Titanium dioxide and carbon black nanoparticles disrupt neuronal homeostasis via excessive activation of cellular prion protein signaling

Abstract

Our in vitro and in vivo study thus posits for the first time normal cellular prion protein PrP^C as being a neuronal receptor of TiO₂- and CB-NPs and identifies PrP^C-coupled signaling pathways by which those nanoparticles alter redox equilibrium, augment the intrinsic sensitivity of neurons to neuroinflammation, and provoke a rise of Aβ peptides. By identifying signaling cascades dysregulated by TiO₂- and CB-NPs in neurons, our data shed light on how human exposure to some NPs might be related to AD.