摘要
In this mini-review,we summarize recent findings relating to the prion-like propagation ofα-synuclein(α-syn)and the development of novel therapeutic strategies to target synucleinopathy in Parkinson’s disease(PD).We link the Braak’s staging hypothesis of PD with the recent evidence from in-vivo and in-vitro studies for the prion-like cell-to-cell propagation ofα-syn(via exocytosis and endocytosis).The classical accumulation of aggregatedα-syn in PD may result from an increased production or a failure in the mechanisms of clearance ofα-syn.We discuss novel agents,currently in clinical trial for PD including the ones that impact the aggregation ofα-syn and others that interfere withα-syn endocytosis as a means to target the progression of the disease.
