ArticleCellular and molecular neurobiology2018
Cuprizone Administration Alters the Iron Metabolism in the Mouse Model of Multiple Sclerosis.
Article in Cellular and molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Potential therapeutic effects of ibudilast and retinoic acid against cuprizone-induced behavioral and biochemical changes in mouse brain.Frontiers in molecular neuroscience · 2025Article
- Multisensory gamma stimulation mitigates the effects of demyelination induced by cuprizone in male mice.Nature communications · 2024Article
- Quantitative Analysis of Early White Matter Damage in Cuprizone Mouse Model of Demyelination Using 7.0 T MRI Multiparametric Approach.ASN neuro · 2024Article
- Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination.Molecular neurodegeneration · 2022Review
- The mechanistic target of rapamycin as a regulator of metabolic function in oligodendroglia during remyelination.Current opinion in pharmacology · 2022Review
- Expression of antimicrobial host defence peptides in the central nervous system during health and disease.Discovery immunology · 2022Review
- 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
- Revisiting the Pathoetiology of Multiple Sclerosis: Has the Tail Been Wagging the Mouse?Frontiers in immunology · 2020Review
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- Diffusion tensor imaging identifies aspects of therapeutic estrogen receptor β ligand-induced remyelination in a mouse model of multiple sclerosis.Neurobiology of disease · 2019Article
- Relationship of Iron Metabolism and Short-Term Cuprizone Treatment of C57BL/6 Mice.International journal of molecular sciences · 2019Article
- Serum hepcidin levels in multiple sclerosis.Multiple sclerosis journal - experimental, translational and clinicalArticle
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Cuprizone (CZ) is a widely used copper chelating agent to develop non-autoimmune animal model of multiple sclerosis, characterized by demyelination of the corpus callosum (CC) and other brain regions. The exact mechanisms of CZ action are still arguable, but it seems that the only affected cells are the mature oligodendrocytes, possibly via metabolic disturbances caused by copper deficiency. During the pathogenesis of multiple sclerosis, high amount of deposited iron can be found throughout the demyelinated areas of the brain in the form of extracellular iron deposits and intracellularly accumulated iron in microglia. In the present study, we used the accepted experimental model of 0.2% CZ-containing diet with standard iron concentration to induce demyelination in the brain of C57BL/6 mice. Our aim was to examine the changes of iron homeostasis in the CC and as a part of the systemic iron regulation, in the liver. Our data showed that CZ treatment changed the iron metabolism of both tissues; however, it had more impact on the liver. Besides the alterations in the expressions of iron storage and import proteins, we detected reduced serum iron concentration and iron stores in the liver, together with elevated hepcidin levels and feasible disturbances in the Fe-S cluster biosynthesis. Our results revealed that the CZ-containing diet influences the systemic iron metabolism in mice, particularly the iron homeostasis of the liver. This inadequate systemic iron regulation may affect the iron homeostasis of the brain, eventually indicating a relationship among CZ treatment, iron metabolism, and neurodegeneration.
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