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Cytokines in Bipolar Disorder: Recent Findings, Deleterious Effects But Promise for Future Therapeutics

Published online by Cambridge University Press:  01 July 2011

Abstract

An emerging body of evidence points to impairments in neuroplasticity, cell resilience, and neuronal survival as major pathophysiological mechanisms in bipolar disorder. Neuronal survival is influenced by several factors including an orchestrated action of neurotransmitters, hormones, and neurotrophins. Patients with bipolar disorder exhibit increased peripheral level of inflammatory mediators such as cytokines, mainly during acute mood episodes. These mediators interact in several pathways involved in regulation of mood and energy including hypothalamic-pituitary-adrenal axis and monoamine metabolism. Importantly, inflammatory cytokines have a potential role in controlling neuronal and glial cell loss that occurs during mood episodes, especially during mania, as they are the most powerful extracellular stimuli to apoptosis. Bipolar patients have been reported to show imbalanced peripheral production of cytokines both at the mRNA and protein levels, associated signal transduction machinery, as well as to have specific functional polymorphisms in the genes that encode these cytokines. Interestingly, lithium, valproate, and several antidepressants have demonstrated to have immunomodulatory properties. Growing evidence supports the involvement of inflammatory mechanisms in bipolar disorder, opening new paths of investigation using immunomodulatory medications. These findings can offer not only an opportunity of treating mood symptoms but also understanding and reverting neurobiological changes associated with the disorder.

Type
Review Article
Copyright
Copyright © Cambridge University Press 2012

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Footnotes

Faculty Disclosures: Dr. Brietzke has received a research grant from CAPES. Dr. Grassi‐Oliveira has received research grants from CAPES and Conselho Nacional de Desenvolvimento Cientí fico e Tecnógico (CNPq). Dr. Lafer has has received research grants from CNPq and Fundação de Amparo a Pesquisa do Estado de São Paulo. Dr. Stabellini has received research grants from CNPq.

Acknowledgements: The authors are thankful to Dr. Jorge Kalil and Dr. Edécio Cunha-Neto from the Department of Immunology of University of São Paulo for their helpful inputs during the preparation of the manuscript.

References

Faculty Disclosures: Dr. Brietzke has received a research grant from CAPES. Dr. Grassi‐Oliveira has received research grants from CAPES and Conselho Nacional de Desenvolvimento Cientí fico e Tecnógico (CNPq). Dr. Lafer has has received research grants from CNPq and Fundação de Amparo a Pesquisa do Estado de São Paulo. Dr. Stabellini has received research grants from CNPq.

Acknowledgements: The authors are thankful to Dr. Jorge Kalil and Dr. Edécio Cunha-Neto from the Department of Immunology of University of São Paulo for their helpful inputs during the preparation of the manuscript.

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