The effect of polyphenolic compounds for advanced glycation end products (AGEs) cause Alzheimer''s disease (AD) pathogenesis

• Main Authors: Sung-Fu Hung, 洪松甫
• Other Authors: Shun-Yao Ko
• Format: Others
• Language: zh-TW
• Published: 2012
• Online Access: http://ndltd.ncl.edu.tw/handle/43516161518572399306

碩士 === 長榮大學 === 醫學研究所 === 100 === The characteristic of Alzheimer’s disease (AD) is senile plaques in brain which is a neurodegenerative disease. Senile plaques are β-amyloid (Aβ) accumulation. The formation of Aβ which is amyloid precursor protein (APP) cleaved by β-secretase and γ-secretase. Advanced glycation end products (AGEs) are nonenzymatic glycation of proteins from Maillard reaction. Some reports have suggested that AGEs cause reactive oxygen species (ROS). AGEs increase APP expression and Aβ production via ROS. The combination of AGEs and Aβ has additional neurotoxicity. Resveratrol, epigallocatechin-3-gallate (EGCG) and curcuminoids are polyphenolic compounds, and it has been demostrated that polyphenolic compounds reduce Aβ and risk of AD pathogenesis. But the effection between APP metabolic pathway and polyphenolic compounds is unlear. In this study, we propose that resveratrol, EGCG and curcuminoids affect on APP processing pathway regulated by AGEs. The result show that AGEs increase the expression of beta-site APP-cleaving enzyme (BACE) and Presenilin 1 (PS1). More important, polyphenolic compounds would block the effection of AGEs. Therefore, we demonstrate that the development of AGEs causing AD pathogenesis would be decreased by polyphenolic compounds.