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In Alzheimer disease (AD), amyloid-β (Aβ) oligomer is suggested to play a critical role in imitating neurodegeneration, although its pathogenic mechanism remains to be determined. Recently, the cellular prion protein (PrP C ) has been reported to be an essential co-factor in mediating the neurotoxic effect of Aβ oligomer. However, these previous studies focused on the synaptic plasticity in either the presence or the absence of PrP C  and no study to date has reported whether PrP C  is required for the neuronal cell death, the most critical element of neurodegeneration in AD. Here, we show that  Prnp  −/−  mice are resistant to the neurotoxic effect of Aβ oligomer  in vivo  and  in vitro . Furthermore, application of an anti-PrP C  antibody or PrP C  peptide prevents Aβ oligomer-induced neurotoxicity. These findings are the first to demonstrate that PrP C  is required for Aβ oligomer-induced neuronal cell death, the pathology essential to cognitive loss.

Cellular prion protein is essential for oligomeric amyloid-β-induced neuronal cell death