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Cuprizone (bis-cyclohexanone oxaldihydrazone) induced mouse model recapitulates several MS pathological features in human, including apoptosis of oligodendrocytes, demyelination, microglia activation and infiltration of macrophages. Typical demyelination can be observed after five weeks of cuprizone exposure in mice. Once cuprizone administration is stopped, spontaneous remyelination will subsequently take place in these model animals. Creative Bioarray focuses on drug research and development services and helps customers explore effective therapeutic approaches targeting demyelination and remyelination in multiple brain regions such as corpus callosum and cerebellum.
Figure. 1. Example of the cuprizone induced mouse model study paradigm
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Figure. 2. Representative pictures show myelination (PLP1 and MBP) in the subcortex and cortex of mouse cerebellum for control, 5 weeks of cuprizone exposure and after 4 weeks of fingolimod/placebo treatment.
Figure. 3. Subcortical β-APP (red) and neurofilament (green) staining of control, after 5 weeks of cuprizone exposure and after 4 weeks of recovery.
Figure. 4. NOGO-A positive mature oligodendrocytes (red) and GFAP-expressing astrocytes (green) in subcortex and cortex in control, 5 weeks of cuprizone exposure and after 4 weeks of recovery.
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Maria Nordheim Alme, et al. Fingolimod does not enhance cerebellar remyelination in the cuprizone model[J]. Journal of Neuroimmunology, 2015, 285:180-186.
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Multiple Sclerosis (MS) Models: