Our data showed that both AD 4,4 and AD 3,3 carriers have significantly more neuroinflammation than AMCs, with AD 4,4 having higher expression levels of neuroinflammatory markers like TLR, MyD88, and NFκB and AD 3,3 having lesser expression levels of IL-1β compared to AD 4,4, together with increased levels of IL-1β’s signaling cascade and further neuroinflammation. This evidence concerns the gene IL1B and Alzheimer disease.