ReviewMetabolic brain disease2012
Targeting cyclooxygenase-2 in depression is not a viable therapeutic approach and may even aggravate the pathophysiology underpinning depression.
Review in Metabolic brain disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 56 citations in OpenAlex.
- Therapeutic potential of COX-2 inhibitors in neuropsychiatric disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Association between Regular Use of Analgesics before Cancer Diagnosis and Occurrence of Mood Disorders.Nursing reports (Pavia, Italy) · 2024Article
- Antioxidant Biomolecules and Their Potential for the Treatment of Difficult-to-Treat Depression and Conventional Treatment-Resistant Depression.Antioxidants (Basel, Switzerland) · 2022Review
- Cyclooxygenase Inhibition Safety and Efficacy in Inflammation-Based Psychiatric Disorders.Molecules (Basel, Switzerland) · 2020Review
- Targeting Inflammatory-Mitochondrial Response in Major Depression: Current Evidence and Further Challenges.Oxidative medicine and cellular longevity · 2020Review
- Neurobiology and Therapeutic Potential of Cyclooxygenase-2 (COX-2) Inhibitors for Inflammation in Neuropsychiatric Disorders.Frontiers in psychiatry · 2019Review
- Aspirin and incident depressive symptoms: A longitudinal cohort study over 8 years.International journal of geriatric psychiatry · 2018Article
- Immune-based strategies for mood disorders: facts and challenges.Expert review of neurotherapeutics · 2018Review
- Anti-inflammatory treatment for major depressive disorder: implications for patients with an elevated immune profile and non-responders to standard antidepressant therapy.Journal of psychopharmacology (Oxford, England) · 2017Review
- Anti-inflammatory treatment and risk for depression after first-time stroke in a cohort of 147 487 Danish patients.Journal of psychiatry & neuroscience : JPN · 2017Article
- Toward Omics-Based, Systems Biomedicine, and Path and Drug Discovery Methodologies for Depression-Inflammation Research.Molecular neurobiology · 2016Review
- Inflammation and Immune Regulation as Potential Drug Targets in Antidepressant Treatment.Current neuropharmacology · 2016Review
- Cytosolic phospholipase A2 plays a crucial role in ROS/NO signaling during microglial activation through the lipoxygenase pathway.Journal of neuroinflammation · 2015Article
- Markers of Oxidative Stress and Neuroprogression in Depression Disorder.Oxidative medicine and cellular longevity · 2015Review
- Role of immune-inflammatory and oxidative and nitrosative stress pathways in the etiology of depression: therapeutic implications.CNS drugs · 2014Review
- Mind and body: how the health of the body impacts on neuropsychiatry.Frontiers in pharmacology · 2013Review
- Aspirin: a review of its neurobiological properties and therapeutic potential for mental illness.BMC medicine · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.