Reversal of

Edward S Wickstead, Husnain A Karim, Roberta E Manuel, Christopher S Biggs, Stephen J Getting, Simon McArthur

Open access · hybridAbstract read

In one paragraph

Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it

0cells of the map it votes in

8citing papers in PubMed

1.0field-weighted citation impact, top 23% 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

8 citing papers in PubMed, 17 citations in OpenAlex.

Decoding microglial immunometabolism: a new frontier in Alzheimer's disease research.Molecular neurodegeneration · 2025
Review
Stimulation of the Pro-Resolving Receptor Fpr2 Reverses Inflammatory Microglial Activity by Suppressing NFκB Activity.International journal of molecular sciences · 2023
Article
Moderate intrinsic phenotypic alterations inFrontiers in cellular neuroscience · 2023
Article
Promiscuous Receptors and Neuroinflammation: The Formyl Peptide Class.Life (Basel, Switzerland) · 2022
Review
Near-infrared light reduces β-amyloid-stimulated microglial toxicity and enhances survival of neurons: mechanisms of light therapy for Alzheimer's disease.Alzheimer's research & therapy · 2022
Article
Time-Dependent Protective and Pro-Resolving Effects of FPR2 Agonists on Lipopolysaccharide-Exposed Microglia Cells Involve Inhibition of NF-κB and MAPKs Pathways.Cells · 2021
Article
The Role of Formyl Peptide Receptors in Neurological Diseases via Regulating Inflammation.Frontiers in cellular neuroscience · 2021
Review
Cerebrovascular damage caused by the gut microbe/host co-metaboliteGut microbes
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

6 authors at 2 institutions in 1 country.

Edward S WicksteadInstitute of Dentistry, Barts and the London School of Medicine & Dentistry, Queen Mary, University of London, Blizard Institute, 4, Newark Street, London E1 2AT, UK.

Husnain A KarimInstitute of Dentistry, Barts and the London School of Medicine & Dentistry, Queen Mary, University of London, Blizard Institute, 4, Newark Street, London E1 2AT, UK.

Roberta E ManuelInstitute of Dentistry, Barts and the London School of Medicine & Dentistry, Queen Mary, University of London, Blizard Institute, 4, Newark Street, London E1 2AT, UK.

Christopher S BiggsCollege of Liberal Arts & Sciences, University of Westminster, 115, New Cavendish Street, London W1W 6UW, UK.

Stephen J GettingCollege of Liberal Arts & Sciences, University of Westminster, 115, New Cavendish Street, London W1W 6UW, UK.

Simon McArthurInstitute of Dentistry, Barts and the London School of Medicine & Dentistry, Queen Mary, University of London, Blizard Institute, 4, Newark Street, London E1 2AT, UK.ORCID https://orcid.org/0000-0001-8521-1808

Queen Mary University of London · GBUniversity of Westminster · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglial inflammatory activity is thought to be a major contributor to the pathology of neurodegenerative conditions such as Alzheimer's disease (AD), and strategies to restrain their behaviour are under active investigation. Classically, anti-inflammatory approaches are aimed at suppressing proinflammatory mediator production, but exploitation of inflammatory resolution, the endogenous process whereby an inflammatory reaction is terminated, has not been fully investigated as a therapeutic approach in AD. In this study, we sought to provide proof-of-principle that the major proresolving actor, formyl peptide receptor 2, Fpr2, could be targeted to reverse microglial activation induced by the AD-associated proinflammatory stimulus, oligomeric

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAntioxidantsCell LineCell RespirationEnzyme ActivationHumansInflammationMiceMicrogliaMitochondriaNADPH OxidasesNeuronsPentose Phosphate PathwayReactive Oxygen SpeciesAmyloid beta-PeptidesAntioxidantsformyl peptide receptor 2, mouseFpr3 protein, mouseNADPH OxidasesReactive Oxygen SpeciesReceptors, Formyl Peptide

Identifiers

PMID32617132

DOI10.1155/2020/2139192

PMCPMC7313167

OpenAlexW3034941436

What OpenQuestion holds

Textmetadata

LicenceCC BY

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.