Evidence map›Paper›PMID 24223903›Full record

ArticlePloS one2013

Neuroprotection in a novel mouse model of multiple sclerosis.

Katie Lidster, Samuel J Jackson, Zubair Ahmed, Peter Munro, Pete Coffey, Gavin Giovannoni, Mark D Baker, David Baker

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Semi-invasive and non-invasive recording of visual evoked potentials in mice.Documenta ophthalmologica. Advances in ophthalmology · 2019
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Retinal Cell Degeneration in Animal Models.International journal of molecular sciences · 2016
    Review
  17. Article
  18. Stepchild or Prodigy? Neuroprotection in Multiple Sclerosis (MS) Research.International journal of molecular sciences · 2015
    Review
  19. Article
  20. 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

8 authors at 3 institutions in 1 country.

Katie LidsterBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Samuel J Jackson
Zubair Ahmed
Peter Munro
Pete Coffey
Gavin Giovannoni
Mark D Baker
David Baker
Queen Mary University of London · GBUniversity College London · GBUniversity of Birmingham · GB

Funding

National Centre for the Replacement, Refinement and Reduction of Animals in Research G1000094/1Wellcome TrustWellcome Trust 092539
6 · The paper itself

Abstract

Multiple sclerosis is an immune-mediated, demyelinating and neurodegenerative disease that currently lacks any neuroprotective treatments. Innovative neuroprotective trial designs are required to hasten the translational process of drug development. An ideal target to monitor the efficacy of strategies aimed at treating multiple sclerosis is the visual system, which is the most accessible part of the human central nervous system. A novel C57BL/6 mouse line was generated that expressed transgenes for a myelin oligodendrocyte glycoprotein-specific T cell receptor and a retinal ganglion cell restricted-Thy1 promoter-controlled cyan fluorescent protein. This model develops spontaneous or induced optic neuritis, in the absence of paralytic disease normally associated with most rodent autoimmune models of multiple sclerosis. Demyelination and neurodegeneration could be monitored longitudinally in the living animal using electrophysiology, visual sensitivity, confocal scanning laser ophthalmoscopy and optical coherence tomography all of which are relevant to human trials. This model offers many advantages, from a 3Rs, economic and scientific perspective, over classical experimental autoimmune encephalomyelitis models that are associated with substantial suffering of animals. Optic neuritis in this model led to inflammatory damage of axons in the optic nerve and subsequent loss of retinal ganglion cells in the retina. This was inhibited by the systemic administration of a sodium channel blocker (oxcarbazepine) or intraocular treatment with siRNA targeting caspase-2. These novel approaches have relevance to the future treatment of neurodegeneration of MS, which has so far evaded treatment.

Indexed as

Disease Models, AnimalRNA InterferenceAnimalsAnticonvulsantsCarbamazepineCaspase 2Evoked Potentials, VisualGreen Fluorescent ProteinsHumansMiceMice, Inbred C57BLMice, TransgenicMicroscopy, ConfocalMultiple SclerosisMyelin-Oligodendrocyte GlycoproteinOphthalmoscopyAnticonvulsantsCarbamazepineCaspase 2Cyan Fluorescent ProteinGreen Fluorescent ProteinsMyelin-Oligodendrocyte GlycoproteinOxcarbazepineReceptors, Antigen, T-Cell

Identifiers

PMID24223903
PMCPMC3817036
OpenAlexW2025707873

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.