As the major overexpression was found in subjects with neurodegenerative diseases, who were also the ones who had more misfolded Aβ, tau and α-synuclein, we performed PLA assays to determine whether there was a direct interaction between PrP and amylin, tau, α-synuclein or Aβ in pancreatic tissue in addition to co-expression in pancreatic β-cells, as has been described in brain tissue [17, 24]. Here, PRNP is linked to neurodegenerative disease.