A Comprehensive Study of Inflammation's Contribution to the Pathophysiology of Major Depressive Syndrome

Objective: The research aims to summaries the data demonstrating the connection between persistent low-grade inflammation and the pathophysiology of severe depression, and the effects of chronic low-grade inflammation on the immune system, neurodegeneration, and the neuroendocrine system. Materials and methods: The research examining the connection between severe depression and inflammation. The hypothalamic-pituitary-adrenal (HPA) axis is highlighted, as are the functions of proinflammatory cytokines and the tryptophan-kynurenine pathway in neurotoxicity and oxidative stress. Results: The HPA axis is activated, and cortisol production is enhanced in severe depression, characterized by chronic low-grade inflammation. The tryptophan-kynurenine pathway is also triggered by proinflammatory cytokines, which produce neurotoxic substances such as quinolinic acid and 3-hydroxykynurenine. Particularly in cases of late-life depression, these mechanisms lead to oxidative stress and neurodegeneration. Conclusion: Antidepressant drugs exhibit some mitigation of the immunological and endocrine alterations brought on by inflammation. Not all potent antidepressants, however, focus on these systems. To be more successful, the research advises that innovative antidepressant research should take into account medications specifically targeting the immunological, endocrine, and neurotransmitter systems.