A new study highlights the link between inflammation and depression, challenging traditional neurotransmitter-focused theories. An examination of decades of research suggests that immune system imbalances may trigger and sustain depressive symptoms, particularly in high-risk groups. This research paves the way for personalized treatments targeting inflammation, offering new hope for those unresponsive to conventional therapies.
Depression, recognized as the leading cause of disability worldwide, affects nearly one in six people over their lifetimes. Despite decades of research, much remains unknown about the biological mechanisms underlying this debilitating condition. Professor Raz Yirmiya, a pioneering researcher in the field of inflammation and depression from the Department of Psychology at the Hebrew University of Jerusalem, has recently published a comprehensive review in Brain, Behavior, and Immunity, offering new insights that challenge long-held beliefs and open pathways toward personalized treatment.
Traditional theories of depression have focused on neurotransmitters like serotonin and norepinephrine, suggesting that a deficiency in these brain chemicals may lead to depressive symptoms. While widely accepted, these theories have failed to explain why a significant portion of patients do not respond to conventional antidepressants. Over the last 30 years, Professor Yirmiya's research, along with others', has pointed to a different culprit: chronic inflammation, both.