Cuprizone Model of Demyelination and Remyelination in Mice

Modeling Myelin Loss and Repair for Multiple Sclerosis

The cuprizone model is a well-characterized, toxin-induced model of central nervous system demyelination and remyelination, widely used in multiple sclerosis (MS) research. Unlike autoimmune models such as EAE, cuprizone produces demyelination without a primary peripheral immune response, allowing oligodendrocyte injury, myelin loss, and the subsequent repair process to be studied directly. This makes it especially well suited for evaluating remyelinating and neuroprotective therapies.

Cuprizone Mouse Model: induction, duration and remyelination phase.

Cuprizone, a copper chelator administered in the diet, drives reproducible oligodendrocyte loss and demyelination in defined brain regions, most notably the corpus callosum. Continued exposure sustains demyelination, while withdrawal allows spontaneous remyelination, giving a controlled window to assess both myelin loss and repair. At MD Biosciences, demyelination is induced in C57BL/6 mice and quantified by MBP histology, including optical density and corpus callosum thickness, alongside functional measures.

Scientific Data

Quantitative Demyelination

Corpus callosum thickness, measured from MBP-stained sections, is significantly reduced after 13 weeks of cuprizone exposure compared with naïve controls, providing a reproducible, quantitative readout of demyelination for evaluating therapeutic effect.

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