Epigallocatechin-3-gallate and curcumin suppress amyloid beta-induced beta-site APP cleaving enzyme-1 upregulation

Abstract

Beta-site APP cleaving enzyme-1 (BACE-1), is a rate-limiting enzyme for β amyloid production. Beta amyloid induces the production of radical oxygen species and neuronal injury. Oxidative stress plays a key role in various neurological diseases such as ischemia and Alzheimer's disease. Recent studies suggest that oxidative stress induces BACE-1 protein upregulation in neuronal cells. Here, we demonstrate that naturally occurring compounds (−)-epigallocatechin-3-gallate and curcumin suppress β amyloid-induced BACE-1 upregulation. Exposure of β amyloid 1–42 to neuronal culture increased BACE-1 protein levels. (−)-Epigallocatechin-3-gallate or curcumin significantly attenuated β amyloid-induced radical oxygen species production and β-sheet structure formation. These two compounds have novel pharmacological effects that may be beneficial for Alzheimer's disease treatment.