Intervention of APP/PS1 mice with the active ingredient of Acorus tatarinowii Schott, β-Asarone, revealed that the expression of p-mTOR and p62 was reduced in the treated group and the expression of p-Akt, Beclin-1, and LC3B was reduced in the treated group compared to the blank group, indicating that β-Asarone could inhibit Beclin-1 and LC3B by upregulating the PI3K/Akt/mTOR signaling pathway to inhibit Beclin-1-dependent autophagy to attenuate Aβ1-42-induced neuronal toxicity and improve cognitive performance in AD mice (Xue et al., 2014; Deng et al., 2016). This evidence concerns the gene APP and Alzheimer disease.