Ph.D. Univ. of California, San Diego
Amyloid-beta (Abeta) is known to induce apoptotic cell death and its underlying mechanism has been studied extensively, but the endogenous protection mechanism that results from Abeta insult is less known. In this study, we have found that Abeta(1-42) produced a dose-dependent decrease in cell viability and dose-dependent increase in apoptotic cell death in PC12 cells. Meanwhile, Abeta(1-42) (0.1 muM) increased the phosphorylation of serum- and glucocorticoid-inducible kinase1 (SGK1) at Ser-78 specifically.