Many studies have reported that lutein have positive effects in different clinical conditions, thus ameliorating cognitive function, decreasing the risk of cancer, and improving measures of cardiovascular health. This study investigates the potential neuroprotective effects of lutein, a carotenoid with antioxidant properties against sodium azide-induced amnesia in mice. A total of thirty (30) healthy mice weighing 19g - 35g were used for this study. The mice were acclimatized and divided into six groups (n= 5 per group) which are; Group 1 (Control group), Group 2 (Sodium azide only), Group 3(Sodium azide + 20mg/kg of lutein), Group 4 (Sodium azide + 40mg/kg of lutein), Group 5 (Sodium azide + 60mg/kg of lutein), Group 6 (Sodium azide + Donepezil). Motor deficits were assessed using behavioral tests like Barnes maze test, Hand grip test, Rotarod test and Y maze test. While biochemical analysis was performed to evaluate oxidative stress markers, inflammatory cytokines and neurotransmitters. The results demonstrate that the mice treated with sodium azide only had a significantly higher latency compared to the control group. This suggests that sodium azide negatively impacted spatial learning and memory as indicated by the increased time taken to find the target. Lutein, especially at 40mg/kg and 60mg/kg as well as Donepezil (the standard drug) has neuroprotective effects against the spatial learning and memory deficits induced by sodium azide in mice. This study shows that sodium azide induced both motor symptoms such as agnosia and non-motor symptoms such as impaired memory, oxidative stress in mice and lutein an antioxidant carotenoid possesses a dose dependent increase in learning ability and cognitive functions and decrease in oxidative stress.