Evidence map›Paper›PMID 36875711›Full record

ReviewTherapeutic advances in neurological disorders2023

Microglia as a cellular target of diclofenac therapy in Alzheimer's disease.

Barbara E Stopschinski, Rick A Weideman, Danni McMahan, David A Jacob, Bertis B Little, Hsueh-Sheng Chiang, Nil Saez Calveras, Olaf Stuve

Open access · goldAbstract readReview
In one paragraph

Review in Therapeutic advances in neurological disorders, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Mechanisms of comorbidity between Alzheimer's disease and pain.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Personalized, Precision Medicine to Cure Alzheimer's Dementia: Approach #1.International journal of molecular sciences · 2024
    Review
  13. Review
  14. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Barbara E StopschinskiDepartment of Neurology, University of Texas Southwestern Medical Center, Dallas, TX, USA.ORCID https://orcid.org/0000-0002-5715-4567
Rick A WeidemanPharmacy Service, Dallas VA Medical Center, Dallas, TX, USA.
Danni McMahanPharmacy Service, Dallas VA Medical Center, Dallas, TX, USA.
David A JacobVeterans Integrated Service Network 17, Arlington, TX, USA.
Bertis B LittleSchool of Public Health and Information Sciences, University of Louisville, Louisville, KY, USA.
Hsueh-Sheng ChiangDepartment of Neurology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Nil Saez CalverasDepartment of Neurology, University of Texas Southwestern Medical Center, Dallas, TX, USA.ORCID https://orcid.org/0000-0002-9153-9700
Olaf StuveDepartment of Neurology, University of Texas Southwestern Medical Center, Dallas, TX, USA.ORCID https://orcid.org/0000-0002-0469-6872
Dallas VA Medical Center · USThe University of Texas Southwestern Medical Center · USUniversity of Louisville · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is an untreatable cause of dementia, and new therapeutic approaches are urgently needed. AD pathology is defined by extracellular amyloid plaques and intracellular neurofibrillary tangles. Research of the past decades has suggested that neuroinflammation plays a critical role in the pathophysiology of AD. This has led to the idea that anti-inflammatory treatments might be beneficial. Early studies investigated non-steroidal anti-inflammatory drugs (NSAIDS) such as indomethacin, celecoxib, ibuprofen, and naproxen, which had no benefit. More recently, protective effects of diclofenac and NSAIDs in the fenamate group have been reported. Diclofenac decreased the frequency of AD significantly compared to other NSAIDs in a large retrospective cohort study. Diclofenac and fenamates share similar chemical structures, and evidence from cell and mouse models suggests that they inhibit the release of pro-inflammatory mediators from microglia with leads to the reduction of AD pathology. Here, we review the potential role of diclofenac and NSAIDs in the fenamate group for targeting AD pathology with a focus on its potential effects on microglia.

Indexed as

Alzheimer’s diseasediclofenacmicroglianeuroinflammationNLRP3 inflammasomeNSAID

Identifiers

PMID36875711
PMCPMC9974624
OpenAlexW4323286837

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.