All five of these proteins have been implicated in AD pathogenesis: LRP1 is a receptor that interacts with Abeta and APOE, which may influence LRP1’s ability to aid in Abeta clearance[86]; EGFR polymorphisms were found to be inversely proportional to AD risk in a Han Chinese cohort[91]; 14-3-3 can be found around Abeta plaques and facilitates GSKbeta-mediated phosphorylation of tau[92]; SUMO1 expression is altered in cortices of AD patients[93]; and EGR1 inhibition leads to decreased Abeta and p-tau while reversing cognitive deficits in 3xTg AD mice[94]. This evidence concerns the gene APOE and Cognitive impairment.