Evidence map›Paper›PMID 32710244›Full record

ArticleActa neuropathologica2020

Lesion stage-dependent causes for impaired remyelination in MS.

Katharina Heß, Laura Starost, Nicholas W Kieran, Christian Thomas, Maria C J Vincenten, Jack Antel, Gianvito Martino, Inge Huitinga, Luke Healy, Tanja Kuhlmann

Abstract read
In one paragraph

Article in Acta neuropathologica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing 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

81 citing papers in PubMed.

  1. Astrocytes in Multiple Sclerosis: Getting to the Core.International journal of molecular sciences · 2026
    Review
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  7. Targeting neuroinflammation in neurodegenerative disorders: the emerging potential of semaglutide.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Multiple sclerosis: molecular pathogenesis and therapeutic intervention.Signal transduction and targeted therapy · 2025
    Review
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  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

21 more citing papers are in PubMed but not listed here.

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

10 authors.

Katharina HeßInstitut für Neuropathologie, Universitätsklinikum Münster, Pottkamp 2, 48149, Münster, Germany.
Laura StarostInstitut für Neuropathologie, Universitätsklinikum Münster, Pottkamp 2, 48149, Münster, Germany.
Nicholas W KieranMontreal Neurological Institute, McGill University, Montreal, Canada.
Christian ThomasInstitut für Neuropathologie, Universitätsklinikum Münster, Pottkamp 2, 48149, Münster, Germany.
Maria C J VincentenDepartment of Neuroimmunology, The Netherlands Institute for Neuroscience, Amsterdam, The Netherlands.
Jack AntelMontreal Neurological Institute, McGill University, Montreal, Canada.
Gianvito MartinoNeuroimmunology Unit, Division of Neuroscience, Institute of Experimental Neurology, IRCCS San Raffaele Hospital, 20132, Milan, Italy.
Inge HuitingaDepartment of Neuroimmunology, The Netherlands Institute for Neuroscience, Amsterdam, The Netherlands.
Luke HealyMontreal Neurological Institute, McGill University, Montreal, Canada.
Tanja KuhlmannInstitut für Neuropathologie, Universitätsklinikum Münster, Pottkamp 2, 48149, Münster, Germany. tanja.kuhlmann@ukmuenster.de.ORCID http://orcid.org/0000-0002-0174-5042

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is the most frequent demyelinating disease and a leading cause for disability in young adults. Despite significant advances in immunotherapies in recent years, disease progression still cannot be prevented. Remyelination, meaning the formation of new myelin sheaths after a demyelinating event, can fail in MS lesions. Impaired differentiation of progenitor cells into myelinating oligodendrocytes may contribute to remyelination failure and, therefore, the development of pharmacological approaches which promote oligodendroglial differentiation and by that remyelination, represents a promising new treatment approach. However, this generally accepted concept has been challenged recently. To further understand mechanisms contributing to remyelination failure in MS, we combined detailed histological analyses assessing oligodendroglial cell numbers, presence of remyelination as well as the inflammatory environment in different MS lesion types in white matter with in vitro experiments using induced-pluripotent stem cell (iPSC)-derived oligodendrocytes (hiOL) and supernatants from polarized human microglia. Our findings suggest that there are multiple reasons for remyelination failure in MS which are dependent on lesion stage. These include lack of myelin sheath formation despite the presence of mature oligodendrocytes in a subset of active lesions as well as oligodendroglial loss and a hostile tissue environment in mixed active/inactive lesions. Therefore, we conclude that better in vivo and in vitro models which mimic the pathological hallmarks of the different MS lesion types are required for the successful development of remyelination promoting drugs.

Indexed as

AdultAgedCell DifferentiationDemyelinating DiseasesHumansMicrogliaMiddle AgedMultiple SclerosisMyelin SheathOligodendrogliaRemyelinationStem CellsMicrogliaMultiple sclerosisOligodendrocytesRemyelination

Identifiers

PMID32710244
PMCPMC7424408

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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.