Parkinson's disease (PD) is one of the most common neurodegenerative disorders and is characterized by progressive motor impairment due to the death of dopaminergic neurons in the substantia nigra (SN) of the brain. PD affects more than 1% of the population over 60 years of age worldwide. Despite significant progress in understanding the pathogenesis of PD, including genetic and biochemical aspects, current therapy is limited to symptomatic treatments. Recent evidence suggests that impaired autophagy leads to the accumulation of abnormal proteins and, particularly, α-synuclein, aggregated forms of which are neurotoxic to dopaminergic neurons in the SN. Notably, PD is predominantly sporadic. However, monogenic PD forms have also been described. PD forms associated with mutations of the GBA1 or LRRK2 gene are among the most common PD forms with known etiology. Leucine-rich repeat kinase 2 (LRRK2), which is encoded by LRRK2, and the lysosomal enzyme glucocerebrosidase (GCase), which is encoded by GBA1, are involved in the same endolysosomal pathway. LRRK2 and GCase dysfunction reported in PD, especially in cases with mutations of the respective genes, can impair the endolysosomal pathway, the lysosomal function, and possibly autophagy. The review highlights the molecular mechanisms of autophagy and the prospects for targeted therapy of PD via induction of autophagy by influencing the key players in the process.