Long-xuan LI2,Jia-pei DAI3,Li-qiang RU4,Guang-fu YIN4,Bin ZHAO Department of Neurology,Affiliated Hospital,Guangdong Medical College,Zhanjiang 524001,China; 3The Netherlands Institute for Brain Research,Amsterdam 1105AZ,the Netherlands; 4Department of Neurobiology,TongjiMedical College of Huazhong Universityof Science and Technology,Wuhan 430030,China
基金项目:
Project supported by the National Natural Science Foundation of China, No 30171082.
摘 要:
INTRODUCTION Alzheimer’s disease (AD) is characterized by neu-ronal loss and extracellular senile plaque, whose majorconstituentis amyloid β-peptide(Aβ), a 39-43 amino acidspeptide derived from amyloid precursor protein (APP).It is widely believed that the cellular actions of Aβ areresponsible for the neuronal cell loss observed in ADand play a causal role in the pathogenesis of AD[1,2].Aggregated Aβ and its activefragmentshave beenshownto have clear neurotoxic effect[3]. …