ReviewJournal of molecular neuroscience : MN2013
Cuprizone-induced demyelination as a tool to study remyelination and axonal protection.
Review in Journal of molecular neuroscience : MN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.
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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
60 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.
- Remyelination promoting therapies in multiple sclerosis animal models: a systematic review and meta-analysis.Scientific reports · 2019Pooled it
- Spatiotemporal APLNR Expression Dynamics During Oligodendroglial Remodeling of the Corpus Callosum in the Cuprizone Model.International journal of molecular sciences · 2026Article
- Unveiling the neuroprotective potential of vortioxetine on inflammation in the cuprizone-induced demyelination model.Experimental brain research · 2026Article
- Early-Age Cuprizone Exposure Induces Region-Specific Demyelination and Neuroinflammation in Mice.Neuromolecular medicine · 2026Article
- Article
- Transient juvenile demyelination impairs maturation and function of parvalbumin-positive interneurons in the prefrontal cortex.PLoS biology · 2025Article
- Betaine alleviates deficits in motor behavior, neurotoxic effects, and neuroinflammatory responses in a rat model of demyelination.Toxicology reports · 2025Article
- Impact of calcitriol and PGDDrug delivery and translational research · 2024Article
- Neurobehavioral, biochemical and histological assessment of the effects of resveratrol on cuprizone-induced demyelination in mice: role of autophagy modulation.Journal of physiology and biochemistry · 2023Article
- Dietary Polyphenols, Microbiome, and Multiple Sclerosis: From Molecular Anti-Inflammatory and Neuroprotective Mechanisms to Clinical Evidence.International journal of molecular sciences · 2023Review
- Genetic models of cleavage-reduced and soluble TREM2 reveal distinct effects on myelination and microglia function in the cuprizone model.Journal of neuroinflammation · 2023Article
- L-Theanine Improves Locomotor Function in a Model of Multiple Sclerosis Mice.Archives of Razi Institute · 2023Article
- A case of primary optic pathway demyelination caused by oncocytic oligodendrogliopathy of unknown origin.Acta neuropathologica communications · 2022Article
- Modulation of pacemaker channel function in a model of thalamocortical hyperexcitability by demyelination and cytokines.Cerebral cortex (New York, N.Y. : 1991) · 2022Article
- Siponimod ameliorates metabolic oligodendrocyte injury via the sphingosine-1 phosphate receptor 5.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Combination effects of mesenchymal stem cells transplantation and anodal transcranial direct current stimulation on a cuprizone-induced mouse model of multiple sclerosis.Journal of molecular histology · 2022Article
- Stemazole Promotes Oligodendrocyte Precursor Cell Survival In Vitro and Remyelination In Vivo.International journal of molecular sciences · 2022Article
- Colony-stimulating factor 1 receptor signaling in the central nervous system and the potential of its pharmacological inhibitors to halt the progression of neurological disorders.Inflammopharmacology · 2022Review
- Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination.Molecular neurodegeneration · 2022Review
- Locomotor and histological changes in a cuprizone-induced animal model of multiple sclerosis: comparison between alpha-tocopherol and fingolimod.Research in pharmaceutical sciences · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the brain of multiple sclerosis (MS) patients, the conduction block of axons due to demyelination and inflammation underlies early neurological symptoms, whereas axonal transection accounts for permanent deficits occurring during later disease stages. The beneficial function of myelin for the protection of the axonal compartment and network stability between neurons has been shown in numerous studies. Thus, rapid and adequate remyelination is an important factor for axonal patronage during neuroinflammatory conditions. In this review article, we discuss frequently used experimental in vivo and in vitro animal models to examine remyelination and repair in MS. The focus of the discussion is the relevance of the toxin model 'cuprizone' to study the pathology of demyelination and the physiology of remyelination. This also includes recent findings in this animal model which implicate that axonal damage is an ongoing process independent of the initiation of endogenous remyelination.
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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.