AD was associated with damage to the intestinal barrier, through which LPS and proinflammatory factors produced by pathogens entered the body, disrupted the integrity of the blood-brain barrier (BBB), enhanced the uptake of Aβ and α-syn in the brain, and activated microglia-induced immune reactions through the LPS/TLR4/NF-κB pathway, resulting in neuronal loss [116, 117]. Here, NFKB1 is linked to Alzheimer disease.