IL1B and Alzheimer disease: This is consistent with the idea that neuroinflammation is the most significant characteristic feature of Alzheimer’s neuropathogenesis, with or without the impact of inheritance of APOE 4,4, as even AD 3,3 carriers have significant levels of Aβ accumulation, which is correlated with the expression of IL-1β, without which Aβ plaques and neurofibrillary tangles, the hallmarks of Alzheimer’s, are not produced.