Though primarily a sporadic condition, Parkinson’s disease is increasingly recognized to be a multifactorial disease with a strong genetic component. At a cellular level, disruptions of protein trafficking and recycling, particularly by misfolding, accumulation, and aggregation of α-synuclein, mitochondrial dysfunction, oxidative stress, and other etiopathogenic mechanisms, have been found to result in the death of vulnerable neuronal populations and appear to drive the neurodegeneration underlying Parkinson’s disease. The improved understanding of these mechanisms has led to the development of novel pathogenesis-targeted and potentially disease-modifying therapeutic approaches in Parkinson’s disease. Until these treatments are fully developed and approved, clinicians must rely on therapies designed to improve quality of life of patients by treating various motor and non-motor symptoms of the disease.