The potential ability of DHA to reduce caspase activation [114, 115], Aβ peptide accumulation, and Tau hyperphosphorylation [126, 127] also strongly supports the notion that DHA deficiency, as a result of iPLA2 deficiency, could represent a precursor event that could initiate the cellular manifestations of AD pathology. This evidence concerns the gene PLA2G6 and Alzheimer disease.