In this mini-review, we summarize recent findings relating to the prion-like propagation of α-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 of α-syn (via exocytosis and endocytosis). The classical accumulation of aggregated α-syn
in PD may result from an increased production or a failure in the mechanisms of clearance of α-syn. We discuss
novel agents, currently in clinical trial for PD including the ones that impact the aggregation of α-syn and others
that interfere with α-syn endocytosis as a means to target the progression of the disease.

EB00000002378K

Available

• Mini-review on initiatives to interfere with the propagation and clearance of alpha- synuclein in Parkinson’s disease