| First Author | Lin CL | Year | 2009 |
| Journal | Neurobiol Aging | Volume | 30 |
| Issue | 1 | Pages | 81-92 |
| PubMed ID | 17590240 | Mgi Jnum | J:145820 |
| Mgi Id | MGI:3836115 | Doi | 10.1016/j.neurobiolaging.2007.05.012 |
| Citation | Lin CL, et al. (2009) Epigallocatechin gallate (EGCG) suppresses beta-amyloid-induced neurotoxicity through inhibiting c-Abl/FE65 nuclear translocation and GSK3 beta activation. Neurobiol Aging 30(1):81-92 |
| abstractText | Alzheimer's disease (AD) is the most common neurodegenerative disease and is caused by an accumulation of A beta plaque deposits in the brains. Evidence is increasing that green tea flavonoids can protect cells from A beta-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 A beta levels by enhancing endogenous APP nonamyloidogenic proteolytic processing. Furthermore, EGCG also decreased nuclear translocation of c-Abl and blocked APP-C99-dependent GSK3 beta 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. |
