By preventing hippocampal neurodegeneration, it developed behavioral disorder and decreased BACE-1 activity. It has monoamine oxidase and AChE inhibitory properties. In addition, it has been shown to attenuate the accumulation of Aβ plaques and inhibit the expression of BACE-1. It reduces the hyperphosphorylation of tau on calyculin-A treatment by restoring protein phosphatase-2A activity and inhibiting GSK-3β activation in HEK293 cells. This evidence concerns the gene ACHE and Neurodegeneration.