Objective. In the course of the research, the effect of vincamine (nootropic drug) on neurological status, as well as the activity of antioxidant enzymes and the level of their coding genes’ expression in the somatosensory cortex of rats within the model of experimental allergic encephalomyelitis (EAE) were being studied. Relevance: the topicality of studying the mechanisms of multiple sclerosis in the early stages of its development is dictated by the need to search for markers of the disease and its therapy before the onset of its clinical manifestation. Materials and methods. The animals’ neurological status was studied using muscular strength, balance, tenacity and traction tests. Rates of survival and the rats’ body weight were also being evaluated. The study of activity antioxidant enzymes: superoxide dismutase (SOD), glutathione peroxidase (GPO), and glutathione reductase (GR), as well as the expression of SOD1, GPX4, GPX6, and GSR genes was conducted on the 14th and 30th day of immunization. Results. The percentage of vincamine-injected animals’ survival was 100% versus 87% among rats that were not injected with the nootropic drug during immunization (р<0,05) . Besides, after the injection of vincamine, a less significant decrease in body weight (р<0,01) and a less pronounced neurological deficit (р<0,05) in comparison with immunized non-injected animals were reported. The vincamine injection contributed to an increase in all studied antioxidant enzymes’ activity and the level of their genes’ expression in the somatosensory cortex. Conclusion. Against the background of vincamine injection, a minimization of neurological deficit is being observed, probably due to a decrease in oxidative stress in the rat brain during the clinical stage of experimental allergic encephalomyellitis.