dorsolateral prefrontal cortex, and thalamus. Previous studies have shown that the number of episodes of depression has been also correlated with hippocampal atrophy."
"If we can figure out the function of the neurochemical systems of the brain," says Bremner, "we can develop treatments that will more effectively target the affected circuitry and possibly prevent recurrence in those patients who are predisposed to repeated episodes of depression." The combined results of these studies will bring neuroscientists another step closer to verifying the baseline areas that they have long-suspected are involved in depression. If baseline metabolism can be determined as the key to predicting a patient's susceptibility to a return of depressive symptoms, physicians can better outline a successful course of treatment for their patients.
This study was supported by a VA Merit Review Grant to co-author Dennis S. Charney, MD, the National Alliance for Research in Schizophrenia and Affective Disorders (NARSAD) Young Investigator Award and National Institute of Mental Health grant to Dr. Bremner, and a Veterans Administration Career Development Award grant to Dr. Bremner.