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Researchers found significant relationship between inflammation and depression

by Sandhya Hirani
January 1, 2025
भारत में कम उम्र के लोग करते हैं सबसे ज्यादा आत्महत्या : विशेषज्ञ

New Delhi, January 1, 2025 (IANS). Scientists have revealed a deep connection between depression and inflammation, which may change the way we understand depression.

The research of neuroscientist Professor Raz Yirmiya of the Hebrew University of Jerusalem is not limited to laboratories only.

Their discovery shows how microglia cells and interleukin-1 play a role in stress-induced depression. This raises the question whether the treatment of depression can be improved by understanding the process of inflammation? And do different types of immune responses influence different forms of depression?

Professor Yirmiya told in an interview published in the journal Brain Medicine, “Most depressed patients do not have any obvious inflammatory disease. But we and other scientists found that stress, which is the biggest cause of depression, increases the inflammatory processes in the brain. “Activates.”

Jeremiah’s team identified several potential treatment targets through advanced technologies and behavioral studies. His work focuses on the microglial checkpoint system and stress tolerance, opening new avenues of understanding how the immune system influences mental health.

Their research indicates that personalized treatments could be developed based on controlling inflammation.

“My main effort is to use my research and that of other scientists to develop new antidepressants that target inflammation processes,” says Yirmiya.

Their findings suggest that activating or suppressing the immune system may trigger depression symptoms. Therefore, individual treatment is needed for every patient.

This interview with Jeremiah is part of a series that highlights the people behind new thinking in science. The authors of this series say that in every interview a unique mix of scientists’ research and their personal views has been presented.

–IANS

AS/

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