The anti-inflammatory drugs to treat depression?

The death of nerve cells caused by stress was blocked by anti-inflammatory molecule in a study published in the Proceedings of the National Academy of Sciences. This suggests that one way to treat certain symptoms of depression and stress could reduce the activity of the immune system that causes inflammation.

The idea that some cases of depression could be caused by an inflammatory response has gained prominence over the last decade, from a clinical trial of an anti-inflammatory drug for psoriasis had an antidepressant side effects unexpected.

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Previous research has suggested that cytokines block the birth of new neurons (nerve cells) in the hippocampi of stressed and depressed, an effect that may underlie some symptoms of depression such as memory problems.

Ronald Duman and his colleagues at Yale University studied the cytokine NF-kB is known to control several immune responses, to see if its release could reduce neurogenesis (the creation of new neurons) and whether these effects could be prevented .

After stress, whether acute or chronic, there were fewer neurons created in the brain of rodents. When they received an inhibitor of NF-kB before the stress, the birth of new neurons continued at a normal rate.

Duman hopes that a cytokine inhibitor can be developed as a treatment option for people with depression who do not respond to conventional treatment with antidepressants. “Depression is not a single disease,” he said. “A sub-group of depressed people may have an inflammatory condition, while other sub-groups could be better treated with existing antidepressant medications.”

While other anti-inflammatory drugs are in clinical trials for the treatment of depression, Tad Pace of Emory University, who studies the immune system function in people with major depression, said that NF -kB might be a better target for a drug because it is the first of a signaling cascade involving several other citokines.

Joe Herbert of Cambridge University, who studies the factors that affect neurogenesis, warns of possible complications with this type of treatment. “Developing drugs that interfere with the cytokine NF-kB can be problematic given its widespread function in the organization and its involvement in the development of cancer.

Pace remains optimistic, hoping to see the anti-inflammatory drugs, such as an inhibitor of NF-kB, regularly prescribed for the treatment of depression in the next 10 years.

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