Because AD is pathologically characterized by β-amyloid protein (Aβ) deposition in amyloid plaques (APs) and by tau phosphorylation in neurofibrillary tangles (NFTs) [2], numerous investigations have since been carried out to evaluate the roles of COX-2 and its metabolic products, prostaglandins (PGs), in Aβ deposition. This evidence concerns the gene PTGS2 and Alzheimer disease.