The PARLance of Parkinson disease

Mitochondrial biology has recently emerged as a key regulatory event in Parkinson disease (PD). Notably, defects in the clearance of damaged mitochondria, termed mitophagy, have been recently highlighted as a possible mechanistic explanation for neuronal loss. We have recently identified the mitochondrial rhomboid, termed PARL, as a regulator of the cells mitophagic response. Further, we have identified PD-linked mutations at a functional site in the PARL gene. Here we discuss the benefit of combining molecular genetic and cell biology approaches in understanding human disease.