Previous studies have demonstrated a neuroprotective effect of vitamin B12. This study investigates these effects on paralysis induced by amyloid-beta in Caenorhabditis elegans (C. elegans) to determine an effective dose of vitamin B12. The transgenic strain CL4176, which expresses amyloid-beta upon a temperature shift, was used to model toxicity and subsequent paralysis. A paralysis assay was conducted over eight hours to evaluate time-to-paralysis in four experimental groups: control, and animals grown on plates supplemented with 75 nM, 150 nM, or 300 nM vitamin B12. Our results show that C. elegans expressing amyloid-beta exhibit an 80% reduction in motility compared to the wild-type strain CL802. However, motility was rescued in animals grown on plates containing vitamin B12, regardless of the concentration. Immunostaining confirmed amyloid-beta aggregation following the temperature upshift, although vitamin B12 treatment did not reduce aggregate size. This study builds on existing research by reaffirming vitamin B12's neuroprotective effects against amyloid-beta toxicity and highlighting the complexity of its mechanisms. These findings contribute to a deeper understanding of potential therapeutic interventions for amyloid-beta pathology.