Our results reveal that the administrations of HE-Et or HE-My to APP/PS1 mice for 30 days eliminated amyloid plaque burden, prevented recruitments and activations of plaque-associated microglia and astrocytes, promoted the expression of IDE, the NGF/proNGF ratio, and the proliferation of neuron progenitors and the number of newly born neurons in dentate gyrus. The gene discussed is APP; the disease is amyloidosis.