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Selenomethionine Protects Mutant Tau N27A Cell from Oxidative Stress and Decreases Phosphorylation of Tau

Alzheimer’s Disease (AD) is neurodegenerative disease characterized by loss of cells and aggregated tau in the hippocampus. Hyperphosphorylated tau causes the misfolding of tau proteins (aggregated tau), which are responsible for proper neuronal activity. Selenium-methionine has been known to decrease the amount of phosphorylated tau within mutant and wild type 3xTg- AD mice. However, selenium can be toxic to cell depending on the type of cells and the concentration of selenium. The purpose of this study is to determine the effect selenium-methionine has on decreasing hyperphosphorylation of tau, protecting cells from oxidative stress, and decreasing the amount of aggregated tau in N27a cell cultures. After treating N27a mutant tau and wild type cell cultures with different concentrations of selenium-methionine and hydrogen peroxide, we found selenium- methionine decreases the amount of phosphorylated tau for mutant tau cell at 20uM, protect mutant tau cells at 20uM and WT tau cells at 10uM and 20uM from oxidative stress, and that it is toxic to cells at 80uM concentration. We conclude that Set-Met could be preventing further phosphorylation to continue and protecting cells from oxidative stress, but are not destroying aggregated tau.