Cuprizone does not induce CNS demyelination in nonhuman primates

• Published in: Annals of clinical and translational neurology Vol. 2; no. 2; pp. 208 - 213
• Main Authors: Chen, Zhihong, Chen, Jacqueline T., Johnson, Matthew, Gossman, Zachary C., Hendrickson, Megan, Sakaie, Ken, Martinez‐Rubio, Clarissa, Gale, John T., Trapp, Bruce D.
• Format: Journal Article
• Language: English
• Published: United States John Wiley & Sons, Inc 01.02.2015; BlackWell Publishing Ltd
• Subjects: Animal cognition; Brain; Brief Communications; Dietary supplements; Feeds; Health care; Laboratory animals; Multiple sclerosis; NMR; Nuclear magnetic resonance; Primates; Studies; Young adults; United States > US
• ISSN: 2328-9503; 2328-9503
• DOI: 10.1002/acn3.159

Cognitive decline is a common symptom in multiple sclerosis patients, with profound effects on the quality of life. A nonhuman primate model of multiple 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 nonhuman 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.