Although numerous studies have shown that cadmium disturbs the normal biological processes in central nervous system the mechanism of toxicity is not well understood The present study has investigated the effect of cadmium on oxidative stress Na+/K- ATPase activity and the aggregation of amyloid beta peptide(β-amyloid) in neuronal cell line. HT22 cell LC5 and LC50 of cadmium for HT22 cell resulted from MTT assay was 4 1 uM and 9 5 uM, respectively Cadmium (2 to 8 uM) dose-dependently increased the lipid peroxlidation and decreased the content of glutathione Cadmium 4 uM showed a significant decrease in Na- /K+ ATPase activity as compared with control group The dggregation of β-amyloid Was accelerated in a dose-dependent manner by the treatment with 2 to 8uM cadmium These results suggest that the neurotoxicity of cadmium can be mediated by the increase in oxidative stress and decrease in Na /K ¹ ATPase activity