Evidence map›Paper›PMID 24434190›Full record

ReviewBiochemical pharmacology2014

Therapeutic implications of the prostaglandin pathway in Alzheimer's disease.

Eiron Cudaback, Nikolas L Jorstad, Yue Yang, Thomas J Montine, C Dirk Keene

Abstract readReview
In one paragraph

Review in Biochemical pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
9.8field-weighted citation impact, top 1% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Effect of Bushen Huoxue Prescription on Cognitive Dysfunction of KK-Ay Type 2 Diabetic Mice.Evidence-based complementary and alternative medicine : eCAM · 2021
    Article
  9. Article
  10. Article
  11. 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
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
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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

5 authors at 2 institutions in 1 country.

Eiron CudabackUniversity of Washington Harborview Medical Center, Department of Pathology, Box 359791, 325 Ninth Ave, Seattle, WA 98104, USA.
Nikolas L JorstadUniversity of Washington Harborview Medical Center, Department of Pathology, Box 359791, 325 Ninth Ave, Seattle, WA 98104, USA.
Yue YangUniversity of Washington Harborview Medical Center, Department of Pathology, Box 359791, 325 Ninth Ave, Seattle, WA 98104, USA.
Thomas J MontineUniversity of Washington Harborview Medical Center, Department of Pathology, Box 359791, 325 Ninth Ave, Seattle, WA 98104, USA.
C Dirk KeeneUniversity of Washington Harborview Medical Center, Department of Pathology, Box 359791, 325 Ninth Ave, Seattle, WA 98104, USA. Electronic address: cdkeene@uw.edu.
University of Washington · USHarborview Medical Center · US

Funding

THERAPEUTIC EFFECTS OF INTRA-NASAL INSULIN DETEMIRP50AG005136 · NIA · UNIVERSITY OF WASHINGTON · PI GRABOWSKI, THOMAS J. · 1985 to 2019
$57.2M
Toxicants and innate immunity in models of Parkinson's diseaseR01ES016754 · NIEHS · UNIVERSITY OF WASHINGTON · PI MONTINE, THOMAS J · 2009 to 2013
$1.7M
NIA NIH HHS P50 AG005136NIA NIH HHS P50AG05136NIEHS NIH HHS ES16754NIEHS NIH HHS R01 ES016754
6 · The paper itself

Abstract

An important pathologic hallmark of Alzheimer's disease (AD) is neuroinflammation, a process characterized in AD by disproportionate activation of cells (microglia and astrocytes, primarily) of the non-specific innate immune system within the CNS. While inflammation itself is not intrinsically detrimental, a delicate balance of pro- and anti-inflammatory signals must be maintained to ensure that long-term exaggerated responses do not damage the brain over time. Non-steroidal anti-inflammatory drugs (NSAIDs) represent a broad class of powerful therapeutics that temper inflammation by inhibiting cyclooxygenase-mediated signaling pathways including prostaglandins, which are the principal mediators of CNS neuroinflammation. While historically used to treat discrete or systemic inflammatory conditions, epidemiologic evidence suggests that protracted NSAID use may delay AD onset, as well as decrease disease severity and rate of progression. Unfortunately, clinical trials with NSAIDs have thus far yielded disappointing results, including premature discontinuation of a large-scale prevention trial due to unexpected cardiovascular side effects. Here we review the literature and make the argument that more targeted exploitation of downstream prostaglandin signaling pathways may offer significant therapeutic benefits for AD while minimizing adverse side effects. Directed strategies such as these may ultimately help to delay the deleterious consequences of brain aging and might someday lead to new therapies for AD and other chronic neurodegenerative diseases.

Indexed as

Alzheimer DiseaseAnti-Inflammatory Agents, Non-SteroidalClinical Trials as TopicHumansProstaglandin-Endoperoxide SynthasesProstaglandinsSignal TransductionAnti-Inflammatory Agents, Non-SteroidalProstaglandin-Endoperoxide SynthasesProstaglandinsAlzheimer's diseaseCyclooxygenaseNeuroinflammationNSAIDProstaglandin

Identifiers

PMID24434190
PMCPMC3972296
OpenAlexW2008002430

What OpenQuestion 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 OpenQuestion graph.