IL1B and Alzheimer disease: It has become increasingly clear that IL-1β is by far the principal actor in the development of AD in response to any and all neuronal insults, including direct acute brain injury as in contact sports and motor vehicle accidents, or sustained insults, including the excess neuronal activity in epilepsy [13], especially in the context of the overlay of inheritance of the Alzheimer’s gene, which we showed manifests as frank mature Alzheimer’s plaques even in childhood, as noted in a 10-year-old with numerous, frank Aβ plaques [13].