These effects were not produced by nonspecific CD81+ and total plasma EVs from AD patients or AEVs and NEVs from FTLD or cognitively normal participants and were blocked by the MAC inhibitor CD59 and additional endogenous complement inhibitors, suggesting that neuronal MAC assembly represents a necessary effector for AEV and NEV-mediated neurotoxicity in AD. The gene discussed is CD59; the disease is Alzheimer disease.