文献类型：期刊文献

英文题名：Copper Enhances Amyloid-beta Peptide Neurotoxicity and non beta-Aggregation: A Series of Experiments Conducted upon Copper-Bound and Copper-Free Amyloid-beta Peptide

作者：Dai, Xueling[1,2];Sun, Yaxuan[2];Gao, Zhaolan[2];Jiang, Zhaofeng[1,2]

第一作者：戴雪伶

通讯作者：Jiang, ZF[1]

机构：[1]Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing 100191, Peoples R China;[2]Beijing Union Univ, Dept Biol, Coll Appl Sci & Humanities, Beijing 100191, Peoples R China

第一机构：北京联合大学应用文理学院|北京联合大学生物化学工程学院

通讯机构：[1]corresponding author), Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing 100191, Peoples R China.|[114172]北京联合大学应用文理学院;[11417]北京联合大学;[1141726]北京联合大学生物化学工程学院;

年份：2010

卷号：41

期号：1

起止页码：66-73

外文期刊名：JOURNAL OF MOLECULAR NEUROSCIENCE

收录：;Scopus(收录号：2-s2.0-77950189704);WOS:【SCI-EXPANDED(收录号:WOS:000275905400009)】；

基金：This work was supported by grants from the Key Program of the Beijing Natural Science Foundation (Project No: KZ200311417015) and the Funding Project for Academic Human Resources Development in Institutions of Higher Learning Under the Jurisdiction of Beijing Municipality, PHR(IHLB) [PHR20090513].

语种：英文

外文关键词：Alzheimer's disease; Amyloid-beta peptide; beta aggregation; Neurotoxicity

摘要：Alzheimer's disease is characterized by the abnormal aggregation of amyloid-beta peptide (A beta) in extracellular deposits known as senile plaques. However, the nature of the toxic A beta species and its precise mechanism of action remain unclear. Previous reports suggest that the histidine residues are involved in copper-A beta interaction, by which resulting in the neurotoxicity of A beta and free radical damage. Here, we employed a mutant A beta (A beta H13R) in which a histidine residue was replaced by arginine. Copper facilitated the precipitation of both wild-type and mutant A beta in the spectrophotometric absorbance assay but suppressed beta-structure aggregates according to Thioflavine-T assay. Wild-type A beta alone is more cytotoxic but produced less amount of H2O2 than A beta H13R-copper complexes, suggesting that A beta-membrane interaction may also implicated in the pathologic progress. A beta toxicity is in positive correlation to its competence to aggregate despite the aggregation is mainly composed of non-beta fibril substances. In short, these findings may provide further evidence on the role of copper in the pathogenesis of Alzheimer's disease.