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