Evidence map›Paper›PMID 35526004›Full record

ReviewMolecular neurodegeneration2022

Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination.

Martin Zirngibl, Peggy Assinck, Anastasia Sizov, Andrew V Caprariello, Jason R Plemel

Open access · goldAbstract readReview
In one paragraph

Review in Molecular neurodegeneration, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed
16.3field-weighted citation impact, top 1% of its field
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

133 citing papers in PubMed, 207 citations in OpenAlex.

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  6. Investigating theResearch in pharmaceutical sciences · 2026
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73 more citing papers are in PubMed but not listed here.

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

5 authors at 4 institutions in 2 countries.

Martin ZirngiblFaculty of Medicine & Dentistry, Neuroscience and Mental Health Institute, University of Alberta, Edmonton, Canada.
Peggy AssinckWellcome Trust- MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge, UK.
Anastasia SizovFaculty of Medicine & Dentistry, Neuroscience and Mental Health Institute, University of Alberta, Edmonton, Canada.
Andrew V CaprarielloDepartment of Clinical Neurosciences, Hotchkiss Brain Institute, University of Calgary, Cumming School of Medicine, Calgary, Canada.
Jason R PlemelFaculty of Medicine & Dentistry, Neuroscience and Mental Health Institute, University of Alberta, Edmonton, Canada. jrplemel@ualberta.ca.
University of Alberta · CAUniversity of Calgary · CAUniversity of Cambridge · GBWomen and Children’s Health Research Institute · CA

Funding

CIHR
6 · The paper itself

Abstract

backgroundThe dietary consumption of cuprizone - a copper chelator - has long been known to induce demyelination of specific brain structures and is widely used as model of multiple sclerosis. Despite the extensive use of cuprizone, the mechanism by which it induces demyelination are still unknown. With this review we provide an updated understanding of this model, by showcasing two distinct yet overlapping modes of action for cuprizone-induced demyelination; 1) damage originating from within the oligodendrocyte, caused by mitochondrial dysfunction or reduced myelin protein synthesis. We term this mode of action 'intrinsic cell damage'. And 2) damage to the oligodendrocyte exerted by inflammatory molecules, brain resident cells, such as oligodendrocytes, astrocytes, and microglia or peripheral immune cells - neutrophils or T-cells. We term this mode of action 'extrinsic cellular damage'. Lastly, we summarize recent developments in research on different forms of cell death induced by cuprizone, which could add valuable insights into the mechanisms of cuprizone toxicity. With this review we hope to provide a modern understanding of cuprizone-induced demyelination to understand the causes behind the demyelination in MS.

Indexed as

CuprizoneDemyelinating DiseasesAnimalsAstrocytesDisease Models, AnimalMiceMice, Inbred C57BLMicrogliaMyelin SheathOligodendrogliaCuprizoneAstrocytesCell deathCNSCuprizoneDemyelinationInflammationMicrogliaMultiple SclerosisOligodendrocytes

Identifiers

PMID35526004
PMCPMC9077942
OpenAlexW4229064788

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.