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

The beta-amyloid (A beta) peptide and the A beta-oligomer receptor, prion protein (PrP), both influence neurogenesis. Using in vitro murine neural stem cells (NSCs), we investigated whether A beta and PrP interact to modify neurogenesis. A beta 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 A beta-treated NSCs into mature cells was unaffected by PrP expression. Such marked PrP-dependent differences in NSC growth responses to A beta provides further evidence of biologically significant interactions between these two factors and an important new insight into regulation of NSC self-renewal in vivo.