Evidence map›Paper›PMID 42426932›Full record

ArticleActa neuropathologica communications2026

CSF1R inhibition following antibody mediated demyelination has limited impact on remyelination.

Lisa C Golden, Graham C Peet, Rebecca E Rodriguez, Nicholas J Jahahn, Gregory P Owens, Jeffrey L Bennett, Wendy B Macklin

Abstract read
In one paragraph

Article in Acta neuropathologica communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Lisa C Golden *Department of Cell and Developmental Biology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Graham C Peet *Department of Cell and Developmental Biology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Rebecca E RodriguezDepartment of Cell and Developmental Biology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Nicholas J JahahnDepartment of Cell and Developmental Biology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Gregory P OwensDepartment of Neurology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Jeffrey L BennettNeuroscience Program, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Wendy B MacklinDepartment of Cell and Developmental Biology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA. wendy.macklin@cuanschutz.edu.

Funding

Microglial impact on remyelinationR01NS115488 · NINDS · UNIVERSITY OF COLORADO DENVER · PI BENNETT, JEFFREY L, MACKLIN, WENDY B · 2020 to 2024
$2.4M
The impact of immunoglobulin induced interferon response on remyelinationF31NS141369 · NINDS · UNIVERSITY OF COLORADO DENVER · PI Graham C Peet · 2025 to 2026
$77k
NINDS NIH HHS F31 NS141369NINDS NIH HHS F31NS141369NINDS NIH HHS R01 NS115488NINDS NIH HHS R01NS115488
6 · The paper itself

Abstract

Multiple sclerosis (MS) is a chronic, immune-mediated, demyelinating disease of the central nervous system. B cell depleting treatments are effective MS therapies, and while antibodies may serve as a biomarker, little is known about how they participate in MS pathology. Using a proteolipid protein 1 complex-specific (PLP1c) recombinant antibody cloned from cerebrospinal fluid plasmablasts of MS patients, we studied the development and resolution of antibody-mediated demyelinating lesions in vivo in mice. Demyelination was complement-dependent and resolved over four weeks. Because of the previously described impact of microglia on remyelination, we targeted microglia depletion with CSF1R inhibition to test their role in this model. Despite a significant reduction in total microglia following CSF1R inhibition, microglia or macrophage density was high in recovering lesions. Premyelinating oligodendrocyte populations were altered without impacting gross lesion recovery. Future work will determine if PLP1c-binding antibodies are representative of other MS-derived antibodies, and how pathogenic MS autoantibodies may contribute to the variability of MS lesion remyelination.

Indexed as

Demyelinating DiseasesMultiple SclerosisReceptors, Granulocyte-Macrophage Colony-Stimulating FactorRemyelinationAnimalsAutoantibodiesDisease Models, AnimalFemaleHumansMiceMice, Inbred C57BLMicrogliaMyelin Proteolipid ProteinOligodendrogliaAutoantibodiesCsf1r protein, mouseMyelin Proteolipid ProteinPlp1 protein, mouseReceptors, Granulocyte-Macrophage Colony-Stimulating FactorComplementDemyelinationImmunoglobulinMicrogliaMultiple sclerosisPLP1Remyelination

Identifiers

PMID42426932
PMCPMC13621750

What OpenQuestion holds

Textmetadata
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.