BACE1 and Alzheimer disease: However, further research is necessary to establish whether there is a direct or indirect correlation between the BACE1 levels and the metabolic pathways of PE, LPE, and ePE and to explain how BACE1 silencing favors the appearance of the PUFAs involved in neuroprotection or if the reduction of BACE1 attenuated cytotoxic βA production for restoring cellular function including lipid metabolism, anti-inflammatory pathway and cognitive function, and to verify which would be the analog modulation of the phospholipid profile and composition in the human AD pathogenesis.