ArticleNature communications2026
A comparative transcriptomic analysis of mouse demyelination models and multiple sclerosis lesions.
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.
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.
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.
Who cites it
2 citing papers in PubMed.
- Type-I IFNs in EAE drive synaptic transcriptional responses in neurons and astrocytes in the brain.bioRxiv : the preprint server for biology · 2026Article
- Oligodendrocyte progenitor cell responses to inflammatory demyelination with aging.Research square · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Demyelinating diseases, including multiple sclerosis (MS), are characterized by loss of myelin and progressive neurodegeneration. It remains unclear if demyelination mouse models, such as cuprizone (CPZ) and lysophosphatidylcholine (LPC) elicit distinct responses or are comparable to human disease. Here, we integrate new and published single-cell transcriptomic datasets from CPZ- and LPC-induced demyelination and compare them with human MS data. We find that CPZ induces a distinct, stressed oligodendrocyte (OL) state, marked by Cdkn1a and Nupr1, that resembles phenotypes in MS lesions. The models converge on an immune responsive OL state expressing Socs3, B2m, and interferon-response genes during remyelination. Mouse microglia share a conserved activation program, although LPC drives a stronger, prolonged response. However, neither model captures the oligodendrocyte progenitor and microglial heterogeneity observed in MS. These results provide a cross-model, cross-species atlas of glial states and offer a framework to strategically leverage mouse models to study myelin injury and repair.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.