PRRT2 and Alzheimer disease: Finally, to validate this finding we used ASPD derived from the brains of the three AD patients displaying the most severe AD pathology and the highest ASPD concentrations, which we also used in our previous studies (Noguchi et al., 2009; Ohnishi et al., 2015), to confirm that patient-derived ASPD truly inactivate eNOS activity by increasing the phosphorylation of eNOS-Thr495 through a mitochondrial ROS-PKC pathway.