ReviewFrontiers in molecular neuroscience2022
Animal models to investigate the effects of inflammation on remyelination in multiple sclerosis.
Review in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- Neuroprotective effects of glucotropaeolin as the major glucosinolate of cress seed on cuprizone-induced mouse model of multiple sclerosis.Biochemistry and biophysics reports · 2026Article
- Therapeutic Effects of Combined 6-Shogaol and Ibudilast on Neuroinflammation and Behavioral Deficits in a Cuprizone Mouse Model of Multiple Sclerosis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Co-Administration of LPC and LPS Enhanced the Spinal Cord Vulnerability in a Mouse Model of Focal Demyelination.Journal of molecular neuroscience : MN · 2026Article
- From insights to innovations: evaluating preclinical paradigms in demyelinating disease therapeutics.Lab animal · 2026Review
- Spatiotemporal APLNR Expression Dynamics During Oligodendroglial Remodeling of the Corpus Callosum in the Cuprizone Model.International journal of molecular sciences · 2026Article
- Repeated ablations of mature Tmem10Cell death & disease · 2025Article
- Critical analysis of translational potential of rodent models of white matter pathology across a wide spectrum of human diseases.Cell death & disease · 2025Review
- MiR-124 and MiR-155 as Therapeutic Targets in Microglia-Mediated Inflammation in Multiple Sclerosis.Cellular and molecular neurobiology · 2025Review
- Microbiota-Driven Mechanisms in Multiple Sclerosis: Pathogenesis, Therapeutic Strategies, and Biomarker Potential.Biology · 2025Review
- Neuroprotective effects of ghrelin in cuprizone-induced rat model of multiple sclerosis.Metabolic brain disease · 2025Article
- Article
- Potential therapeutic effects of ibudilast and retinoic acid against cuprizone-induced behavioral and biochemical changes in mouse brain.Frontiers in molecular neuroscience · 2025Article
- A Morphological and Behavioral Study of Demyelination and Remyelination in the Cuprizone Model: Insights into APLNR and NG2+ Cell Dynamics.International journal of molecular sciences · 2024Article
- Meningeal lymphatic function promotes oligodendrocyte survival and brain myelination.Immunity · 2024Article
- A preclinical mice model of multiple sclerosis based on the toxin-induced double-site demyelination of callosal and cerebellar fibers.Biological research · 2024Article
- Experimental Autoimmune Encephalomyelitis Influences GH-Axis in Female Rats.International journal of molecular sciences · 2024Article
- Fasudil-modified macrophages reduce inflammation and regulate the immune response in experimental autoimmune encephalomyelitis.Neural regeneration research · 2024Article
- Star power: harnessing the reactive astrocyte response to promote remyelination in multiple sclerosis.Neural regeneration research · 2024Review
- The Mouse Model of Internal Capsule Demyelination: A Novel Tool for Investigating Motor Functional Changes Caused by Demyelination and for Evaluating Drugs That Promote Remyelination.Acta histochemica et cytochemica · 2024Review
- Central Versus Peripheral Drug Exposure Ratio, a Key Differentiator for Siponimod Over Fingolimod?Neurology and therapy · 2023Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Multiple sclerosis (MS) is a chronic inflammatory, demyelinating, and neurodegenerative disease of the central nervous system (CNS). In people with MS, impaired remyelination and axonal loss lead to debilitating long-term neurologic deficits. Current MS disease-modifying drugs mainly target peripheral immune cells and have demonstrated little efficacy for neuroprotection or promoting repair. To elucidate the pathological mechanisms and test therapeutic interventions, multiple animal models have been developed to recapitulate specific aspects of MS pathology, particularly the acute inflammatory stage. However, there are few animal models that facilitate the study of remyelination in the presence of inflammation, and none fully replicate the biology of chronic demyelination in MS. In this review, we describe the animal models that have provided insight into the mechanisms underlying demyelination, myelin repair, and potential therapeutic targets for remyelination. We highlight the limitations of studying remyelination in toxin-based demyelination models and discuss the combinatorial models that recapitulate the inflammatory microenvironment, which is now recognized to be a major inhibitor of remyelination mechanisms. These models may be useful in identifying novel therapeutics that promote CNS remyelination in inflammatory diseases such as MS.
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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.