ArticleBiochemistry2017
Cuprizone Intoxication Induces Cell Intrinsic Alterations in Oligodendrocyte Metabolism Independent of Copper Chelation.
Article in Biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- Cell-specific isotope labeling identifiesbioRxiv : the preprint server for biology · 2026Article
- Ferroptosis and Cuproptosis in Cancer and Neurodegeneration: A Comprehensive Review of Modulation by Iron and Copper Chelators and Related Agents.Biomolecules · 2026Review
- Apolipoprotein D Expression Dynamics During Cuprizone-Induced Demyelination and Remyelination in a Mouse Model of Multiple Sclerosis.International journal of molecular sciences · 2025Article
- Betaine alleviates deficits in motor behavior, neurotoxic effects, and neuroinflammatory responses in a rat model of demyelination.Toxicology reports · 2025Article
- Neuroprotective effects of ghrelin in cuprizone-induced rat model of multiple sclerosis.Metabolic brain disease · 2025Article
- Microglial Neuroinflammation-Independent Reversal of Demyelination of Corpus Callosum by Arsenic in a Cuprizone-Induced Demyelinating Mouse Model.Molecular neurobiology · 2024Article
- CNS Resident Innate Immune Cells: Guardians of CNS Homeostasis.International journal of molecular sciences · 2024Review
- Microglia/macrophage polarization regulates spontaneous remyelination in intermittent cuprizone model of demyelination.Biochemistry and biophysics reports · 2024Article
- How to Use the Cuprizone Model to Study De- and Remyelination.International journal of molecular sciences · 2024Review
- Astrocytes: Lessons Learned from the Cuprizone Model.International journal of molecular sciences · 2023Review
- Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination.Molecular neurodegeneration · 2022Review
- Cuprizone feed formulation influences the extent of demyelinating disease pathology.Scientific reports · 2021Article
- mTOR Signaling Regulates Metabolic Function in Oligodendrocyte Precursor Cells and Promotes Efficient Brain Remyelination in the Cuprizone Model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Dysregulated copper transport in multiple sclerosis may cause demyelination via astrocytes.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Cuprizone-Induced Neurotoxicity in Human Neural Cell Lines Is Mediated by a Reversible Mitochondrial Dysfunction: Relevance for Demyelination Models.Brain sciences · 2021Article
- Cannabidiol Displays Proteomic Similarities to Antipsychotics in Cuprizone-Exposed Human Oligodendrocytic Cell Line MO3.13.Frontiers in molecular neuroscience · 2021Article
- In Vivo Measurement of Neurochemical Abnormalities in the Hippocampus in a Rat Model of Cuprizone-Induced Demyelination.Diagnostics (Basel, Switzerland) · 2020Article
- Ferroptosis Mediates Cuprizone-Induced Loss of Oligodendrocytes and Demyelination.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Metabolomic and Signaling Programs Induced by Immobilized versus Soluble IFN γ in Neural Stem Cells.Bioconjugate chemistry · 2020Article
- Betaine restores epigenetic control and supports neuronal mitochondria in the cuprizone mouse model of multiple sclerosis.Epigenetics · 2020Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Cuprizone intoxication is a common animal model used to test myelin regenerative therapies for the treatment of diseases such as multiple sclerosis. Mice fed this copper chelator develop reversible, region-specific oligodendrocyte loss and demyelination. While the cellular changes influencing the demyelinating process have been explored in this model, there is no consensus about the biochemical mechanisms of toxicity in oligodendrocytes and about whether this damage arises from the chelation of copper in vivo. Here we have identified an oligodendroglial cell line that displays sensitivity to cuprizone toxicity and performed global metabolomic profiling to determine biochemical pathways altered by this treatment. We link these changes with alterations in brain metabolism in mice fed cuprizone for 2 and 6 weeks. We find that cuprizone induces widespread changes in one-carbon and amino acid metabolism as well as alterations in small molecules that are important for energy generation. We used mass spectrometry to examine chemical interactions that are important for copper chelation and toxicity. Our results indicate that cuprizone induces global perturbations in cellular metabolism that may be independent of its copper chelating ability and potentially related to its interactions with pyridoxal 5'-phosphate, a coenzyme essential for amino acid metabolism.
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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.