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Working model for α-synuclein-induced endocytic defects and amelioration by Hsc70. A, In the presence of excess α-synuclein, endogenous Hsc70 becomes depleted at synapses, leading to impaired CCV uncoating and an inhibition of synaptic vesicle recycling. B, Addition of exogenous Hsc70 restores CCV uncoating and leads to more normal synaptic vesicle recycling. (Graphics by Jack Cook and Tim Silva, Woods Hole Oceanographic Institution.)
