Inflammatory mechanisms in major depressive disorder : Current Opinion in Psychiatry (original) (raw)
Clinical therapeutics: Edited by Dieter Naber and Harold Pincus
aDepartment of Psychiatry
bHotchkiss Brain Institute, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada
Correspondence to Thomas J. Raedler, MD, Foothills Medical Centre, TRW Building, Suite 4D62, 3280 Hospital Drive NW, Calgary, AB T2N 4Z6, Canada Tel: +1 403 210 6899; fax: +1 403 210 9114; e-mail: [email protected]
Abstract
Purpose of review
As the ‘monoamine hypothesis of depression’ fails to explain all aspects of major depression, additional causes are being investigated. Several observations suggest that inflammatory mechanisms pay a role in the cause of major depressive disorder (MDD). This article reviews their role in major depression.
Recent findings
Recent studies support the concept that inflammatory mechanisms play a crucial role in the pathomechanisms of major depression. Major depression shares similarities with ‘sickness behavior’, a normal response to inflammatory cytokines. Elevations in proinflammatory cytokines and other inflammation-related proteins in major depression were found in plasma and cerebrospinal fluid (CSF) as well as in postmortem studies. Elevated levels of proinflammatory cytokines persist after clinical symptoms of depression are in remission and can also predict the onset of a depressive episode. Antidepressant treatment can lead to a normalization of elevated cytokine levels in major depression. Finally, we understand how inflammatory mechanisms affect the metabolism of tryptophan and how nonsteroidal antiinflammatory drugs (NSAIDs) can interfere with the effects of antidepressants.
Summary
Further studies are needed to fully understand the role of inflammatory mechanisms in major depression and the potential treatment implications.
© 2011 Lippincott Williams & Wilkins, Inc.