To more clearly define the role of neuroinflammation in Alzheimer’s neuropathogenesis, particularly as it may be influenced by the inheritance of one or both APOEε4 alleles, we assessed the roles played by IL-1β in the regulation of its downstream signaling proteins, in particular the TLR-MyD88-NFκB signaling cascade, leading to increases in Cox-1 and Cox 2 and further increases in IL-1β in a self-perpetuating cycle, more in AD 4,4 carriers than in AD 3,3 or AMC 3,3. The gene discussed is MYD88; the disease is Alzheimer disease.