EAE is an animal model of multiple sclerosis (MS), which is most commonly used in rodents. Due to the recent diversification of therapeutic modalities, including gene modification, and given the structural similarities in the central nervous system (CNS) to humans, non-human primates become to be considered a better animal model for MS research. In the present study, we evaluated neurological signs, magnetic resonance images (MRI), and histopathology in the CNS to examine whether immunization with myelin oligodendrocyte glycolipid (MOG) could induce EAE in cynomolgus monkeys. After MOG treatment, the animals showed motor dysfunction and visual impairment, indicating neurological deficits. However, there were individual differences in onset and severity of the neurological deficits. MRI and histopathological examination revealed disseminated inflammation in brain and optic nerve, similar to the pathology of MS in humans. Although further research is required to reduce the individual differences of the neurological deficits, these results indicate that MOG treatment can induce EAE in cynomolgus monkeys, and this can be used as a translational animal model for the development of new therapeutic modalities for MS.