Evidence map›Paper›PMID 32293054›Full record

ArticleAnnals of neurology2020

Nimodipine Reduces Dysfunction and Demyelination in Models of Multiple Sclerosis.

Roshni A Desai, Andrew L Davies, Natalie Del Rossi, Mohamed Tachrount, Alex Dyson, Britta Gustavson, Pardis Kaynezhad, Lewis Mackenzie, Marieke A van der Putten, Daniel McElroy and 7 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Annals of neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.0field-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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Hypoxia in multiple sclerosis.Redox biology · 2025
    Review
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  6. Review
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  14. Protective Effect of Nimodipine Against Valproic-acid Induced Biochemical and Behavioral Phenotypes of Autism.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2022
    Article
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  18. 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

17 authors at 8 institutions in 1 country.

Roshni A DesaiDepartment of Neuroinflammation, UCL Queen Square Institute of Neurology, University College London, London, UK.ORCID 0000-0001-5005-3678
Andrew L DaviesDepartment of Neuroinflammation, UCL Queen Square Institute of Neurology, University College London, London, UK.
Natalie Del RossiDepartment of Neuroinflammation, UCL Queen Square Institute of Neurology, University College London, London, UK.
Mohamed TachrountDepartment of Brain Repair and Rehabilitation, UCL Queen Square Institute of Neurology, University College London, London, UK.
Alex DysonBloomsbury Institute for Intensive Care Medicine, Division of Medicine, University College London, London, UK.
Britta GustavsonDepartment of Neuroinflammation, UCL Queen Square Institute of Neurology, University College London, London, UK.
Pardis KaynezhadBiomedical Optics Research Laboratory, Department of Medical Physics and Biomedical Engineering, University College London, London, UK.
Lewis MackenzieSchool of Physics & Astronomy, University of Glasgow, Glasgow, UK.
Marieke A van der PuttenSchool of Physics & Astronomy, University of Glasgow, Glasgow, UK.
Daniel McElroyGlasgow Biomedical Research Centre, Room B3-19, 120 University Place, University of Glasgow, Glasgow, UK.
Dimitra SchizaDepartment of Neuroinflammation, UCL Queen Square Institute of Neurology, University College London, London, UK.
Christopher LiningtonGlasgow Biomedical Research Centre, Room B3-19, 120 University Place, University of Glasgow, Glasgow, UK.
Mervyn SingerBloomsbury Institute for Intensive Care Medicine, Division of Medicine, University College London, London, UK.
Andrew R HarveySchool of Physics & Astronomy, University of Glasgow, Glasgow, UK.
Ilias TachtsidisBiomedical Optics Research Laboratory, Department of Medical Physics and Biomedical Engineering, University College London, London, UK.
Xavier GolayDepartment of Brain Repair and Rehabilitation, UCL Queen Square Institute of Neurology, University College London, London, UK.
Kenneth J SmithDepartment of Neuroinflammation, UCL Queen Square Institute of Neurology, University College London, London, UK.
Queen Mary University of London · GBUniversity of Glasgow · GBBury College · GBUniversity College London · GBDurham University · GBFreeman Hospital · GBJohn Radcliffe Hospital · GBMRC Prion Unit · GB

Funding

National Centre for the Replacement, Refinement and Reduction of Animals in Research NC/L001969/1Wellcome Trust
6 · The paper itself

Abstract

objectiveTreatment of relapses in multiple sclerosis (MS) has not advanced beyond steroid use, which reduces acute loss of function, but has little effect on residual disability. Acute loss of function in an MS model (experimental autoimmune encephalomyelitis [EAE]) is partly due to central nervous system (CNS) hypoxia, and function can promptly improve upon breathing oxygen. Here, we investigate the cause of the hypoxia and whether it is due to a deficit in oxygen supply arising from impaired vascular perfusion. We also explore whether the CNS-selective vasodilating agent, nimodipine, may provide a therapy to restore function, and protect from demyelination in 2 MS models.

methodsA variety of methods have been used to measure basic cardiovascular physiology, spinal oxygenation, mitochondrial function, and tissue perfusion in EAE.

resultsWe report that the tissue hypoxia in EAE is associated with a profound hypoperfusion of the inflamed spinal cord. Treatment with nimodipine restores spinal oxygenation and can rapidly improve function. Nimodipine therapy also reduces demyelination in both EAE and a model of the early MS lesion.

interpretationLoss of function in EAE, and demyelination in EAE, and the model of the early MS lesion, seem to be due, at least in part, to tissue hypoxia due to local spinal hypoperfusion. Therapy to improve blood flow not only protects neurological function but also reduces demyelination. We conclude that nimodipine could be repurposed to offer substantial clinical benefit in MS. ANN NEUROL 2020 ANN NEUROL 2020;88:123-136.

Indexed as

AnimalsCalcium Channel BlockersDisease ProgressionEncephalomyelitis, Autoimmune, ExperimentalFemaleMagnetic Resonance ImagingMaleMyelin SheathNimodipineRatsRats, Sprague-DawleySpinal CordCalcium Channel BlockersNimodipine

Identifiers

PMID32293054
PMCPMC7737229
OpenAlexW3015778590

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.