Topic: Synaptic Vesicle Endocytosis

Membrane trafficking defects are one of the core components of Parkinson’s Disease (PD), a progressive neurodegenerative disorder that results in severe motor deficits. Several genes associated with Clathrin-Mediated Endocytosis (CME) have been identified as PD risk genes, suggesting a putative link between trafficking defects and early nigrostriatal dysfunction. Intriguingly, recent work on endocytosis-defective mutants has implicated a renowned PD protein: Parkin (or PARK2), an E3 Ubiquitin ligase conventionally involved in mitochondrial quality control, in CME. Parkin is reported to mono-ub