Evidence map›Paper›PMID 26979823›Full record

ReviewACS chemical neuroscience2016

Untangling the Web: Toxic and Protective Effects of Neuroinflammation and PGE2 Signaling in Alzheimer's Disease.

Nathaniel S Woodling, Katrin I Andreasson

Open access · greenAbstract readReview
In one paragraph

Review in ACS chemical neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Frontiers in aging · 2026
    Article
  4. Neuroinflammation and Disease: Pathways and Opportunities.Annual review of pharmacology and toxicology · 2026
    Review
  5. Article
  6. Article
  7. Inhibition of neuroinflammation and neuronal damage by the selective non-steroidal ERβ agonist AC-186.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. The inducible prostaglandin E synthase (mPGES-1) in neuroinflammatory disorders.Experimental biology and medicine (Maywood, N.J.) · 2023
    Review
  13. Article
  14. Dihydroquercetin ameliorates LPS-induced neuroinflammation and memory deficit.Current research in pharmacology and drug discovery · 2022
    Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Review
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

2 authors at 1 institution in 1 country.

Nathaniel S WoodlingDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine , 1201 Welch Road, Stanford, California 94305, United States.
Katrin I AndreassonDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine , 1201 Welch Road, Stanford, California 94305, United States.
Stanford University · US

Funding

Working Memory in Parkinson Disease: A Cognitive & Systems Neuroscience ApproachP50AG047366 · NIA · STANFORD UNIVERSITY · PI GREICIUS, MICHAEL D · 2015 to 2019
$7.9M
Targeting the kynurenine pathway in Alzheimer's diseaseR01AG048232 · NIA · STANFORD UNIVERSITY · PI ANDREASSON, KATRIN I. · 2014 to 2018
$2.4M
Prostanoid signaling and inflammation in aging and Alzheimer's diseaseR01AG030209 · NIA · STANFORD UNIVERSITY · PI ANDREASSON, KATRIN I. · 2009 to 2013
$1.6M
MODELS OF ALZHEIMER'S DISEASER01AG015799 · NIA · JOHNS HOPKINS UNIVERSITY · PI ANDREASSON, KATRIN I · 2000 to 2003
$982k
Validation of the PGE2 EP4 receptor as a therapeutic target in ADR21AG033914 · NIA · STANFORD UNIVERSITY · PI ANDREASSON, KATRIN I. · 2009 to 2010
$892k
Cellular and Molecular Mechanisms of Inflammation in Alzheimer's DiseaseF31AG039195 · NIA · STANFORD UNIVERSITY · PI WOODLING, NATHANIEL S · 2011 to 2012
$55k
NIA NIH HHS F31 AG039195NIA NIH HHS F31AG039195NIA NIH HHS P50 AG047366NIA NIH HHS R01 AG030209NIA NIH HHS R01AG030209NIA NIH HHS R01 AG048232NIA NIH HHS R01AG048232NIA NIH HHS R01AG15799NIA NIH HHS R21 AG033914NIA NIH HHS R21AG033914
6 · The paper itself

Abstract

The neuroinflammatory response has received increasing attention as a key factor in the pathogenesis of Alzheimer's disease (AD). Microglia, the innate immune cells and resident phagocytes of the brain, respond to accumulating Aβ peptides by generating a nonresolving inflammatory response. While this response can clear Aβ peptides from the nervous system in some settings, its failure to do so in AD accelerates synaptic injury, neuronal loss, and cognitive decline. The complex molecular components of this response are beginning to be unraveled, with identification of both damaging and protective roles for individual components of the neuroinflammatory response. Even within one molecular pathway, contrasting effects are often present. As one example, recent studies of the inflammatory cyclooxygenase-prostaglandin pathway have revealed both beneficial and detrimental effects dependent on the disease context, cell type, and downstream signaling pathway. Nonsteroidal anti-inflammatory drugs (NSAIDs), which inhibit cyclooxygenases, are associated with reduced AD risk when taken by cognitively normal populations, but additional clinical and mouse model studies have added complexities and caveats to this finding. Downstream of cyclooxygenase activity, prostaglandin E2 signaling exerts both damaging pro-inflammatory and protective anti-inflammatory effects through actions of specific E-prostanoid G-protein coupled receptors on specific cell types. These complexities underscore the need for careful study of individual components of the neuroinflammatory response to better understand their contribution to AD pathogenesis and progression.

Indexed as

Alzheimer DiseaseAnimalsDinoprostEncephalitisHumansMicrogliaSignal TransductionDinoprostAlzheimer’s diseaseamyloid βand EP4 receptorcyclooxgenasesEP2 receptorEP3 receptormicroglianeuroinflammationprostaglandin E2

Identifiers

PMID26979823
PMCPMC5239037
OpenAlexW2301642572

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.