Although it has been suggested that Aβ-stimulated microglial activation contributes to the pathophysiology of AD [24]‐[26,28]‐[30,33,67] and a broad range of microglial secreted inflammatory markers are elevated in AD brains, including IL-1α, IL-1β, TGF-β and TNF-α [68,69], enthusiasm for an anti-inflammatory approach to treating AD has decreased, in part, due to lack of drug efficacy of a number of human trials that targeted cyclooxygenase (Cox) activity in AD patients [70]‐[74]. This evidence concerns the gene IL1A and Alzheimer disease.