Evidence map›Paper›PMID 42115623›Full record

ArticleNature communications2026

Neuregulin-1 facilitates myelin regeneration through microglia-mediated mechanisms in a mouse model of chronic demyelination.

Seyyed Mohyeddin Ziaee, Shiva Nemati, Hardeep Kataria, Elisabet Jakova, Seyed Mojtaba Hosseini, Pejman Ghelich, Graham McLeod, Ali Tamayol, V Wee Yong, Soheila Karimi-Abdolrezaee

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
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.

Seyyed Mohyeddin Ziaee *Department of Physiology and Pathophysiology, Manitoba Multiple Sclerosis Research Centre, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.
Shiva Nemati *Department of Physiology and Pathophysiology, Manitoba Multiple Sclerosis Research Centre, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.
Hardeep KatariaDepartment of Physiology and Pathophysiology, Manitoba Multiple Sclerosis Research Centre, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.ORCID http://orcid.org/0000-0001-8413-0600
Elisabet JakovaDepartment of Physiology and Pathophysiology, Manitoba Multiple Sclerosis Research Centre, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.
Seyed Mojtaba HosseiniDepartment of Physiology and Pathophysiology, Manitoba Multiple Sclerosis Research Centre, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.
Pejman GhelichDepartment of Biomedical Engineering, University of Connecticut, Farmington, CT, USA.
Graham McLeodDepartment of Physiology and Pathophysiology, Manitoba Multiple Sclerosis Research Centre, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.
Ali TamayolDepartment of Biomedical Engineering, University of Connecticut, Farmington, CT, USA.ORCID http://orcid.org/0000-0003-1801-2889
V Wee YongHotchkiss Brain Institute and the Department of Clinical Neurosciences, University of Calgary, Calgary, AB, Canada.ORCID http://orcid.org/0000-0002-2600-3563
Soheila Karimi-AbdolrezaeeDepartment of Physiology and Pathophysiology, Manitoba Multiple Sclerosis Research Centre, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Soheila.Karimi@umanitoba.ca.ORCID http://orcid.org/0000-0002-0683-2663

Funding

Gouvernement du Canada | Canadian Institutes of Health Research (Instituts de Recherche en Santé du Canada) PJT-191850Multiple Sclerosis Society of Canada (Société Canadienne de la Sclérose en Plaques) EGID3742 and 1241879
6 · The paper itself

Abstract

Impaired myelin repair, or remyelination, is a hallmark of progressive multiple sclerosis (MS) that drives brain degeneration and enduring neurological disabilities. Microglia crucially support remyelination through myelin phagocytosis and lipid metabolism. However, in chronic demyelinated MS lesions, microglia lose their reparative function by acquiring a foamy dysfunctional phenotype characterized by accumulation of lipid droplets due to impaired cholesterol processing of myelin debris. Here, we show a positive correlation between dysregulation of neuregulin-1 and impaired oligodendrocyte remyelination in mice with chronic demyelination. Therapeutic restoration of neuregulin-1 fosters myelin regeneration through microglia-dependent mechanisms. We demonstrate that Nrg-1 signaling supports microglia integrity and function in chronic demyelinated lesions by exploiting their capacity for the clearance of myelin debris and cholesterol recycling, biosynthesis and efflux. These findings signify the promise of neuregulin-1 as an endogenous target to facilitate microglia mediated-repair in progressive MS in which there is an unmet need for new treatments.

Indexed as

Demyelinating DiseasesMicrogliaMyelin SheathNeuregulin-1RemyelinationAnimalsCholesterolDisease Models, AnimalFemaleMaleMiceMice, Inbred C57BLMultiple SclerosisOligodendrogliaPhagocytosisSignal TransductionCholesterolNeuregulin-1Nrg1 protein, mouse

Identifiers

PMID42115623
PMCPMC13309555

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.