Evidence map›Paper›PMID 20157512›Full record

ArticleAging2009

Cyclooxygenase-1 null mice show reduced neuroinflammation in response to beta-amyloid.

Sang-Ho Choi, Francesca Bosetti

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Microglia as a cellular target of diclofenac therapy in Alzheimer's disease.Therapeutic advances in neurological disorders · 2023
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Is cyclooxygenase-1 involved in neuroinflammation?Journal of neuroscience research · 2021
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Sang-Ho ChoiMolecular Neuroscience Unit, Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892, USA.
Francesca Bosetti
National Institute on Aging · US

Funding

Role of cyclooxygenases in neuroinflammationZIAAG000425 · NIA · NATIONAL INSTITUTE ON AGING · PI BOSETTI, FRANCESCA · 2009 to 2010
$682k
Intramural NIH HHS
6 · The paper itself

Abstract

Several independent epidemiological studies indicate that chronic use of non-steroidal anti-inflammatory drugs can reduce the risk of developing Alzheimer's disease (AD), supporting the inflammatory cascade hypothesis. Although the first clinical trial with indomethacin, a preferential cyclooxygenase (COX)-1 inhibitor, showed beneficial effects, subsequent large clinical trials, mostly using COX-2 inhibitors, failed to show any beneficial effect in AD patients with mild to severe cognitive impairment. These combined data suggest that either an early treatment is crucial to stop the mechanisms underlying the disease before the onset of the symptoms, or that preferential COX-1 inhibition, rather than COX-2, is beneficial. Therefore, a full understanding of the physiological, pathological, and/or neuroprotective role of COX isoforms may help to develop better therapeutic strategies for the prevention or treatment of AD. In this study, we examined the effect of COX-1 genetic deletion on the inflammatory response and neurodegeneration induced by beta-amyloid. beta-amyloid (Abeta(1-42)) was centrally injected in the lateral ventricle of COX-1-deficient (COX-1(-/-)) and their respective wild-type (WT) mice. In COX-1(-/-) mice, Abeta(1-42)-induced inflammatory response and neuronal damage were attenuated compared to WT mice, as shown by Fluoro-Jade B and nitrotyrosine staining. These results indicate that inhibition of COX-1 activity may be valid therapeutic strategy to reduce brain inflammatory response and neurodegeneration.

Indexed as

Amyloid beta-PeptidesAnimalsBrain DiseasesCyclooxygenase 1HippocampusInflammationMiceMice, KnockoutNeurogliaOxidative StressPeptide FragmentsAmyloid beta-Peptidesamyloid beta-protein (1-42)Cyclooxygenase 1Peptide Fragmentscyclooxygenasemicroglianeuroinflammationneurotoxicityoxidative stress

Identifiers

PMID20157512
PMCPMC2806008
OpenAlexW2154176348

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.