TLR4 and Alzheimer disease: LPS can contribute to the development of AD pathology by stimulating the phagocytic state of microglia via Toll-like receptor 4 (TLR4) and activated nuclear factor-κB (NF-kB) (Figure 2) [93,94,95], which leads to the secretion of multiple pro-inflammatory cytokines and the promotion of the oxidative stress (Figure 2).