ReviewBrain pathology (Zurich, Switzerland)2017
Multiple sclerosis animal models: a clinical and histopathological perspective.
Review in Brain pathology (Zurich, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 1 of them a synthesis that pooled it.
What it found
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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
115 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Immunomodulatory Potential of Cannabidiol in Multiple Sclerosis: a Systematic Review.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021Pooled it
- Neural Stem Cells in Multiple Sclerosis: A Comprehensive Review of Preclinical and Clinical Evidence for CNS Repair and Translational Hurdles.Applied biochemistry and biotechnology · 2026Review
- Tmem117, an oligodendrocyte-enriched regulator of NCX activity, links myelin homeostasis to counterregulation and metabolic health.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- S3I-201, a STAT3 Inhibitor, Inhibits Proinflammatory Mediator Signalling in CD19 and CD45R/B220 Cells in a Mouse Model of Multiple Sclerosis.Cellular and molecular neurobiology · 2026Article
- Early Reduction in Mitochondrial Membrane Potential in Synaptic Mitochondria Contribute to Synaptic Pathology in the EAE Mouse Model of Multiple Sclerosis.International journal of molecular sciences · 2026Article
- Oligodendrocytes Are Active Participants in the Pathogenesis of Multiple Sclerosis and Its Animal Models.International journal of molecular sciences · 2026Review
- Oligodendrocyte progenitor cell responses to inflammatory demyelination with aging.Research square · 2025Article
- Novel Animal Models for Multiple Sclerosis: R-Ras GTPases in Myelin Pathophysiology.Biomolecules · 2025Review
- Article
- Alpha-mangostin Ameliorates Apoptosis, Inflammation and Oxidative Stress in Cuprizone-induced Demyelination in C57BL/6 Mice.Basic and clinical neuroscience · 2025Article
- Profiling Blood-Based Neural Biomarkers and Cytokines in Experimental Autoimmune Encephalomyelitis Model of Multiple Sclerosis Using Single-Molecule Array Technology.International journal of molecular sciences · 2025Article
- Investigating mechanisms underlying the development of paralysis symptom in a model of MS.Brain research bulletin · 2025Article
- Plasma and Visceral Organ Kynurenine Metabolites Correlate in the Multiple Sclerosis Cuprizone Animal Model.International journal of molecular sciences · 2025Article
- Oligodendrocyte and Myelin Pathophysiology in Multiple Sclerosis.Advances in neurobiology · 2025Review
- Novel insights into vascular dysfunction in cuprizone-induced demyelination through functional ultrasound imaging.Imaging neuroscience (Cambridge, Mass.) · 2025Article
- Intrinsic ecto-5'-Nucleotidase/AMolecular neurobiology · 2024Article
- Impact of Neuron-Derived HGF on c-Met and KAI-1 in CNS Glial Cells: Implications for Multiple Sclerosis Pathology.International journal of molecular sciences · 2024Article
- Modulation of αv integrins by lebecetin, a viper venom-derived molecule, in experimental neuroinflammation and demyelination models.Scientific reports · 2024Article
- The physiological and pathophysiological roles of copper in the nervous system.The European journal of neuroscience · 2024Review
- N-butyl-β-carboline-3-carboxylate (β-CCB) systemic administration promotes remyelination in the cuprizone demyelinating model in mice.Scientific reports · 2024Article
55 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is a broad consensus that multiple sclerosis (MS) represents more than an inflammatory disease: it harbors several characteristic aspects of a classical neurodegenerative disorder, that is, damage to axons, synapses and nerve cell bodies. While we are equipped with appropriate therapeutic options to prevent immune-cell driven relapses, effective therapeutic options to prevent the progressing neurodegeneration are still missing. In this review article, we will discuss to what extent pathology of the progressive disease stage can be modeled in MS animal models. While acute and relapsing-remitting forms of experimental autoimmune encephalomyelitis (EAE), which are T cell dependent, are aptly suited to model relapsing-remitting phases of MS, other EAE models, especially the secondary progressive EAE stage in Biozzi ABH mice is better representing the secondary progressive phase of MS, which is refractory to many immune therapies. Besides EAE, the cuprizone model is rapidly gaining popularity to study the formation and progression of demyelinating CNS lesions without T cell involvement. Here, we discuss these two non-popular MS models. It is our aim to point out the pathological hallmarks of MS, and discuss which pathological aspects of the disease can be best studied in the various animal models available.
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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.