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Inflammation, stress and depression: an exploration of ketamine’s therapeutic profile

J. Johnston, Maximillian Greenwald, Ioline D. Henter, Christoph Kraus, A. Mkrtchian, Neil G Clark, Lawrence T. Park, P. Gold, Carlos A. Zarate, Bashkim Kadriu

Drug Discovery Today February 1, 2023 DOI: 10.1016/j.drudis.2023.103518 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Review Peer reviewed
Topics Depression Esketamine Ketamine
Citations 64
Key findings Ketamine's antidepressant effects may be partly due to its anti-inflammatory actions on the HPA axis, kynurenine pathway, or cytokine suppression, and stress-induced inflammation may contribute to treatment-resistant depression.

Abstract

Well-established animal models of depression have described a proximal relationship between stress and central nervous system (CNS) inflammation – a relationship mirrored in the peripheral inflammatory biomarkers of individuals with depression. Evidence also suggests that stress-induced proinflammatory states can contribute to the neurobiology of treatment-resistant depression. Interestingly, ketamine, a rapid-acting antidepressant, can partially exert its therapeutic effects via anti-inflammatory actions on the hypothalamic-pituitary-adrenal (HPA) axis, the kynurenine pathway or by cytokine suppression. Further investigations into the relationship between ketamine, inflammation and stress could provide insight into ketamine’s unique therapeutic mechanisms and stimulate efforts to develop rapid-acting, anti-inflammatory-based antidepressants.

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