Cuprizone does not induce CNS demyelination in nonhuman primates

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 be...

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Detalles Bibliográficos
Autores principales: Chen, Zhihong, Chen, Jacqueline T, Johnson, Matthew, Gossman, Zachary C, Hendrickson, Megan, Sakaie, Ken, Martinez-Rubio, Clarissa, Gale, John T, Trapp, Bruce D
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BlackWell Publishing Ltd 2015
Materias:
Brief Communications
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4338961/
https://www.ncbi.nlm.nih.gov/pubmed/25750925
http://dx.doi.org/10.1002/acn3.159
Descripción
Sumario: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.

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