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Parkinson's Disease (PD) is a neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra, leading to motor dysfunction and non-motor symptoms. Current treatments primarily offer symptomatic relief without halting disease progression. This has driven the exploration of natural compounds with neuroprotective properties. In previous studies, α-phellandrene, a monoterpene present in essential oils of various aromatic plants, has shown promise in mitigating neurodegenerative processes. This study focuses on alpha-phellandrene's therapeutic potential in a rotenone-induced Parkinson's Disease model. Rotenone, a mitochondrial complex I inhibitor, is commonly used to induce PD-like symptoms in experimental models due to its ability to mimic the neurodegenerative processes observed in human PD. Our review explores the neuroprotective effects of alpha-phellandrene, focusing on its antioxidant, anti-inflammatory, and anti-apoptotic properties. Experimental groups of rodents received rotenone to induce PD-like symptoms, followed by alpha-phellandrene treatment. Biochemical analyses were performed to measure oxidative stress markers, inflammatory cytokines, and apoptotic signals in brain tissues. Results indicated that alpha-phellandrene administration significantly improved motor function and reduced rotenone-induced oxidative stress, inflammation, and apoptosis in dopaminergic neurons. Histopathological examinations revealed a notable preservation of neuronal integrity in alpha-phellandrene-treated groups compared to controls. In conclusion, alpha-phellandrene demonstrates considerable neuroprotective effects in a rotenone-induced Parkinson's dmodel. These findings suggest that alpha-phellandrene could be a promising natural therapeutic agent for PD, warranting further investigation into its mechanisms of action and potential clinical applications. Specifically, our review indicates that alpha-phellandrene may exert neuroprotective effects by various mechanisms, such as reducing oxidative stress, modulating neurotransmitter levels, or inhibiting neuroinflammation. These mechanisms highlight its potential to alleviate PD symptoms and slow disease progression, underscoring the need for in-depth studies to validate these therapeutic effects in clinical settings