Abstract: Parkinson’s disease (PD), characterized by the loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc) of the midbrain, is a prototype neurological disease that is suitable for cellular replacement therapy. Levodopa has been utilized to replace the insufficient dopamine released by degenerating DA neurons since the 1960s and it remains the cornerstone of PD treatment. However, as the disease progresses, the diminishing DA neurons become inadequate to convert administered levodopa to functional dopamine, and the affected axonal projections fail to deliver dopamine to target brain regions. As a result, the dopamine replacement eventually loses its efficacy after the initial honeymoon period, and chronic levodopa therapy is associated with debilitating side effects, including motor and non-motor complications.