dc.contributorUniv Toronto
dc.contributorUniv Western Ontario
dc.contributorUniversidade Federal de São Paulo (UNIFESP)
dc.creatorRosenblat, Joshua D.
dc.creatorCha, Danielle S.
dc.creatorMansur, Rodrigo B. [UNIFESP]
dc.creatorMcIntyre, Roger S.
dc.date.accessioned2016-01-24T14:37:42Z
dc.date.available2016-01-24T14:37:42Z
dc.date.created2016-01-24T14:37:42Z
dc.date.issued2014-08-04
dc.identifierProgress in Neuro-psychopharmacology & Biological Psychiatry. Oxford: Pergamon-Elsevier B.V., v. 53, p. 23-34, 2014.
dc.identifier0278-5846
dc.identifierhttp://repositorio.unifesp.br/handle/11600/38079
dc.identifier10.1016/j.pnpbp.2014.01.013
dc.identifierWOS:000338813600004
dc.description.abstractMood disorders have been recognized by the World Health Organization (WHO) as the leading cause of disability worldwide. Notwithstanding the established efficacy of conventional mood agents, many treated individuals continue to remain treatment refractory and/or exhibit clinically significant residual symptoms, cognitive dysfunction, and psychosocial impairment. Therefore, a priority research and clinical agenda is to identify pathophysiological mechanisms subserving mood disorders to improve therapeutic efficacy.During the past decade, inflammation has been revisited as an important etiologic factor of mood disorders. Therefore, the purpose of this synthetic review is threefold: 1) to review the evidence for an association between inflammation and mood disorders, 2) to discuss potential pathophysiologic mechanisms that may explain this association and 3) to present novel therapeutic options currently being investigated that target the inflammatory-mood pathway.Accumulating evidence implicates inflammation as a critical mediator in the pathophysiology of mood disorders. Indeed, elevated levels of pro-inflammatory cytokines have been repeatedly demonstrated in both major depressive disorder (MDD) and bipolar disorder (BD) patients. Further, the induction of a pro-inflammatory state in healthy or medically ill subjects induces 'sickness behavior' resembling depressive symptomatology.Potential mechanisms involved include, but are not limited to, direct effects of pro-inflammatory cytokines on monoamine levels, dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, pathologic microglial cell activation, impaired neuroplasticity and structural and functional brain changes.Anti-inflammatory agents, such as acetyl-salicylic acid (ASA), celecoxib, anti-TNF-alpha agents, minocycline, curcumin and omega-3 fatty acids, are being investigated for use in mood disorders. Current evidence shows improved outcomes in mood disorder patients when anti-inflammatory agents are used as an adjunct to conventional therapy; however, further research is needed to establish the therapeutic benefit and appropriate dosage. (C) 2014 Elsevier Inc. All rights reserved.
dc.languageeng
dc.publisherElsevier B.V.
dc.relationProgress in Neuro-psychopharmacology & Biological Psychiatry
dc.rightshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.rightsAcesso restrito
dc.subjectBipolar disorder
dc.subjectCytokines
dc.subjectInflammation
dc.subjectMajor depressive disorder
dc.subjectMood disorder
dc.subjectNon-steroidal anti-inflammatory drug (NSAID)
dc.titleInflamed moods: A review of the interactions between inflammation and mood disorders
dc.typeResenha


Este ítem pertenece a la siguiente institución