Role of inflammatory mechanisms in major depressive disorder: From etiology to potential pharmacological targets

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dc.contributor.authorKouba, Bruna R.
dc.contributor.authorde Araujo Borba, Laura
dc.contributor.authorBorges de Souza, Pedro
dc.contributor.authorGil-Mohapel, Joana
dc.contributor.authorRodrigues, Ana LĂșcia S.
dc.date.accessioned2024-10-10T17:23:12Z
dc.date.available2024-10-10T17:23:12Z
dc.date.issued2024
dc.description.abstractThe involvement of central and peripheral inflammation in the pathogenesis and prognosis of major depressive disorder (MDD) has been demonstrated. The increase of pro-inflammatory cytokines (interleukin (IL)-1?, IL-6, IL-18, and TNF-?) in individuals with depression may elicit neuroinflammatory processes and peripheral inflammation, mechanisms that, in turn, can contribute to gut microbiota dysbiosis. Together, neuroinflammation and gut dysbiosis induce alterations in tryptophan metabolism, culminating in decreased serotonin synthesis, impairments in neuroplasticity-related mechanisms, and glutamate-mediated excitotoxicity. This review aims to highlight the inflammatory mechanisms (neuroinflammation, peripheral inflammation, and gut dysbiosis) involved in the pathophysiology of MDD and to explore novel anti-inflammatory therapeutic approaches for this psychiatric disturbance. Several lines of evidence have indicated that in addition to antidepressants, physical exercise, probiotics, and nutraceuticals (agmatine, ascorbic acid, and vitamin D) possess anti-inflammatory effects that may contribute to their antidepressant properties. Further studies are necessary to explore the therapeutic benefits of these alternative therapies for MDD.
dc.description.reviewstatusReviewed
dc.description.scholarlevelFaculty
dc.description.sponsorshipThe authors acknowledge funding from Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq; #312215/2021-5) and Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) and Fundação de Amparo à Pesquisa e Inovação de Santa Catarina (FAPESC, Brazil). J.G.M. acknowledges funding from the University of Victoria (UVic, Victoria, BC, Canada)—São Paulo Research Foundation (FAPESP, São Paulo, SP, Brazil) SPRINT partnership (UVic-FAPESP SPRINT 1/2018). A.L.S.R. is CNPq Research Fellow.
dc.identifier.citationKouba, B. R., de Araujo Borba, L., Borges de Souza, P., Gil-Mohapel, J., & Rodrigues, A. L. S. (2024). Role of inflammatory mechanisms in major depressive disorder: From etiology to potential pharmacological targets. Cells, 13(5), Article 5. https://doi.org/10.3390/cells13050423
dc.identifier.urihttps://doi.org/10.3390/cells13050423
dc.identifier.urihttps://hdl.handle.net/1828/20555
dc.language.isoen
dc.publisherCells
dc.rightsAttribution CC BY
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectanti-inflammatory approaches
dc.subjectgut dysbiosis
dc.subjectinflammation
dc.subjectmajor depressive disorder
dc.titleRole of inflammatory mechanisms in major depressive disorder: From etiology to potential pharmacological targets
dc.typeArticle

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