Cuprizone does not induce CNS demyelination in nonhuman primates. (18th December 2014)

• Record Type: Journal Article
• Authors: Chen, Zhihong; Chen, Jacqueline T.; Johnson, Matthew; Gossman, Zachary C.; Hendrickson, Megan; Sakaie, Ken; Martinez‐Rubio, Clarissa; Gale, John T.; Trapp, Bruce D.
• Is Part Of: Annals of clinical and translational neurology. Volume 2:Number 2(2015:Feb.)
• Page Start: 208
• Page End: 213
• Publication Date: 2014-12-18
• Subjects: Nervous system -- Diseases -- Periodicals; Neurology -- Periodicals; 616.8005
• DOI: 10.1002/acn3.159
• Languages: English
• ISSNs: 2328-9503

Abstract

<abstract abstract-type="main" id="acn3159-abs-0001"> <title>Abstract</title> <p>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 <italic>per os</italic> 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.</p> </abstract>