Based on the data, Pb inhibited CDR1as expression, and this inhibition may occur by promoting elevated expression levels of miR-671 and AGO2 proteins, and promoting the binding of miR-671 to CDR1as to induce degradation of CDR1as by AGO2 proteins, which in turn promoted the nuclear migration process of NF-κB protein, and ultimately induced elevated expression levels of AD-related proteins, impairing the learning and memory abilities of mice, and thus participating in the pathogenesis of AD. This evidence concerns the gene NFKB1 and Alzheimer disease.