NEVs and AEVs from AD patients at the clinical and preclinical stages carry higher levels of AD pathogenic proteins compared to controls, including total Tau (tTau), phosphorylated Thr181 Tau (p181-Tau), and Aβ42 in NEVs [9,10,12,14,16,17,19], and complement proteins, including C1q, in AEVs [15]. This evidence concerns the gene VTN and Alzheimer disease.