The prion protein regulates beta-Amyloid-mediated self-renewal of neural stem cells in vitro

Abstract

The beta-Amyloid (Aβ) peptide and the Aβ-oligomer receptor, prion protein (PrP), both influence neurogenesis. Using in vitro murine neural stem cells (NSCs), we investigated whether Aβ and PrP interact to modify neurogenesis. Aβ imparted PrP-dependent changes on NSC self-renewal, with PrP-Ablated and wild-Type NSCs displaying increased and decreased cell growth, respectively. In contrast, differentiation of Aβ-Treated NSCs into mature cells was unaffected by PrP expression. Such marked PrP-dependent differences in NSC growth responses to Aβ provides further evidence of biologically significant interactions between these two factors and an important new insight into regulation of NSC self-renewal in vivo.