Objective : To investigate the protective effects of Naoerkang(NEK) on Alzheimer disease (AD) mince induced by chronic Al(AlCl3) toxicity involved in regulating protein expression of amyloid precursor protein(APP) and β-amyloid(Aβ). Method : Sixty male mice were randomly divided into normal control group

model group

piracetam group

low-dose NEK group

medium-dose NEK group

and high-dose NEK group

with 10 mice in each group

AlCl3(100 mg·kg-1) were injected into abdominal cavity in mice to establish AD model whereas the normal control mice were injected with same volume of saline for comparisom.The mice in the NEK groups were intragastrically treated respectively with high

medium and low dose(1.36

0.68

0.34 g·mL-1) NEK for 50 days consecutively; piracetam(10 g·mL-1) was intragastrically administered to mice in the piracetam group; and normal saline was applied in the control and model groups. Jumping stand was used to examine their abilities in learning and memory. The positive protein expression of APP and Aβ in cortex and hippocampal region of the mice in each group were detected by immunohistochemistry

and the results were analyzed by gray scale adopting Qwin550CW images and signals cllection and analysis system. Result : Compared with the control group

the Latent Period of memory was shortened significantly (P<0.01)

while that of learning had been prolonged obviously (P<0.05)and the times of mistakes for learning and memory increased significantly (P<0.01) for the mice of the model group. Compared with the model group

the Latent Period memory in the groups treatment with drug shortened significantly (P<0.01)

while that of learning had been prolonged obviously (P<0.05)and the Frequency of Error for learning and memory had been increased evidently(P<0.01). The expressions of APP

Aβ in cortex and hippocampus had been increased significantly(P<0.05 orP<0.01) for the mice of the model group

and it had shown a more obvious reduction campared with the group using Naoerkang (P<0.01). Conclusion : Naoerkang can ameliorate the AD induced by Aβ

the mechanism maybe involve in regulating APP and Aβ.