Here, nasal administration of a miR-146a agomir relieved the progression of AD-associated neuroinflammation by inhibiting the expression of the TLR4 signaling pathway and its related inflammatory genes NF-κB, IL-1 receptor-associated kinase 1 (IRAK1), and TNF receptor-associated factor 6 (TRAF6) as well as reducing the release of inflammatory factors IL-1β, IL-6, and TNF-α [220, 466]. This evidence concerns the gene IL1B and Alzheimer disease.