In conclusion, this present study revealed that TA derived from PCP could promote the autophagic degradation of the NLRP3 inflammasome in Aβ(1–42)-induced BV-2 cells via the AMPK/ULK1 and Raf/MEK/ERK signaling pathways and improve the cognitive and behavioral functions in C. elegans and APP/PS1 mice (Fig. 9), which may provide a potential novel therapeutic reagent for TA in the prevention and treatment of AD in the future. This evidence concerns the gene NLRP3 and Alzheimer disease.