Evidence map›Paper›PMID 32290524›Full record

ArticleCells2020

Delayed Demyelination and Impaired Remyelination in Aged Mice in the Cuprizone Model.

Stefan Gingele, Florian Henkel, Sandra Heckers, Thiemo M Moellenkamp, Martin W Hümmert, Thomas Skripuletz, Martin Stangel, Viktoria Gudi

Abstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
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

30 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. White Matter Injury in Central Nervous System Disorders.Neuropsychiatric disease and treatment · 2025
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Remyelination in Multiple Sclerosis: Findings in the Cuprizone Model.International journal of molecular sciences · 2022
    Review
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.

Stefan GingeleDepartment of Neurology, Hannover Medical School, D-30625 Hannover, Germany.
Florian HenkelDepartment of Neurology, Hannover Medical School, D-30625 Hannover, Germany.ORCID 0000-0003-1465-8172
Sandra HeckersDepartment of Neurology, Hannover Medical School, D-30625 Hannover, Germany.
Thiemo M MoellenkampDepartment of Neurology, Hannover Medical School, D-30625 Hannover, Germany.
Martin W HümmertDepartment of Neurology, Hannover Medical School, D-30625 Hannover, Germany.
Thomas SkripuletzDepartment of Neurology, Hannover Medical School, D-30625 Hannover, Germany.
Martin StangelDepartment of Neurology, Hannover Medical School, D-30625 Hannover, Germany.ORCID 0000-0003-2504-5398
Viktoria GudiDepartment of Neurology, Hannover Medical School, D-30625 Hannover, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To unravel the failure of remyelination in multiple sclerosis (MS) and to test promising remyelinating treatments, suitable animal models like the well-established cuprizone model are required. However, this model is only standardized in young mice. This does not represent the typical age of MS patients. Furthermore, remyelination is very fast in young mice, hindering the examination of effects of remyelination-promoting agents. Thus, there is the need for a better animal model to study remyelination. We therefore aimed to establish the cuprizone model in aged mice. 6-month-old C57BL6 mice were fed with different concentrations of cuprizone (0.2-0.6%) for 5-6.5 weeks. De- and remyelination in the medial and lateral parts of the corpus callosum were analyzed by immunohistochemistry. Feeding aged mice 0.4% cuprizone for 6.5 weeks resulted in the best and most reliable administration scheme with virtually complete demyelination of the corpus callosum. This was accompanied by a strong accumulation of microglia and near absolute loss of mature oligodendrocytes. Subsequent remyelination was initially robust but remained incomplete. The remyelination process in mature adult mice better represents the age of MS patients and offers a better model for the examination of regenerative therapies.

Indexed as

AnimalsCuprizoneDemyelinating DiseasesDisease Models, AnimalMaleMiceMonoamine Oxidase InhibitorsMultiple SclerosisRemyelinationCuprizoneMonoamine Oxidase Inhibitorsageastrocytecuprizonedemyelinationmicrogliamultiple sclerosismyelinoligodendrocyteremyelination

Identifiers

PMID32290524
PMCPMC7226973

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Registered trials

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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.