Dopamine release from Parkinson's patient-derived neurons is disrupted due to impaired synaptic vesicle loading
This study demonstrates that dopamine release deficits in human Parkinson's disease neurons carrying the SNCA-triplication mutation stem from impaired vesicular monoamine transporter 2 (VMAT2) function, which reduces dopamine storage capacity, disrupts vesicle recycling, and elevates cytosolic dopamine levels, thereby contributing to both symptomatic dysfunction and neuronal degeneration.