As life expectancy increases, the prevalence of age-related disorders, including neurodegenerative diseases (ND), is also rising. Oxidative stress (OS) is a key factor accelerating ND progression. For instance, in Parkinson’s disease (PD), impaired free radical scavenging promotes α-synuclein (α-syn) aggregation and neuronal damage. Therefore, antioxidant compounds are considered promising therapeutic candidates. In this study, we investigated the biological effects of Geraniol (GER), a plant-derived compound with antioxidant properties. Caenorhabditis elegans is a valuable model in biomedical research due to its genetic conservation with mammals and ease of manipulation. We evaluated GER’s effects in C. elegans PD models and explored the conserved molecular mechanisms involved. In wild-type animals, GER increased survival under OS, confirming its antioxidant activity in vivo. To elucidate the underlying mechanisms, we used mutants in key stress-response pathways and found that SKN-1/NRF2 mediates GER’s protective effect. Given the connection between OS and PD, we assessed GER in a muscle-expressed α-syn model, where it improved locomotion and reduced protein aggregation. In a neuronal α-syn model, GER significantly preserved dopaminergic neuron morphology and function. Overall, our results show that GER exerts antioxidant, antiproteotoxic, and neuroprotective effects in C. elegans PD models, supporting its potential as a therapeutic candidate for neurodegenerative diseases.