To investigate the effect of lutein intervention on cognitive competence in mice with Alzheimer's disease (AD) and the related mechanism.Methods Use 5-month male senescence-accelerated mouse prone 8 (SAMP8) as a natural model of AD. SAMP8s were randomly assigned into 1 AD model group and 3 lutein intervention groups; senescence-accelerated mouse resistant 1(SAMR1) were used as control.15,0, 60 mg/kg BW lutein was given to the 3 intervention groups, once a day via intragastric administration for 8 weeks. Cognitive competence was assessed by the Morris water maze after intervention. Levels of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), malondialdehyde (MDA) and acetylcholinesterase (AchE) in brain tissue were measured. The pathological observation of the hippocampus was performed. Results Medium and high level of lutein intervention lowered the escape latency SAMP8(P＜0.05). Lutein intervention increased the levels of CAT, GSH, AchE and lowered MDA(P＜0.05). High level lutein reduced the number of abnormal cells in hippocampus(P＜0.05).Conclusion Lutein can improve the cognitive competence of SAMP8 and one of its possible mechanisms was by enhancing oxidation resistance and reducing oxidative damage.