Parkinson’s disease (PD) is a neurodegenerative disorder that is characterized by dopaminergic neuronal damage. We evaluated the neuroprotective effect of γ-amino butyric acid (GABA) in PD and the underlying mechanism focusing on WNT/β-catenin signaling mediated by the MAPK pathway. We treated MPTP-induced SH-SY5Y cells with GABA Low and High concentrations, and we also treated PD model mice with GABA. GABA treatment effectively reduced the expression of biomarkers associated with PD, particularly lewy’s bodies and α-synuclein, and increased the number of tyrosine hydroxylase positive cells. GABA also improved the motor dysfunction in MPTP-induced PD model mice as measured by the rotarod test. The levels of several pro-inflammatory mediators, TNF-α, IL-6, COX-2, and MAC-1, were overexpressed in PD, however, these were reduced following GABA treatment. Our results indicate that GABA is neuroprotective and had anti-inflammatory effects that could be beneficial for treating Parkinson's disease.