Targeting cyclooxygenase-2 in depression is not a viable therapeutic approach and may even aggravate the pathophysiology underpinning depression Maes, Michael 2012, Targeting cyclooxygenase-2 in depression is not a viable therapeutic approach and may even aggravate the pathophysiology underpinning depression, Metabolic brain disease, vol. 27, no. 4, pp. 405-413, doi: 10.1007/s11011-012-9326-6. Attached Files Name Description MIMEType Size Downloads Title Targeting cyclooxygenase-2 in depression is not a viable therapeutic approach and may even aggravate the pathophysiology underpinning depression Author(s) Maes, Michael Journal name Metabolic brain disease Volume number 27 Issue number 4 Start page 405 End page 413 Total pages 9 Publisher Springer New York LLC Place of publication New York, N. Y. Publication date 2012-12 ISSN 0885-7490 1573-7365 Keyword(s) depression cytokines inflammation COX-2 cardiovascular disorder leaky gut oxidative and nitrosative stress Summary Depression is a complex progressive disorder accompanied by activation of inflammatory and Th-1 driven pathways, oxidative and nitrosative stress (O&NS), lowered antioxidant levels, mitochondrial dysfunctions, neuroprogression and increased bacterial translocation. In depression, activation of immuno-inflammatory pathways is associated with an increased risk for cardio-vascular disorder (CVD). Because of the inflammatory component, the use of cyclooxygenase 2 (COX-2) inhibitors, such as celecoxib, has been advocated to treat depression. Electronic databases, i.e. PUBMED, Scopus and Google Scholar were used as sources for this selective review on the effects of COX-2 inhibitors aggravating the abovementioned pathways. COX-2 inhibitors may induce neuroinflammation, exacerbate Th1 driven responses, increase lipid peroxidation, decrease the levels of key antioxidants, damage mitochondria and aggravate neuroprogression. COX-2 inhibitors may aggravate bacterial translocation and CVD through Th1-driven mechanisms. COX-2 inhibitors may aggravate the pathophysiology of depression. Since Th1 and O&NS pathways are risk factors for CVD, the use of COX-2 inhibitors may further aggravate the increased risk for CVD in depression. Selectively targeting COX-2 may not be a viable therapeutic approach to treat depression. Multi-targeting of the different pathways that play a role in depression is more likely to yield good treatment results. Language eng DOI 10.1007/s11011-012-9326-6 Field of Research 119999 Medical and Health Sciences not elsewhere classified Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences HERDC Research category C1.1 Refereed article in a scholarly journal Copyright notice ©2012, Springer Science+Business Media, LLC Persistent URL http://hdl.handle.net/10536/DRO/DU:30047547 Document type: Journal Article Collections: Faculty of Health School of Medicine Related Links Link Description Connect to published version (restricted access) Go to link with your DU access privileges     Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved. Versions Version Filter Type Thu, 30 Aug 2012, 09:41:48 EST Thu, 30 Aug 2012, 10:38:28 EST Wed, 19 Sep 2012, 10:14:27 EST Wed, 19 Sep 2012, 10:20:37 EST Thu, 13 Dec 2012, 15:47:43 EST Thu, 13 Dec 2012, 15:49:34 EST Thu, 13 Dec 2012, 15:50:19 EST Mon, 17 Jun 2013, 17:54:15 EST Filtered Full Citation counts:   Cited 39 times in TR Web of Science Cited 43 times in Scopus Search Google Scholar Access Statistics: 98 Abstract Views, 2 File Downloads  -  Detailed Statistics Created: Thu, 30 Aug 2012, 09:41:48 EST

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