Evidence map›Paper›PMID 28542521›Full record

ArticlePloS one2017

Regeneration of myelin sheaths of normal length and thickness in the zebrafish CNS correlates with growth of axons in caliber.

Marja J Karttunen, Tim Czopka, Marieke Goedhart, Jason J Early, David A Lyons

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.0field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
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  8. Observational
  9. Article
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  11. CNS Hypomyelination Disrupts Axonal Conduction and Behavior in Larval Zebrafish.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  12. Article
  13. Review
  14. Review
  15. Proteome Profile of Myelin in the Zebrafish Brain.Frontiers in cell and developmental biology · 2021
    Article
  16. A Novel Lysolecithin Model for Visualizing DamageFrontiers in cell and developmental biology · 2021
    Article
  17. Article
  18. Article
  19. Review
  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

5 authors at 1 institution in 2 countries.

Marja J KarttunenCentre for Neuroregeneration, MS Society Centre for Translational Research, Euan MacDonald Centre for Motor Neurone Disease Research, University of Edinburgh, Edinburgh, United Kingdom.
Tim CzopkaCentre for Neuroregeneration, MS Society Centre for Translational Research, Euan MacDonald Centre for Motor Neurone Disease Research, University of Edinburgh, Edinburgh, United Kingdom.
Marieke GoedhartCentre for Neuroregeneration, MS Society Centre for Translational Research, Euan MacDonald Centre for Motor Neurone Disease Research, University of Edinburgh, Edinburgh, United Kingdom.
Jason J EarlyCentre for Neuroregeneration, MS Society Centre for Translational Research, Euan MacDonald Centre for Motor Neurone Disease Research, University of Edinburgh, Edinburgh, United Kingdom.
David A LyonsCentre for Neuroregeneration, MS Society Centre for Translational Research, Euan MacDonald Centre for Motor Neurone Disease Research, University of Edinburgh, Edinburgh, United Kingdom.ORCID http://orcid.org/0000-0003-1166-4454
Mott MacDonald (United Kingdom) · GB

Funding

Wellcome Trust 102836/Z/13/Z
6 · The paper itself

Abstract

Demyelination is observed in numerous diseases of the central nervous system, including multiple sclerosis (MS). However, the endogenous regenerative process of remyelination can replace myelin lost in disease, and in various animal models. Unfortunately, the process of remyelination often fails, particularly with ageing. Even when remyelination occurs, it is characterised by the regeneration of myelin sheaths that are abnormally thin and short. This imperfect remyelination is likely to have implications for the restoration of normal circuit function and possibly the optimal metabolic support of axons. Here we describe a larval zebrafish model of demyelination and remyelination. We employ a drug-inducible cell ablation system with which we can consistently ablate 2/3rds of oligodendrocytes in the larval zebrafish spinal cord. This leads to a concomitant demyelination of 2/3rds of axons in the spinal cord, and an innate immune response over the same time period. We find restoration of the normal number of oligodendrocytes and robust remyelination approximately two weeks after induction of cell ablation, whereby myelinated axon number is restored to control levels. Remarkably, we find that myelin sheaths of normal length and thickness are regenerated during this time. Interestingly, we find that axons grow significantly in caliber during this period of remyelination. This suggests the possibility that the active growth of axons may stimulate the regeneration of myelin sheaths of normal dimensions.

Indexed as

AnimalsAnimals, Genetically ModifiedAxonsCentral Nervous SystemDemyelinating DiseasesDisease Models, AnimalMicroscopy, Electron, TransmissionMyelin SheathOligodendrogliaRegenerationZebrafish

Identifiers

PMID28542521
PMCPMC5444792
OpenAlexW2617087134

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.