Results: Using LPS-stimulated BV2 microglial cells and an Aβ-injected ICR mouse model of Alzheimer’s disease, we found that PE significantly suppressed the LPS-induced production of nitric oxide and pro-inflammatory mediators, including IL-6, TNF-α, NF-κB, iNOS, and COX-2, along with inhibition of JNK and p38 MAPK activation. This evidence concerns the gene NFKB1 and early-onset autosomal dominant Alzheimer disease.