PRRT2 and Alzheimer disease: A comprehensive phosphoproteome analysis by Tagawa et al.29 revealed that PKC substrates account for over half of the core molecules that display increased phosphorylation in AD brains, a finding supported by subsequent phosphoproteomics studies identifying PKC as one of the main kinases activated in AD30, and reporting increased phosphorylation of PKCα at Thr63860, a quantitatively phosphorylated C-terminal site that serves as an indicator of PKC steady-state levels61,62.