Researchers at Northwestern University's Feinberg School of Medicine claim that most medical treatments for depression are based upon an oversimplified model of its causes. Despite common beliefs, stress and neurotransmitter imbalances are not the primary causes of human depression.
For this reason, the medications currently popular for treating depression will offer little to no relief in over half the cases, states Eva Redei, the David Lawrence Stein Professor of Psychiatry at Northwestern's Feinberg School.
Using microarray technology, an extensive study by Redei and her team
isolated and identified genes associated with depression in rats. The rats in Redei's study were developed over decades to exhibit severe depression.
Redei explains that because the regions of human and rodent brains that relate to depression, the hippocampus and amygdala, are remarkably similar, depressed rats exhibit many of the same behaviors and physiological changes found in human patients with major depression.
Of 254 genes related to stress and 1275 genes related to depression among the microarray's 30,000 genes, only five overlap, a statistically insignificant number, according to Redei. She states that if chronic stress caused depression, many more genes associated with both stress and depression would have been found.
In the second part of the study Redei found few differences in the levels of genes controlling neurotransmitter functioning among depressed and normal animals. She concluded that antidepressants aimed at the molecules involved in neurotransmitter imbalances are missing the deeper, initial causes of depression — abnormal neuron development and functioning.
Redei's study was presented in Chicago at the Neuroscience 2009 conference. She hopes her team's findings will lead to different targets for new drug development.