Abstract: Parkinson’s disease is a progressive neurodegenerative disorder characterized by dopaminergic neuronal loss, motor dysfunction, and cognitive impairment, largely associated with oxidative stress and neurotransmitter imbalance. The present study was designed to evaluate the neuroprotective potential of the ethanolic extract of Alstonia scholaris in a chlorpromazine-induced Parkinsonism model in experimental animals. Animals were divided into five groups: normal control, chlorpromazine-treated negative control, standard treated group receiving Levodopa (10 mg/kg), and two test groups treated with ethanolic extract of Alstonia scholaris (200 and 400 mg/kg) along with chlorpromazine (3 mg/kg). Behavioral assessments were performed using Morris Water Maze, Elevated Plus Maze, and Y-maze tests to evaluate learning, memory, and exploratory activity. Biochemical parameters including malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and acetylcholinesterase (AChE) were estimated to assess oxidative stress and cholinergic function. Chlorpromazine administration significantly impaired cognitive performance and induced oxidative stress, as evidenced by increased MDA and AChE levels and decreased antioxidant enzyme activities. Treatment with the ethanolic extract of Alstonia scholaris produced a dose-dependent improvement in behavioral and biochemical parameters. The higher dose (400 mg/kg) showed effects comparable to the standard drug, indicating significant neuroprotective activity. The results suggest that Alstonia scholaris possesses potent antioxidant and neuroprotective properties, which may contribute to its beneficial effects against chlorpromazine-induced Parkinsonian symptoms. Further studies are required to isolate active constituents and elucidate the precise mechanisms underlying its neuroprotective action.