High levels of mitochondrial DNA deletions have been found in dopaminergic neurons of Parkinson Disease patients, suggesting a role in the pathology. However, the reason for this accumulation of mtDNA deletions is unclear. In this work, dopamine was found to drive this phenomenon, probably through forcing continuous DNA strand-break repair events. The results also suggest that mtDNA deletions are acting in combination with other cell-specific factors, to promote neurodegeneration.