Institute of Medicine, Chung Shan Medical University

Chih-Li Lin (林志立), Assistant Professor

The overexpression of APP-C99 isignificantly increased the c-Abl expression in the nuclei at 72 h. 4,6-Diamidino-2-phenylindole stained nuclei are detected in the

images on the right. It was also shown that EGCG treatment inhibits the nuclear translocation of c-Abl when APP-C99 is overexpressed in MC65 cells.

Arrows indicated the c-Abl nuclear translocation of MC65 cells.

Laboratory of Neuroscience

     Alzheimer's disease (AD) is a progressive neurodegenerative disorder. It’s pathological characteristics are the presence of senile plaques and neurofibrillary tangles (NFTs) in the brain. It is well known that NFTs-induced cortical neurons loss is the major pathological findings of AD. Although this amyloid cascade hypothesis indicating the deposit of the dysregulated Aβ forms the plaque core and subsequently induces tau aggregation, the underlying mechanism of this hypothesis is still not fully understood. Our lab demonstrated that treatment with EGCG enhanced tau proteolytic degradation by reduced its hyperphosphorylation. Furthermore, we also found EGCG decreased hyperphosphorylation of tau by blocking APP-C99-dependent GSK3β activation, and these inhibitory effects may be occurred through the interruption of c-Abl/Fe65 interaction.

 

 

Institute of Medicine, College of Medicine,

Chung Shan Medical University.

No. 110,  Sec. 1, Chien-Kuo N. Road,

Taichung, Taiwan 402

Contact with us

 

 

Tel: +886-4-2473-0022 ext. 11607

Fax: +886-4-2472-3229

Email: dll@csmu.edu.tw