According to our results, BACE1 silencing down-regulated the composition of AA in LPE at 6 and 12 months post-treatment, and decreased the phosphorylation state of cPLA2, which could be involved in the cell membrane homeostasis of treated AD mice at 12 months post-injection, with the consequent down-regulation of AA levels and COX2 pro-inflammatory pathway in the same time-line (Figures 7C,D), suggesting a more effective anti-inflammatory regulation by the long-term BACE1’s silencing. Here, BACE1 is linked to Alzheimer disease.