ArticlePloS one2020
Increased blood-brain barrier hyperpermeability coincides with mast cell activation early under cuprizone administration.
Article in PloS one, 2020. 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, 29 citations in OpenAlex.
- Oligodendrocyte and Astrocyte Dynamics During Short-Term Cuprizone Treatment.Brain and behavior · 2026Article
- Comparative Analysis of Mouse CSF Proteins in Experimental Autoimmune Encephalomyelitis Model and Cuprizone-Induced Demyelination Model by Olink Proteomics.Molecular neurobiology · 2026Article
- Review
- Neurovascular and synaptic milieu of brain-resident cells in cognitive dysfunction of myalgic encephalomyelitis/chronic fatigue syndrome.Journal of translational medicine · 2026Review
- Prevalence and treatment response of neuropsychiatric disorders in mast cell activation syndrome.Brain, behavior, & immunity - health · 2025Article
- Co-administration of Naringin and NLRP3 Inhibitor Improves Myelin Repair and Mitigates Oxidative Stress in Cuprizone-Induced Demyelination Model.Current neuropharmacology · 2025Article
- Hypermobile Ehlers-Danlos syndrome and spontaneous CSF leaks: the connective tissue conundrum.Frontiers in neurology · 2024Review
- Neuropsychiatric Manifestations of Mast Cell Activation Syndrome and Response to Mast-Cell-Directed Treatment: A Case Series.Journal of personalized medicine · 2023Article
- Localized Increased Permeability of Blood-Brain Barrier for Antibody Conjugates in the Cuprizone Model of Demyelination.International journal of molecular sciences · 2023Article
- Cu,Zn-Superoxide Dismutase has Minimal Effects Against Cuprizone-Induced Demyelination, Microglial Activation, and Neurogenesis Defects in the C57BL/6 Mouse Hippocampus.Neurochemical research · 2023Article
- Direct association with the vascular basement membrane is a frequent feature of myelinating oligodendrocytes in the neocortex.Fluids and barriers of the CNS · 2023Article
- Inhibiting nighttime melatonin and boosting cortisol increase patrolling monocytes, phagocytosis, and myelination in a murine model of multiple sclerosis.Experimental & molecular medicine · 2023Article
- Reaction of different cell types of the brain on neurotoxin cuprizone and hormone melatonin treatment in young and aging mice.Frontiers in cellular neuroscience · 2023Article
- Mast cell-mediated immune regulation in health and disease.Frontiers in medicine · 2023Review
- Single-cell microglial transcriptomics during demyelination defines a microglial state required for lytic carcass clearance.Molecular neurodegeneration · 2022Article
- Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination.Molecular neurodegeneration · 2022Review
- Article
- Animal models to investigate the effects of inflammation on remyelination in multiple sclerosis.Frontiers in molecular neuroscience · 2022Review
- CAQK, a peptide associating with extracellular matrix components targets sites of demyelinating injuries.Frontiers in cellular neuroscience · 2022Article
- Cuprizone feed formulation influences the extent of demyelinating disease pathology.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cuprizone induced animal model of demyelination is characterized by demyelination in many regions of the brain with high levels of demyelination in the corpus callosum as well as changes in neuronal function by 4-6 weeks of exposure. The model is used as a tool to study demyelination and subsequent degeneration as well as therapeutic interventions on these effects. Historically, the cuprizone model has been shown to contain no alterations to blood-brain barrier integrity, a key feature in many diseases that affect the central nervous system. Cuprizone is generally administered for 4-6 weeks to obtain maximal demyelination and degeneration. However, emerging evidence has shown that the effects of cuprizone on the brain may occur earlier than measurable gross demyelination. This study sought to investigate changes to blood-brain barrier permeability early in cuprizone administration. Results showed an increase in blood-brain barrier permeability and changes in tight junction protein expression as early as 3 days after beginning cuprizone treatment. These changes preceded glial morphological activation and demyelination known to occur during cuprizone administration. Increases in mast cell presence and activity were measured alongside the increased permeability implicating mast cells as a potential source for the blood-brain barrier disruption. These results provide further evidence of blood-brain barrier alterations in the cuprizone model and a target of therapeutic intervention in the prevention of cuprizone-induced pathology. Understanding how mast cells become activated under cuprizone and if they contribute to blood-brain barrier alterations may give further insight into how and when the blood-brain barrier is affected in CNS diseases. In summary, cuprizone administration causes an increase in blood-brain barrier permeability and this permeability coincides with mast cell activation.
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Registered trials
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