AD and β- 淀粉样蛋白的代谢与调控.pdf

19 4 Vol. 19, No. 4 2007 8 Chinese Bulletin of Life Sciences Aug., 2007 1004-0374(2007)04-0409-08 β- (201203) β- (A β) β- A β A βA βA β A β ; β- ; R749.1 Q513.2 A Metabolism and regulation of β-amyloid: a potential target for Alzheimer therapy YAN Han, TANG Xican* (State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 201203, China) Abstract: Being the main component of senile plaques in Alzheimer’s disease (AD), β-amyloid protein (Aβ) is derived from amyloid precursor protein via β-secretase-mediated pathway. The neurotoxicity of Aβ has been proven by abundant studies, which can be intensified by aggregation. There is a homeostasis of A β production and clearance in the physiological state. Genetic mutation and environment can interrupt this balance and lead to assembly and deposition of Aβ, in turn cause or accelerate the progress of AD, via oxidative stress, apoptosis, inflammation, etc. In this paper, the formation, clearance and neurotoxicity of Aβ as well as its possible role in AD are reviewed. Key words: Alzheimer’s disease; β-amyloid; neurotoxicity (Alzheimer’s disease, AD) Alzheimer AD AD 65 AD AD 1% 5%85 AD AD 20% 40%[1]1907 Alois 2007-03-08 2007-03-18 ( 1 9 8 0 ) ( 1 9 3 2 ) * E-mail xctang@ 410 19 AD α (tumor necrosis factor-α convertase, TACE, (senile plaques) ADAM17)