Taken together, it seems evident that M1 activation of microglia in combination with proinflammatory cytokine secretion (IL-1β, IL-6, TNF-α, INF-γ) and the associated reactive oxygen/nitrogen species (ROS/RNS) secretion result in an increase in AD susceptibility via indirect tissue damage or direct enhancement of Aβ synthesis and agglomeration [31,35,46,54,74,75,76,77]. This evidence concerns the gene IL1B and Alzheimer disease.