ReviewAnnals of the New York Academy of Sciences2016
Prostaglandin J2: a potential target for halting inflammation-induced neurodegeneration.
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.
What it found
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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
19 citing papers in PubMed, 43 citations in OpenAlex.
- Unique/Rapid Feedback Mechanisms of PGDBioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Multi-omic insight into the molecular mechanism of cuproptosis-related genes in the pathogenesis of Parkinson's disease.NPJ Parkinson's disease · 2026Article
- Prostaglandins: Biological Action, Therapeutic Aspects, and Pathophysiology of Autism Spectrum Disorders.Current issues in molecular biology · 2025Review
- Editorial: Current chemical approaches in combating neuroinflammation in Alzheimer's disease (AD).Frontiers in aging neuroscience · 2025Article
- Differential effect of an evolving amyloid and tau pathology on brain phospholipids and bioactive lipid mediators in rat models of Alzheimer-like pathology.Journal of neuroinflammation · 2024Article
- Plasma metabolome analysis for predicting antiviral treatment efficacy in chronic hepatitis B: diagnostic biomarkers and therapeutic insights.Frontiers in immunology · 2024Article
- Short Survey on the Protein Modifications in Plasma during SARS-CoV-2 Infection.International journal of molecular sciences · 2023Article
- Spatial Metabolomics Reveals the Multifaceted Nature of Lamprey Buccal Gland and Its Diverse Mechanisms for Blood-Feeding.Communications biology · 2023Article
- Cytosolic condensates rich in polyserine define subcellular sites of tau aggregation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Effect of feeding a dried distillers' grains with solubles diet on the metabolism of the intestinal wall in Guanling crossbred cattle: a preliminary assessment.Frontiers in veterinary science · 2023Article
- Article
- Ablation of Selenbp1 Alters Lipid Metabolism via the Pparα Pathway in Mouse Kidney.International journal of molecular sciences · 2021Article
- Pharmacological Modulators of Small GTPases of Rho Family in Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2021Article
- 15-Deoxy-ΔJournal of cancer prevention · 2020Article
- Quantitative Profiling of Oxylipins in Acute Experimental Intracerebral Hemorrhage.Frontiers in neuroscience · 2020Article
- PACAP27 mitigates an age-dependent hippocampal vulnerability to PGJ2-induced spatial learning deficits and neuroinflammation in mice.Brain and behavior · 2020Article
- The Role of Eicosanoids in Alzheimer's Disease.International journal of environmental research and public health · 2019Review
- 15-Deoxy-ΔThe Journal of biological chemistry · 2019Article
- 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 · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
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.
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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 Socratic graph.