In light of these facts, the therapeutic strategies are mostly symptomatic treatments with non-steroidal anti-inflammatory drugs (NSAIDs) shown to decrease the risk of AD and delay progression, but only in prospective observational studies by halting cyclooxygenase 2 (COX-2) or the prostaglandin E2 receptor, activating phagocytosis by microglia, triggering peroxisome proliferator-activated receptor gamma (PPAR-γ), and selective decrease of Aβ42 [19]. This evidence concerns the gene PPARG and Alzheimer disease.