Parkinson's disease (PD) is one of the most common of the neurodegenerative disorders, affecting 1-2% of the population worldwide. Multiple lines of evidence place mitochondrial dysfunction as a central player in the pathogenesis of sporadic PD, and studies of genes associated with familial PD demonstrate convergent pathways involving oxidative stress and mitochondrial dysfunction. Two proteins commonly mutated in familial PD, PINK1 and Parkin, play a key role in maintaining mitochondrial integrity by identifying damaged mitochondria and degrading them through a selective form of autophagy termed mitophagy. Our lab investigates the molecular mechanisms of PINK1/Parkin mitophagy and how it works together with the mitochondrial unfolded protein response to maintain healthy mitochondria.

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