Fascinating Look Into the War on Mental Depression Fascinating Look Into the War on Mental Depression

Northwestern University researcher Eva Redei recently presented her research on the underlying causes of depression at the Neuroscience 2009 in Chicago. The sophistication of the research is impressive, and suggests the promise of hugely important advances in the study of human cognition and mental illness in the relatively near future.

Redei used microarray technology to isolate and identify the specific genes related to depression in these animals. She examined the genes in the brain regions -- the hippocampus and amygdala -- commonly associated with depression in rats and humans.

Then she took four genetically different strains of rats and exposed them to chronic stress for two weeks. Afterwards, she identified the genes that had consistently increased or decreased in response to the stress in all four strains in the same brain regions.

Redei now had one set of depression-related genes that came out of an animal model of depression and one set of stress-related genes that came our of her chronic stress study.

Next she compared the two sets of genes to see if there were any similarities. "If the 'stress causes depression theory' was correct, there should have been a significant overlap between these two sets of genes," she said. "There weren't."

Out of a total of over 30,000 genes on the microarray, she discovered approximately 254 genes related to stress and 1275 genes related to depression, with an overlap of only five genes between the two.

"This overlap is insignificant, a very small percentage," Redei said. "This finding is clear evidence that at least in an animal model, chronic stress does not cause the same molecular changes as depression does." _SD

Redei claims to have shown that modern methods of treating depression are misconceived -- since they are aimed more at stress than at the real cause of depression. She also claims to have demonstrated that depression is caused by something significantly more profound than an imbalance of neurotransmitters. Redei believes that her findings point to potentially more powerful and effective treatments for depression.

I have not read the full study, so I cannot comment on Redei's claims. But I do admit to being impressed by the powerful genetic and bioinformatic methods used to tease out the differences between the genetics of stress and the genetics of depression. These tools can be used to solve many genetic problems that have been the source of heated philosophical arguments for centuries. But powerful and exotic tools do not guarantee valid results. Logical and philosophical rigour must be combined with a creative and adventurous spirit.

Redei suggests that the "real" problem of depression originates in the developmental stages of neurons, and may have to be solved at the same level. There is some evidence that some neurotransmitters can trigger neurogenesis via stem cell migration and differentiation. Better therapies for selective neurogenesis may well find their way into psychiatric treatment for depression. It is likely that deep brain stimulation, for example, and other electromagnetic stimulation techniques, will be found to stimulate neurogenesis at least indirectly.

For the animal depression model, Redei was apparently using a strain of rats that has been bred for decades to mimic physical and physiological human symptoms and signs of depression. The rats are said to be "the most depressed rats in the world." If so, they should be helpful in screening new therapies for depression.

It is not surprising that some therapies will work for depression and others will not.