Evidence mapPaperPMID 26748744Full record

ReviewAnnals of the New York Academy of Sciences2016

Prostaglandin J2: a potential target for halting inflammation-induced neurodegeneration.

Maria E Figueiredo-Pereira, Chuhyon Corwin, John Babich

Abstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.1field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 43 citations in OpenAlex.

  1. Unique/Rapid Feedback Mechanisms of PGDBioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
  2. Article
  3. Review
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  5. Article
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  9. Cytosolic condensates rich in polyserine define subcellular sites of tau aggregation.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. 15-Deoxy-ΔJournal of cancer prevention · 2020
    Article
  15. Article
  16. Article
  17. The Role of Eicosanoids in Alzheimer's Disease.International journal of environmental research and public health · 2019
    Review
  18. 15-Deoxy-ΔThe Journal of biological chemistry · 2019
    Article
  19. Prostaglandin A1 Inhibits the Cognitive Decline of APP/PS1 Transgenic Mice via PPARγ/ABCA1-dependent Cholesterol Efflux Mechanisms.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019
    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

3 authors at 3 institutions in 1 country.

Maria E Figueiredo-PereiraDepartment of Biological Sciences, Hunter College and the Graduate Center, CUNY, New York, New York.
Chuhyon CorwinDepartment of Biological Sciences, Hunter College and the Graduate Center, CUNY, New York, New York.
John BabichDepartment of Radiology, Weill Cornell Medical College, New York, New York.
Cornell University · USHunter College · USThe Graduate Center, CUNY · US

Funding

Clinical and Translational Science CenterUL1TR002384 · WEILL MEDICAL COLL OF CORNELL UNIV · 2025 to 2025
$9.8M
NCATS NIH HHS UL1 TR002384NCRR NIH HHS UL1 RR024996NCRR NIH HHS UL1-RR024996NIMHD NIH HHS G12 MD007599NIMHD NIH HHS MD007599
6 · The paper itself

Abstract

Prostaglandins (PGs) are produced via cyclooxygenases, which are enzymes that play a major role in neuroinflammation. Epidemiological studies show that chronic treatment with low levels of cyclooxygenase inhibitors (nonsteroidal anti-inflammatory drugs (NSAIDs)) lowers the risk for Alzheimer's disease (AD) and Parkinson's disease (PD) by as much as 50%. Unfortunately, inhibiting cyclooxygenases with NSAIDs blocks the synthesis of downstream neuroprotective and neurotoxic PGs, thus producing adverse side effects. We focus on prostaglandin J2 (PGJ2) because it is highly neurotoxic compared to PGA1, D2, and E2. Unlike other PGs, PGJ2 and its metabolites have a cyclopentenone ring with reactive α,β-unsaturated carbonyl groups that form covalent Michael adducts with key cysteines in proteins and GSH. Cysteine-binding electrophiles such as PGJ2 are considered to play an important role in determining whether neurons will live or die. We discuss in vitro and in vivo studies showing that PGJ2 induces pathological processes relevant to neurodegenerative disorders such as AD and PD. Further, we discuss our work showing that increasing intracellular cAMP with the lipophilic peptide PACAP27 counteracts some of the PGJ2-induced detrimental effects. New therapeutic strategies that neutralize the effects of specific neurotoxic PGs downstream from cyclooxygenases could have a significant impact on the treatment of chronic neurodegenerative disorders with fewer adverse side effects.

Indexed as

Alzheimer DiseaseAnimalsDisease Models, AnimalHumansInflammationLipopolysaccharidesNeurodegenerative DiseasesNeuronsParkinson DiseaseProstaglandin D2ProstaglandinsProtein BindingProtein Processing, Post-TranslationalReceptors, ProstaglandinSignal Transduction9-deoxy-delta-9-prostaglandin D2LipopolysaccharidesProstaglandin D2ProstaglandinsReceptors, ProstaglandinAlzheimer's diseaseschronic inflammationcyclooxygenasesMichael adductsNSAIDParkinson's diseaseprostaglandin J2

Identifiers

PMID26748744
PMCPMC4801700
OpenAlexW2233830471

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.