Evidence map›Paper›PMID 34576080›Full record

ArticleInternational journal of molecular sciences2021

Platelet Inhibition by Low-Dose Acetylsalicylic Acid Reduces Neuroinflammation in an Animal Model of Multiple Sclerosis.

Anna Vogelsang, Susann Eichler, Niklas Huntemann, Lars Masanneck, Hannes Böhnlein, Lisa Schüngel, Alice Willison, Karin Loser, Bernhard Nieswandt, Beate E Kehrel and 3 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
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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

13 authors at 5 institutions in 2 countries.

Anna VogelsangDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, 48149 Münster, Germany.
Susann EichlerDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, 48149 Münster, Germany.
Niklas HuntemannDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, 48149 Münster, Germany.ORCID 0000-0003-0015-8484
Lars MasanneckDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, 48149 Münster, Germany.
Hannes BöhnleinDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, 48149 Münster, Germany.
Lisa SchüngelDepartment of Anesthesiology, Intensive Care and Pain Medicine, University Hospital Münster, 48149 Münster, Germany.
Alice WillisonThe Northern Foundation School, Newcastle-upon-Tyne University Hospitals, Newcastle-upon-Tyne NE15 8NY, UK.
Karin LoserDepartment of Human Medicine, Institute of Immunology, Carl von Ossietzky University Oldenburg, 26129 Oldenburg, Germany.ORCID 0000-0002-0007-0936
Bernhard NieswandtRudolf Virchow Center, Research Center for Experimental Biomedicine, University of Würzburg, 97080 Würzburg, Germany.
Beate E KehrelDepartment of Anesthesiology, Intensive Care and Pain Medicine, University Hospital Münster, 48149 Münster, Germany.
Alexander ZarbockDepartment of Anesthesiology, Intensive Care and Pain Medicine, University Hospital Münster, 48149 Münster, Germany.
Kerstin GöbelDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, 48149 Münster, Germany.ORCID 0000-0002-1579-9076
Sven G MeuthDepartment of Neurology, University Hospital Düsseldorf, 40225 Düsseldorf, Germany.
University Hospital Münster · DEDüsseldorf University Hospital · DECarl von Ossietzky Universität Oldenburg · DENewcastle upon Tyne Hospitals NHS Foundation Trust · GBUniversity of Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aside from the established immune-mediated etiology of multiple sclerosis (MS), compelling evidence implicates platelets as important players in disease pathogenesis. Specifically, numerous studies have highlighted that activated platelets promote the central nervous system (CNS)-directed adaptive immune response early in the disease course. Platelets, therefore, present a novel opportunity for modulating the neuroinflammatory process that characterizes MS. We hypothesized that the well-known antiplatelet agent acetylsalicylic acid (ASA) could inhibit neuroinflammation by affecting platelets if applied at low-dose and investigated its effect during experimental autoimmune encephalomyelitis (EAE) as a model to study MS. We found that oral administration of low-dose ASA alleviates symptoms of EAE accompanied by reduced inflammatory infiltrates and less extensive demyelination. Remarkably, the percentage of CNS-infiltrated CD4

Indexed as

AnimalsAspirinBlood PlateletsBrainCD4-Positive T-LymphocytesDisease Models, AnimalDose-Response Relationship, DrugEncephalomyelitis, Autoimmune, ExperimentalInflammationMiceMice, Inbred C57BLMultiple SclerosisPlatelet Aggregation InhibitorsThromboxane A2AspirinPlatelet Aggregation InhibitorsThromboxane A2acetylsalicylic acidexperimental autoimmune encephalomyelitisglycoprotein VImultiple sclerosisplatelet factor 4plateletsthromboxane

Identifiers

PMID34576080
PMCPMC8465626
OpenAlexW3200123530

What OpenQuestion holds

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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.