Cuprizone Model Overview
The cuprizone multiple sclerosis mouse model of demyelination and remyelination is induced by feeding mice the copper-chelating cuprizone toxin. Cuprizone administration in mice models several aspects of human multiple sclerosis (MS), including central nervous system (CNS) loss of myelin, spontaneous remyelination, oligodendrocyte precursor cell (OPC) proliferation & maturation to myelinating oligodendrocytes, astrogliosis, and microgliosis. The pathology observed in the cuprizone model in mice is primarily limited to the corpus callosum with highly predictable pathology that mimics MS lesions.
Unlike EAE, the cuprizone model of multiple sclerosis is not autoimmune mediated and the cuprizone induced white matter demyelination and remyelination are not confounded by a peripheral immune response. EAE and cuprizone mice model different aspects of MS pathology, and therapeutic studies are often performed in parallel.
Cuprizone Model Generation
- C57BL/6 mice are fed 0.2-0.3% cuprizone via powdered chow, food pellets, or oral gavage
- A more severe, chronic, mouse demyelination model can be generated by injecting rapamycin (i.p. 5 days per week)
- In our experience, the powdered chow route of administration provides the most reproducible results
Our Validated Cuprizone Mouse Model Measures
- Body weight
- Myelin-sensitive in vivo MRI
- Immunohistochemistry & multiplex immunofluorescence for multiple cell types in the corpus callosum
Learn more about our characterization of this model, our validated measures, and our Preclinical Neuroscience CRO services.