Thus, while it increases the production of the AD-associated neurotoxic peptide A, by upregulation of the β-site APP cleaving enzyme 1 (BACE-1) activity [138], it results protective in Aβ-driven models of AD, in which it efficiently decreases microglia and astrocyte activation and NF-κB signaling [139]. Here, NFKB1 is linked to Alzheimer disease.