Researchers from Yale University have found that the activity of a particular gene is increased more than two times over in the brains of depressed individuals. That could make the gene, called MKP-1, a new target for antidepressant research.
“This could be a primary cause, or at least a major contributing factor, to the signaling abnormalities that lead to depression,” said Dr. Ronald S. Duman, senior author of the study and professor of psychiatry and pharmacology at Yale.
For some time now, researchers haven’t been able to find a specific biological factor for depression, from which almost 16 percent of Americans suffer in a given year.
Since sufferers of depression experience a vast array of symptoms and because about 40 percent of depressed individuals do not respond to medication, most physicians and scientists suspect that there is a multitude of physiological processes involved in major depressive disorder.
Most antidepressants work by raising levels of the neurotransmitter serotonin, but individuals respond very differently to these medications, which often take weeks or months to take effect.
For the study, researchers conducted whole genome tissue scans from 21 deceased individuals who had been diagnosed with depression and compared their gene expression levels with the tissues of 18 other individuals who had no history of depression. It was discovered that the gene called MKP-1 was more than two times more active in the brain tissues of depressed individuals.
The finding is significant because MKP-1 inactivates a molecular pathway that is extremely important to neuron survival and activity; dysfunction in this gene has been associated with depression and other disorders. Furthermore, when the MKP-1 gene is deactivated in mice, they are able to deal with stress extremely well. However, when the gene is activated, mice develop symptoms analogous to human depression.
Because of these findings, MKP-1 is considered a possible target for a new class of antidepressants, especially for treatment-resistant depression.
This study was funded by the U.S. Health Service and State of Connecticut, Connecticut Mental Health Center and can be found in the Oct. 17 issue of Nature Medicine.
Source: Yale University