Production of seedable Amyloid-β peptides in model of prion diseases upon PrPSc-induced PDK1 overactivation

Abstract

Aβ plaques have been detected in brains of patients with prion diseases. Here, using mice, the authors show that prion infection enhances Aβ production via a PDK1-TACE mechanism and that brain deposition of Aβ induced by Aβ seeds co-transmitted with PrPSc contributes to mortality in prion disease.