Neurological diseases are a leading cause of death affecting a significant portion of the older population. ALS, the third-most common neurodegenerative disorder after Alzheimer’s and Parkinson’s, usually leads to complete paralysis within 2-3 years after diagnosis. Research shows little evidence and agreement in whether antioxidants, such as Vitamin E and C, can delay or suppress symptoms of neurodegeneration in ALS. My study aims to provide evidence that might answer that question, using HA3299 mutant C. elegans as a model. The HA3299 strain possesses a mutant SOD-1 gene that is a cause of inherited ALS. Exposure to 10 mM of Vitamin C and 200 µg/mL of Vitamin E in 40% ethanol was conducted in the first 24 hours after age-synchronization. The worms were transferred onto new NGM seeded plates with .1 µM glyphosate for another 96-hr exposure to induce oxidative stress and catalyze neurodegeneration. The locomotive speeds of C. elegans after both exposures are measured to indicate the nematode’s motor neuron health, with a 1 mm by 1mm grid backdrop under the microscope to measure distance traveled over a 30-second period. My data and relevant ANOVA statistical tests indicate that exposure to glyphosate significantly decreased the motor ability of mutant worms compared to N2 wildtype worms, suggesting that the HA3299 strain can be used as a model for ALS. Furthermore, pretreatment with vitamin C and vitamin E showed a significant improvement in locomotive speed of the mutant worms, implying that vitamin C and E might possess neuroprotective properties against ALS.