In line with the results of proteomics, our in vivo experiments confirmed decreased expression of PP2A and increased phosphorylated GSK3β (p- GSK3β) in the hippocampus of the model group, which further supports the hypothesis that the balance of PP2A and GSK3β, which coordinate synaptic plasticity function, may be an important molecular mechanism in AD treatment. This evidence concerns the gene GSK3B and Alzheimer disease.