Green Tea Research Today is a free monthly online journal that collates and summarizes the latest research about Green Tea, including details on benefits, antioxidants, weight loss, diet, side effects.

Epigallocatechin gallate (EGCG) suppresses beta-amyloid-induced neurotoxicity through inhibiting c-Abl/FE65 nuclear translocation and GSK3beta activation.

Lin CL, Chen TF, Chiu MJ, Way TD, Lin JK

Institute of Biochemistry and Molecular Biology, College of Medicine, National Taiwan University, Taipei, Taiwan.

Alzheimer's disease (AD) is the most common neurodegenerative disease and is caused by an accumulation of Abeta plaque deposits in the brains. Evidence is increasing that green tea flavonoids can protect cells from Abeta-mediated neurotoxicity. However, the underlying mechanism remains unclear. Here, we used a human neuronal cell line MC65 conditional expression of an amyloid precursor protein fragment (APP-C99) to investigate the protection mechanism of epigallocatechin gallate (EGCG), the main constituent of green tea. We demonstrated that treatment with EGCG reduced the Abeta levels by enhancing endogenous APP nonamyloidogenic proteolytic processing. Furthermore, EGCG also decreased nuclear translocation of c-Abl and blocked APP-C99-dependent GSK3beta activation, and these inhibitory effects occurred through the interruption of c-Abl/Fe65 interaction. Our results indicated that the neuroprotective action of EGCG may take place through some mechanisms other than the promotion of APP nonamyloidogenic proteolysis, as was reported previously.

Published 25 June 2007 in Neurobiol Aging.
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