AIM Compound Danshen tablet (CDT), a Traditional Chinese Medicine, has recently been reported to improve spatial cognition in a rat model of Alzheimers disease.However, in vivo neuroprotective mechanism of the CDT in models of spatial memory impairment is not yet evaluated.The present study is aimed to elucidate the cellular mechanism of CDT on Aβ25-35-induced cognitive impairment in mice.METHODS Mice were randomly divided into 5 groups: the control group (sham operated), the AD model group, the positive drug group, and large and small dosage of the CDT groups, respectively.CDT was administered at a dose of 1.62 g· kg-1 and 0.405 g· kg-1 for 3 weeks.The mice in the positive drug group were treated with 0.4 mg· kg-1 of Huperzine A,whereas the mice of the control and AD model groups were administrated orally with equivalent saline.Mter 7 d of preventive treatment, mice were subjected to lateral ventricle injection of Aβ25-35 to establish the mice model of Alzheimers disease.Morris water maze test was used to measure the capability of spatial memory.Levels of TNF-αo, IL-6, ChAT, RACK1 and BDNF were analyzed by RT-PCR, immunohistochemistry and ELISA.RFSULTS The results showed that Aβ25-35 caused spatial memory impairment as demonstrated by performance in the Morris water maze test.CDT was able to confer a significant improvement in spatial memory, and protect mice from Aβ25-35-induced neurotoxicity.Additionally, CDT also inhibited the increase of TNF-ot, IL-6 level, and increased the expression of ChAT, RACK1 and BDNF in brain as compared to model mice.CONCLUSION The findings strongly implicate that CDT may be a useful treatment against learning and memory deficits in mice by rescuing imbalance between cytokines and neurotrophins.