Abstract: Parkinson’s disease (PD) is the most frequent movement disorder and the second most prevalent age-related neurodegenerative disease (ND) worldwide. From the clinical point of view, it is characterized by severe motor complications, including uncontrollable resting tremors, rigidity, bradykinesia, and postural instability. These motor symptoms are caused by the selective and progressive degeneration of midbrain dopaminergic neurons in the subtantia nigra pars compacta and their striatal projections (Kalia and Lang, 2015), which leads to a substantial reduction in dopamine production. Motor features of PD are associated with the accumulation of pathological aggregates of α-synuclein into Lewy bodies, considered the most typical hallmarks of the disease. Non­motor symptoms, including the progressive impairment of cognitive, autonomic, and mood functions, are additional PD-associated clinical complications, consequent to damage in other regions of the central and peripheral nervous system (Kalia and Lang, 2015; Schapira et al., 2017). Indeed, besides dopaminergic neuron degeneration, it is now clear that dysfunction of glial components and other kinds of neurons also participate in PD pathogenesis and progression.