Comparing healthy controls and patients diagnosed with AD according to the NIA-AA criteria, NDEVs of AD patients had other upregulated proteins as well, involved in control of synaptic density and synaptic pruning (complement components), components of the membrane attack complex (shown to co-localize with Aβ plaques and tau tangles), proteins that act as receptors for von Willebrand factor and were associated with endothelial dysfunction (such as platelet glycoprotein Ib beta chain), and upregulated levels of Ras suppressor protein 1 (RSU1) [137]. The gene discussed is RSU1; the disease is endothelial dysfunction.