It could up-regulate BDNF expression, lower down the aggregation of Aβ, as well as be against with oxidative stress and synaptic damage in several AD animal models without affecting AChE activities (Chi et al., 2013; Liu et al., 2013; Qi et al., 2013; Jin et al., 2014; Li et al., 2016; Ji et al., 2017). This evidence concerns the gene ACHE and Alzheimer disease.