Evidence map›Paper›PMID 39501035›Full record

ArticleNature neuroscience2024

Spatially resolved gene signatures of white matter lesion progression in multiple sclerosis.

Astrid M Alsema, Marion H C Wijering, Anneke Miedema, Janssen M Kotah, Mirjam Koster, Merel Rijnsburger, Hilmar R J van Weering, Helga E de Vries, Wia Baron, Susanne M Kooistra and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing 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

31 citing papers in PubMed.

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  12. Astrocyte Functional Heterogeneity in Multiple Sclerosis.Journal of clinical neurology (Seoul, Korea) · 2026
    Review
  13. Article
  14. Article
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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

11 authors.

Astrid M Alsema *Department of Biomedical Sciences, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.ORCID http://orcid.org/0009-0001-2549-409X
Marion H C Wijering *Department of Biomedical Sciences, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.ORCID http://orcid.org/0000-0002-9283-3952
Anneke Miedema *Department of Biomedical Sciences, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Janssen M Kotah *Department of Biomedical Sciences, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.ORCID http://orcid.org/0000-0003-3005-730X
Mirjam KosterDepartment of Biomedical Sciences, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.ORCID http://orcid.org/0000-0002-9286-1486
Merel RijnsburgerDepartment of Molecular Cell Biology and Immunology, Amsterdam UMC, Location Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Hilmar R J van WeeringDepartment of Biomedical Sciences, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.ORCID http://orcid.org/0009-0003-2243-2605
Helga E de VriesDepartment of Molecular Cell Biology and Immunology, Amsterdam UMC, Location Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Wia BaronDepartment of Biomedical Sciences, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.ORCID http://orcid.org/0000-0002-6673-4766
Susanne M KooistraDepartment of Biomedical Sciences, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.ORCID http://orcid.org/0000-0003-0211-8283
Bart J L EggenDepartment of Biomedical Sciences, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands. b.j.l.eggen@umcg.nl.ORCID http://orcid.org/0000-0001-8941-0353

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is an inflammatory disease of the central nervous system characterized by myelin loss and progressive neurodegeneration. To understand MS lesion initiation and progression, we generate spatial gene expression maps of white matter (WM) and grey matter (GM) MS lesions. In different MS lesion types, we detect domains characterized by a distinct gene signature, including an identifiable rim around active WM lesions. Expression changes in astrocyte-specific, oligodendrocyte-specific and microglia-specific gene sets characterize the active lesion rims. Furthermore, we identify three WM lesion progression trajectories, predicting how normal-appearing WM can develop into WM active or mixed active-inactive lesions. Our data shed light on the dynamic progression of MS lesions.

Indexed as

Disease ProgressionGray MatterMultiple SclerosisWhite MatterAdultAstrocytesFemaleHumansMagnetic Resonance ImagingMaleMicrogliaOligodendrogliaTranscriptome

Identifiers

PMID39501035

What OpenQuestion holds

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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.