Over-active genes found in depressed females

New York, July 31: Numerous genes that regulate the activity of a neurotransmitter in the brain, were found to be in abundance in the brain tissue of depressed females.

This could be an underlying cause of the higher incidence of suicide among women, an Indian-origin scientist suggests.


Studying post-mortem tissue from brains of psychiatric patients, Monsheel Sodhi from University of Illinois at Chicago, noted that female patients with depression had abnormally high expression levels of many genes that regulate the glutamate system, which is widely distributed in the brain.

Glutamate is the major excitatory neurotransmitter in the brain. Schizophrenia, epilepsy, autism and Alzheimer's disease have all been linked to abnormalities of the glutamate system.

"Gender plays a role in depression and suicide. Women are two to three times more likely to attempt suicide, but men are four times more likely to die by suicide," said Sodhi

The risk of suicide is associated with changes in several neurotransmitter systems.

Conventional anti-depressants target the monoamine systems, which secrete the neurotransmitters dopamine, serotonin or norepinephrine.

In the new study published in the journal Molecular Psychiatry, Sodhi and her colleagues analysed brain tissue from people who had suffered from depression.

Sodhi discovered that females with depression had the highest levels of expression of several glutamate receptor genes, perhaps making them more prone to depression.

In addition, three of these genes were found to be elevated in both male and female patients who had died by suicide.

"Our data indicate that females with major depression who are at high risk of suicide may have the greatest antidepressant benefit from drugs that act on the glutamate system, such as ketamine," Sodhi said.

The study also suggests new glutamate receptor targets for development of treatments for depression and identifies biochemical markers that could be used to assess suicide risk, she added.


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