Therefore, we established a mouse model of AD in which Pb exposure begins in adulthood and examined the expression differences of several key CDR1as-associated factors, miR-671, AGO2, CDR1as, NF-κB, BACE1, APP, Aβ, and p-tau, under different concentrations of Pb exposure conditions to preliminarily explore the role of miR-671/CDR1as regulation in the effect of Pb exposure on Aβ and p-tau production. The gene discussed is BACE1; the disease is Alzheimer disease.