Evidence map›Paper›PMID 37047344›Full record

ReviewInternational journal of molecular sciences2023

Mechanisms of Demyelination and Remyelination Strategies for Multiple Sclerosis.

Xinda Zhao, Claire Jacob

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

29 citing papers in PubMed, 37 citations in OpenAlex.

  1. Beyond Histamine Blockade: Clemastine Fumarate as a Promoter of Myelin Regeneration, Inflammatory Regulation, and Neuroimmune Modulation in CNS Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Review
  2. Review
  3. Article
  4. CRISPR-Based Gene Therapy for Brain Disease.Molecular neurobiology · 2026
    Review
  5. Review
  6. Rethinking MS Therapeutics: From Disease Pathogenesis Mechanisms to AI-Driven Drug Discovery.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Progressive multiple sclerosis: Evaluating current therapies and exploring future treatment strategies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  13. Repair mechanisms of the central nervous system: From axon sprouting to remyelination.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Linking Pathogenesis to Fall Risk in Multiple Sclerosis.Archives of internal medicine research · 2025
    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

2 authors at 1 institution in 1 country.

Xinda ZhaoInstitute of Developmental Biology and Neurobiology, Faculty of Biology, Johannes-Gutenberg University, Hanns-Dieter-Hüsch-Weg 15, 55128 Mainz, Germany.ORCID 0009-0005-0576-8355
Claire JacobInstitute of Developmental Biology and Neurobiology, Faculty of Biology, Johannes-Gutenberg University, Hanns-Dieter-Hüsch-Weg 15, 55128 Mainz, Germany.ORCID 0000-0001-9567-3950
Johannes Gutenberg University Mainz · DE

Funding

Deutsche Forschungsgemeinschaft SFB/CRC-TR 128
6 · The paper itself

Abstract

All currently licensed medications for multiple sclerosis (MS) target the immune system. Albeit promising preclinical results demonstrated disease amelioration and remyelination enhancement via modulating oligodendrocyte lineage cells, most drug candidates showed only modest or no effects in human clinical trials. This might be due to the fact that remyelination is a sophistically orchestrated process that calls for the interplay between oligodendrocyte lineage cells, neurons, central nervous system (CNS) resident innate immune cells, and peripheral immune infiltrates and that this process may somewhat differ in humans and rodent models used in research. To ensure successful remyelination, the recruitment and activation/repression of each cell type should be regulated in a highly organized spatio-temporal manner. As a result, drug candidates targeting one single pathway or a single cell population have difficulty restoring the optimal microenvironment at lesion sites for remyelination. Therefore, when exploring new drug candidates for MS, it is instrumental to consider not only the effects on all CNS cell populations but also the optimal time of administration during disease progression. In this review, we describe the dysregulated mechanisms in each relevant cell type and the disruption of their coordination as causes of remyelination failure, providing an overview of the complex cell interplay in CNS lesion sites.

Indexed as

Multiple SclerosisRemyelinationCentral Nervous SystemHumansMyelin SheathNeuronsOligodendrogliaepigeneticsimmune cellsmultiple sclerosisoligodendrocytesremyelinationtranscription factors

Identifiers

PMID37047344
PMCPMC10093908
OpenAlexW4361285689

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.