Objective To investigate the molecular mechanism of calcine kinase II（ CaMKII） in improving the memory function of mice with Parkinson disease（ PD）， and to explore the possible mechanism underlying this effect， which will provide a new idea to treat PD. Methods 6-OHDA was stereotactically injected into the left striatum of mouse to prepare the lateral PD mouse model. Then the valid PD model was selected by cylinder test. All valid PD（ n=32） mice were divided into four groups： PD+ no-Ex group（ n=8）， PD+Low-Ex group（ n=8）， PD+Medium-Ex group（ n=8） and PD+High-Ex（ n=8）. Another group of shamoperated mice were involved as control（ n=8， injection of saline at the same site）. Through the analysis and evaluation of their behavioral results， the hippocampus of mice in sham-operated group， PD+no-Ex group and PD + Low-Ex group were selected for Western blot to detect the phosphorylation levels of cAMP-response element binding protein（ CREB）， the extracellular signal-regulated kinase1/2（ ERK1/2）， Tyrosine hydroxylase （TH） and calmodulin kinase Ⅱ（ CaMKII）. Results The navigation test of Morris water maze showed that the mean escape latency of each group was gradually decreased with the prolongation of training time. Different speed of treadmill exercise all improved the memory of mice especially the low speed exercise（ P＜ 0.05）. In addition， spatial probe test showed that compared with mice in sham-operated group， the number of times through the platform were decreased in mice of PD + no-Ex group， and the difference was statistically significant （P ＜ 0.05）. Western blot results showed that the levels of phosphorylated CREB， ERK1/2， CaMKII and TH were decreased in PD mice compared to sham-operated mice（ P＜0.05）. However， compared with PD+no-Ex group， the indicators above in PD+Low-Ex group increased significantly， and the difference was statistically significant（ P＜0.01）. Conclusions Low-exercise training was effective to improve memory in PD mice， which is because that low-exercise training could enhance the activity of PKA pathway， so as to improve the cognition function of PD mice.