Evidence map›Paper›PMID 39384784›Full record

ArticleNature communications2024

CRISPR-edited human ES-derived oligodendrocyte progenitor cells improve remyelination in rodents.

Laura J Wagstaff, Nadine Bestard-Cuche, Maja Kaczmarek, Antonella Fidanza, Lorraine McNeil, Robin J M Franklin, Anna C Williams

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
–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

18 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. CRISPR-Based Gene Therapy for Brain Disease.Molecular neurobiology · 2026
    Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Cutting-edge technologies in neural regeneration.Cell regeneration (London, England) · 2025
    Review
  10. Review
  11. Spinal Cord Injury Remyelination: Pathways to Therapies.International journal of molecular sciences · 2025
    Review
  12. Repair mechanisms of the central nervous system: From axon sprouting to remyelination.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  13. Review
  14. Review
  15. Wrap it up: myelination of transplanted neurons for repair.Frontiers in cellular neuroscience · 2025
    Review
  16. Review
  17. Review
  18. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Laura J WagstaffCentre for Regenerative Medicine, Institute for Regeneration and Repair, University of Edinburgh, Edinburgh, UK. laura.wagstaff@ed.ac.uk.ORCID 0000-0003-3816-6113
Nadine Bestard-CucheCentre for Regenerative Medicine, Institute for Regeneration and Repair, University of Edinburgh, Edinburgh, UK.
Maja KaczmarekCentre for Regenerative Medicine, Institute for Regeneration and Repair, University of Edinburgh, Edinburgh, UK.ORCID 0000-0002-6521-7249
Antonella FidanzaCentre for Regenerative Medicine, Institute for Regeneration and Repair, University of Edinburgh, Edinburgh, UK.ORCID 0000-0002-1266-6454
Lorraine McNeilCentre for Regenerative Medicine, Institute for Regeneration and Repair, University of Edinburgh, Edinburgh, UK.
Robin J M FranklinWellcome - MRC Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, University of Cambridge, Cambridge, UK.
Anna C WilliamsCentre for Regenerative Medicine, Institute for Regeneration and Repair, University of Edinburgh, Edinburgh, UK. anna.williams@ed.ac.uk.ORCID 0000-0002-6329-382X

Funding

Medical Research Council MR/T015594/1Multiple Sclerosis Society (MS Society) MR/T015594/1RCUK | Medical Research Council (MRC) MR/P016022/1
6 · The paper itself

Abstract

In Multiple Sclerosis (MS), inflammatory demyelinated lesions in the brain and spinal cord lead to neurodegeneration and progressive disability. Remyelination can restore fast saltatory conduction and neuroprotection but is inefficient in MS especially with increasing age, and is not yet treatable with therapies. Intrinsic and extrinsic inhibition of oligodendrocyte progenitor cell (OPC) function contributes to remyelination failure, and we hypothesised that the transplantation of 'improved' OPCs, genetically edited to overcome these obstacles, could improve remyelination. Here, we edit human(h) embryonic stem cell-derived OPCs to be unresponsive to a chemorepellent released from chronic MS lesions, and transplant them into rodent models of chronic lesions. Edited hOPCs display enhanced migration and remyelination compared to controls, regardless of the host age and length of time post-transplant. We show that genetic manipulation and transplantation of hOPCs overcomes the negative environment inhibiting remyelination, with translational implications for therapeutic strategies for people with progressive MS.

Indexed as

Multiple SclerosisOligodendrocyte Precursor CellsRemyelinationAnimalsCell DifferentiationCell MovementCRISPR-Cas SystemsDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFemaleGene EditingHuman Embryonic Stem CellsHumansMaleMiceMyelin Sheath

Identifiers

PMID39384784
PMCPMC11464782

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.