In this study, we leverage the advantages of the unilaterally lesioned PD animal model by using the AAV1/2-A53T-alpha-synuclein (α-syn) rat model—which closely mimics human PD, characterized by nigrostriatal deficiency, Lewy body pathology, and motor impairments [13, 14]—and conducted unilateral STN-DBS in the A53T rats and controls (empty vector, EV). Here, SNCA is linked to Parkinson disease.