Cognitive decline is a common symptom in multiple sclerosis patients, with profound effects on the quality of life. A nonhuman primate model ofmultiple sclerosis would be best suited to test the effects of demyelination on complex cognitive functions such as learning and reasoning. Cuprizone has been shown to reliably induce brain demyelination in mice. To establish a non=human primate model of multiple sclerosis, young adult cynomolgus monkeys were administered cuprizone per os as a dietary supplement. The subjects received increasing cuprizone doses (0.3-3% of diet) for up to 18 weeks. Magnetic resonance imaging and immunohistological analyses did not reveal demyelination in these monkeys.
Chen Z, Chen JT, Johnson M, Gossman ZC, Hendrickson M, Sakaie K, Martinez-Rubio C, Gale JT, Trapp BD. Ann Clin Transl Neurol. 2015 Feb;2(2):208-13. Cuprizone does not induce CNS demyelination in nonhuman primates.
Feed cuprizone to a rodents and they can gets demyelination in a few places and this model is increasing been used as a model to assess remyelinating therapies. However in monkeys it did not do anything, So this is not going to bridge the gap between mouse and humans. Is this needed?