Analysis of complement content of plasma-derived AEVs from AD patients versus age- and gender- matched HC indicated significantly increased factors of the classical and alternative pathways (C1q, C4b, C3d, C3b, fB, fD, fBb, and TCC), while mannose-binding lectin levels were unchanged (138, 139). The gene discussed is SFXN1; the disease is Alzheimer disease.