Cellular Prion Protein Mediates α‐Synuclein Uptake, Localization, and Toxicity In Vitro and In Vivo

Abstract

PrP^C 's native trafficking can be misused to internalize misfolded aSyn through a clathrin-based mechanism, which may facilitate the spreading of pathological aSyn. Disruption of aSyn-PrP^C binding is, therefore, an appealing therapeutic target in α-synucleinopathies. © 2021 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.