Mitochondria are dynamic organelles which are required for maintaining cellular homeostasis. Thus, it is not surprising that irregularities in mitochondrial function result in cellular damage and are linked with neurodegenerative diseases, such as Parkinson’s disease. Evidence that mitochondrial dysfunction is key to the pathogenesis of Parkinson’s disease is founded in studies in post-mortem tissue from patients with Parkinson’s disease, and also from genetic studies stemming from patients with familial Parkinson’s disease. Whether triggered by environmental or genetic factors, mitochondrial dysfunction occurs early in the pathogenic process, and is central to Parkinson’s disease pathology. As such, targeting the mitochondria to slow or halt disease progression is an attractive strategy for disease-modifying agents in Parkinson’s disease. Indeed, several therapies which target the mitochondria have been investigated as neuroprotective treatments for Parkinson’s disease. This review will discuss the evidence supporting mitochondrial dysfunction in Parkinson’s disease pathology as well as treatment strategies that target the mitochondria.