Mice that lack functional NF-κB p50 are more sensitive to neurotoxins, display memory deficits [37], show an aberrant microglia-mediated inflammatory response in a rodent Alzheimer’s disease model [31], exhibit a dysfunctional kinetic response of the microglial pro-inflammatory response, and are vulnerable to chronic neuroinflammation [7]. Here, NFKB1 is linked to Alzheimer disease.