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Cuprizone Models

The cuprizone MS mouse model of demyelination & remyelination is induced by feeding mice the copper-chelating cuprizone toxin. Cuprizone administration in mice models several aspects of human multiple sclerosis (MS), including demyelination, spontaneous remyelination, oligodendrocyte precursor cell (OPC) proliferation & maturation, astrogliosis, and microgliosis.

The pathology in this demyelination model is primarily limited to the corpus callosum with highly predictable pathology. This demyelination mouse model is well-suited to therapeutic efficacy studies.

Two brain cross-sections stained for Myelin Basic Protein (MBP), used in studying demyelination in a cuprizone mouse model of Multiple Sclerosis (MS), with varying levels of myelin indicated by the staining intensity

EAE Models

Experimental Autoimmune Encephalomyelitis (EAE) is a gold-standard multiple sclerosis mouse model for assessing therapeutic agents targeting autoimmune-mediated CNS disease. The EAE induction is most commonly performed by immunizing mice against myelin-derived antigens, such as MOG, MBP, and PLP. EAE mice model several aspects of human MS.

This model of multiple sclerosis is a T cell-mediated autoimmune disease with several key pathologic features, including demyelination, inflammation, microgliosis, astrogliosis, and axonal damage.

Histological section, which is often used in the study of Experimental Autoimmune Encephalomyelitis (EAE) models

Learn more about our characterization of these MS mouse models, our validated measures, and our Preclinical Neuroscience CRO services.


What is Cuprizone?

Cuprizone [oxalic acid bis(cyclohexylidene hydrazide)] is a copper-chelating compound. The chemical properties of cuprizone are well-established. It is used to produce a toxic demyelination in mice to generate a model of multiple sclerosis. A good review of this MS model can be found in Torkildsen et al., 2008.

Administration of cuprizone to mice induces damage to oligodendrocytes with concomitant microglial activation and astrogliosis, primarily in the corpus callosum. When mice are put back on normal chow, spontaneous remyelination occurs via the migration and maturation of oligodendrocyte precursor cells (OPCs).

What is MOG EAE?

Myelin Oligodendrocyte Glycoprotein (MOG) is a transmembrane protein expressed by oligodendrocytes and forms part of the myelin sheath. It is used as an antigen to induce autoimmune-mediated demyelination in C57BL/6 mice to serve as a multiple sclerosis model.

Are motor symptoms observed in these multiple sclerosis mouse models?

We observe motor symptoms, including ascending paralysis, in the EAE mouse model. We use a well-established motor scoring system to evaluate disease progression. We can also quantitatively measure grip strength in these mice.

Can Biospective identify different stages of oligodendrocyte maturation?

Yes, we can use multiplex immunofluorescence to identify different stages of the oligodendrocyte lineage in the cuprizone MS model.

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