ArticleJournal of neurochemistry2013
Cyclooxygenase-1 inhibition reduces amyloid pathology and improves memory deficits in a mouse model of Alzheimer's disease.
Article in Journal of neurochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.
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
62 citing papers in PubMed, 1 synthesis or guideline pooled it, 128 citations in OpenAlex.
- Differential expression of MicroRNAs in Alzheimer's disease: a systematic review and meta-analysis.Molecular psychiatry · 2022Pooled it
- Capillary-Associated Microglia in Neurovascular Coupling: Localization, Mechanisms, and Disease Implications.Journal of neuroinflammation · 2026Review
- Exploring the Mechanism of 2,4-Dichlorophenoxyacetic Acid in Causing Neurodegenerative Diseases Based on Network Toxicology and Molecular Docking.International journal of molecular sciences · 2025Article
- Synergistic neuroprotective effects of Vitexin and Thymol against Okadaic acid-induced neurotoxicity: Computational and In vitro evaluation.Molecular biology reports · 2025Article
- Cyclooxygenase-1 deletion in 5 × FAD mice protects against microglia-induced neuroinflammation and mitigates cognitive impairment.Translational neurodegeneration · 2025Article
- The Role and Pathogenesis of Tau Protein in Alzheimer's Disease.Biomolecules · 2025Review
- Neuroinflammation in Alzheimer disease.Nature reviews. Immunology · 2025Review
- Playing Around the Coumarin Core in the Discovery of Multimodal Compounds Directed at Alzheimer's-Related Targets: A Recent Literature Overview.Molecules (Basel, Switzerland) · 2025Review
- Highlighting the Effect of Pro-inflammatory Mediators in the Pathogenesis of Periodontal Diseases and Alzheimer's Disease.Journal of pharmacy & bioallied sciences · 2024Review
- Neuroinflammation of Microglial Regulation in Alzheimer's Disease: Therapeutic Approaches.Molecules (Basel, Switzerland) · 2024Review
- A review of the roles of pathogens in Alzheimer's disease.Frontiers in neuroscience · 2024Review
- Exploring the role of COX-2 in Alzheimer's disease: Potential therapeutic implications of COX-2 inhibitors.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023Review
- Neuroaxonal and cellular damage/protection by prostanoid receptor ligands, fatty acid derivatives and associated enzyme inhibitors.Neural regeneration research · 2023Review
- Inflammation context in Alzheimer's disease, a relationship intricate to define.Biological research · 2022Review
- Synthesis and Preclinical Evaluation ofJournal of nuclear medicine : official publication, Society of Nuclear Medicine · 2022Article
- Therapeutic Antiaging Strategies.Biomedicines · 2022Review
- Cyclooxygenases as Potential PET Imaging Biomarkers to Explore Neuroinflammation in Dementia.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2022Review
- Low-Dose Aspirin Augments the Anti-Inflammatory Effects of Low-Dose Lithium in Lipopolysaccharide-Treated Rats.Pharmaceutics · 2022Article
- Lipid-Based Nanocarriers for Neurological Disorders: A Review of the State-of-the-Art and Therapeutic Success to Date.Pharmaceutics · 2022Review
- Alzheimer's disease and epilepsy: An increasingly recognized comorbidity.Frontiers in aging neuroscience · 2022Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Several epidemiological and preclinical studies suggest that non-steroidal anti-inflammatory drugs (NSAIDs), which inhibit cyclooxygenase (COX), reduce the risk of Alzheimer's disease (AD) and can lower β-amyloid (Aβ) production and inhibit neuroinflammation. However, follow-up clinical trials, mostly using selective cyclooxygenase (COX)-2 inhibitors, failed to show any beneficial effect in AD patients with mild to severe cognitive deficits. Recent data indicated that COX-1, classically viewed as the homeostatic isoform, is localized in microglia and is actively involved in brain injury induced by pro-inflammatory stimuli including Aβ, lipopolysaccharide, and interleukins. We hypothesized that neuroinflammation is critical for disease progression and selective COX-1 inhibition, rather than COX-2 inhibition, can reduce neuroinflammation and AD pathology. Here, we show that treatment of 20-month-old triple transgenic AD (3 × Tg-AD) mice with the COX-1 selective inhibitor SC-560 improved spatial learning and memory, and reduced amyloid deposits and tau hyperphosphorylation. SC-560 also reduced glial activation and brain expression of inflammatory markers in 3 × Tg-AD mice, and switched the activated microglia phenotype promoting their phagocytic ability. The present findings are the first to demonstrate that selective COX-1 inhibition reduces neuroinflammation, neuropathology, and improves cognitive function in 3 × Tg-AD mice. Thus, selective COX-1 inhibition should be further investigated as a potential therapeutic approach for AD.
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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.