ArticleHistochemistry and cell biology2019
Continuous cuprizone intoxication allows active experimental autoimmune encephalomyelitis induction in C57BL/6 mice.
Article in Histochemistry and cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- CD44 as a Conserved Biomarker and Functional Modulator of Neuroinflammation in Multiple Sclerosis and Beyond.Molecular neurobiology · 2026Article
- Insights and challenges on animal models for progressive multiple sclerosis.Journal of neuroinflammation · 2026Review
- A Novel Mouse Model for Cerebral Inflammatory Demyelination in X-Linked Adrenoleukodystrophy: Insights into Pathogenesis and Potential Therapeutic Targets.Annals of neurology · 2025Article
- Investigation of choroid plexus variability in schizophrenia-spectrum disorders-insights from a multimodal study.Schizophrenia (Heidelberg, Germany) · 2024Article
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- Glial cell changes in the corpus callosum in chronically-starved mice.Journal of eating disorders · 2023Article
- Chemogenetic activation of locus coeruleus neurons ameliorates the severity of multiple sclerosis.Journal of neuroinflammation · 2023Article
- Article
- Article
- Review
- Translational value of choroid plexus imaging for tracking neuroinflammation in mice and humans.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Revisiting the Pathoetiology of Multiple Sclerosis: Has the Tail Been Wagging the Mouse?Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oligodendrocyte degeneration is a hallmark of multiple sclerosis pathology, and protecting oligodendrocytes and myelin is likely to be of clinical relevance. Traditionally, oligodendrocyte and myelin degeneration are viewed as a direct consequence of an inflammatory attack, but metabolic defects might be equally important. Appropriate animal models to study the interplay of inflammation and metabolic injury are, therefore, needed. Here, we describe that in spite of its immunosuppressive effects, a continuous intoxication with cuprizone allows the induction of active experimental autoimmune encephalomyelitis (EAE) by myelin oligodendrocyte glycoprotein (MOG
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