Our previous studies showed that PNS could improve learning and memory performance in AD model mice senescence-accelerated mouse-prone 8 (SAMP8), alleviate the deposition of amyloid β-peptide (Aβ)1–40 and Aβ1–42 through inhibiting the expressions of APP, BACE1 and ADAM9 (a disintegrin and metalloprotease 9), increasing α-secretase activity and reducing β-secretase activity [11], and prevent oxidative stress injury via increasing the gene expressions and activities of SOD, CAT, and GSH-PX in the brains of SAMP8 [12], suggesting that PNS may be a promising candidate for AD treatment. This evidence concerns the gene ADAM9 and Alzheimer disease.