Objective To investigate the effects of quercetin on learning and memory and pathway of cerebral inflammation in D-galactose-induced aging mice. Methods Thirty-two Kunming mice were randomly divided into control group (NC group), model group (M group), Q1 treatment group (Q1 group) and Q2 treatment group (Q2 group), with 8 in each group. The aging mouse model was induced by subcutaneous administration of D-galactose 100 mg/(kg·d) in M, Q1 and Q2 groups, and the same amount of normal saline was administered in the same way in the NC group. Quercetin were then given in different doses in Q1 [5 mg/(kg·d)] and Q2 [10 mg/(kg·d)] groups, and the same dose of saline was given to the NC group and M group. Intervention duration was 8 weeks. Morris water maze was used to assess the escape latency, frequency of crossing the platform and retention time in the platform quadrant in the mice. Western blotting was employed to detect the expression of advanced glycation end products (AGEs) and their receptor (RAGE), nuclear factor-κB (NF-κB) and its downstream inflammatory factors, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and cyclooxygenase-2 (COX-2). SPSS statistics 20.0 was used for data analysis, and one-way ANOVA for complete randomized design or Student′s t test for comparison between the groups. Results Compared with NC group, M group had lower escape latency, fewer crossings and shorter retention in target quadrant, but significantly higher AGEs, RAGE, NF-κB, TNF-α, IL-1β and COX-2. Compared with M group, treatment groups had lower escape latency, more crossings and longer retention in the quadrant of the platforms, and lower indices of cerebral inflammation (P<0.05). Compared with Q1 group, Q2 group had lower escape latency, more crossings and longer retention in the quadrant of platforms, and significantly lower expression of RAGE, IL-1β and COX-2. Conclusion Quercetin could effectively improve learning and memory dysfunction in the aging mice and reduce production of inflammatory factors in the brain by inhibiting AGEs/RAGE/NF-κB inflammatory pathway, hence having antiaging potential.