Open AccessCuprizone does not induce CNS demyelination in nonhuman primates
Author(s) -
Chen Zhihong,
Chen Jacqueline T.,
Johnson Matthew,
Gossman Zachary C.,
Hendrickson Megan,
Sakaie Ken,
MartinezRubio Clarissa,
Gale John T.,
Trapp Bruce D.
Publication year - 2015
Publication title -
annals of clinical and translational neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.824
H-Index - 42
ISSN - 2328-9503
DOI - 10.1002/acn3.159
Subject(s) - multiple sclerosis , medicine , primate , nonhuman primate , cognition , magnetic resonance imaging , neuroscience , immunology , psychology , biology , psychiatry , radiology , evolutionary biology
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.