The complex etiology of PD is linked with mitochondrial integrity and a variety of evidence has been shown in Mendelian genetics, aging, and pesticide epidemiological analysis. Both genetic and non-genetic factors directly or indirectly affect mitochondrial function. Moreover, multiple research studies indicate that the PD-gene alpha-synuclein (SNCA) also impacts mitochondrial function. However, the exact mitochondrial mechanism that contributes to the development of PD remains unclear and no mitochondrially-targeted medications are on the horizon. Here we continue from our previous work which shows that β2AR activation down-regulates alpha-synuclein and offers neuroprotection in cellular and animal models of PD. In this study, we showed that activation of the β2AR can restore mitochondrial bioenergetics and morphology in PD models. Results show that activation of β2AR dramatically restores α-synuclein-mediated loss of ATP production in SNCA-Trip neurons. In addition, quantification of 3D images showed the increased sphericity SNCA-Trip neurons compared to the control line. In contrast, treatment with clenbuterol showed less spherical and more branched mitochondria.