Parkinson's disease (PD) is a common neurodegenerative disease, and, currently, there is no cure for patients with PD. Studies have shown that Ginkgo biloba extract (EGb) has good neuroprotective effects against PD. The cerebellum is widely involved in cognitive function and may be related to the regulation of static tremors in PD. However, research on the corresponding microstructures is limited. Purkinje cells (PCs) are the only efferent neurons present in the cerebellum, and dendritic spines in PCs are considered the key structures for transmitting neuronal excitatory signals. When neurons are activated, polo-like kinase 2 (PLK2) is expressed, leading to the degradation of spine-associated Rap guanosine triphosphatase activating protein (SPAR) and, ultimately, the loss of postsynaptic density protein 95 (PSD-95), causing changes in the morphology or quantity of dendritic spines. This raises the question of whether the neuroprotective effect of EGb involves the PLK2-SPAR pathway. In this study, we used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to establish a mouse model of dopamine neuronal injury. Golgi staining was performed to observe the dendritic spine changes. Immunohistochemistry was used to detect the expression of PLK2, SPAR, and PSD-95. The results showed that EGb improves MPTP-induced behavioral changes, dopamine neuronal injury, and dendritic spine damage in mice. In addition, EGb reversed the changes in PLK2, SPAR, and PSD-95 expressions caused by MPTP, revealing the potential mechanism by which EGb improves the condition of patients with PD.