Reply to: “Parkin Deficiency Appears Not to Be Associated with Cardiac Damage in Parkinson's Disease”

effect of a conditional cardiac-specific Parkin deletion in adult mouse hearts indicates that Parkin has a limited role in normal homeostatic cardiac mitochondrial quality control. Our results are in line with studies reporting more severely impaired cardiac autonomic innervation in IPD than in Parkin-PD, possibly indicating no or less α-synuclein deposition in cardiac tissue in Parkin-PD. Interestingly, metabolic syndrome is not only a risk factor for cardiovascular diseases but has been positively associated with the development of IPD. Therefore, our findings indicate that in contrast to IPD, cardiovascular metabolic abnormalities do not appear to play a major role in the etiology of Parkin-PD. To conclude, we did not find evidence for subclinical cardiac damage in Parkin-PD based on TropT analysis. Further functional studies investigating IPD and cardiac disease are warranted, combined with in-depth epidemiological studies, including confounding factors and appropriate control groups.