Neuronal dysfunction during sporadic and familial forms of Parkinson’s disease is intimately connected to mitochondrial dysfunction. Diverse genetic and environmental factors contributing to Parkinson’s disease development and progression have been shown to interfere with and to compromise mitochondrial bioenergetics, dynamics and trafficking. Mitochondria are highly dynamic organelles, constantly changing shape and abundance via coordinated fission and fusion events to adapt to cellular needs. Moreover, direct contact between mitochondria and other organelles allows interconnected signaling, and exchange of metabolites and ions. Several proteins associated with familial Parkinson’s disease modulate the equilibrium between fission and fusion, govern distinct mitochondrial degradation pathways and impact the formation of tethering complexes that facilitate interorganellar contact. Here, we discuss molecular mechanisms of mitochondrial dysfunction in Parkinson’s disease, focusing on mitochondrial dynamics and contact sites.