Objective  To study the  effect and mechanism of astaxanthin on learning and memory ability of vascular dementia (VaD) mice.    Methods  The mice were used to establish VaD model by occlusion of bilateral common carotid artery. The mice were randomly divided into sham group, model group, astaxanthin low-dose group and astaxanthin high-dose group and then given corresponding forms of drug treatments. Morris water maze was used to investigate the learning, memory and space exploration abilities of mice in each group. At the same time, the pathological morphology of brain neurons, the expression of amyloid beta-peptides 42(Aβ42) protein in brain and the content of interleukin (IL)-4 and IL-6 were respectively examined by Nissl staining, immunohistochemical staining, Western blotting and ELISA.    Results  The average escape latency of mice in the model group on the 4th and 5th days was significantly higher than sham-operated group (P<0.05), and the number of plateau crossings and the duration of stay decreased significantly (P<0.05). At the same time, Nissl staining showed that the neurons in the hippocampus of the model group were shrinking and disordered. The number of neurons in the model group was significantly reduced compared with the sham-operated group. The average escape latency of mice treated with different doses of astaxanthin on the 4th and 5th day was significantly lower than the model group (P<0.05).The number and duration of platform crossing were significantly longer than model group (P<0.05). The number of neurons in the intervention group was obviously higher than model group, and the effect was dose-dependent. In addition, immunohistochemical staining, Western blotting analysis and ELISA detection showed that the levels of Aβ42 protein and IL-6 in the astaxanthin intervention group decreased significantly compared with the model group (P<0.05), while the levels of IL-4 increased significantly (P<0.05).   Conclusion  Astaxanthin can reduce the expression of neurotoxic protein Aβ42 protein and inhibit the inflammatory response in the brain, which can protect neurons and improve the learning and memory ability of mice.