AGGREGATION OF AMYLOID BETA-PROTEIN AND ITS NEUROTOXICITY - ENHANCEMENT BY ALUMINUM AND OTHER METALS

被引:39
作者
KURODA, Y
KAWAHARA, M
机构
[1] Department of Molecular & Cellular Neurobiology, Tokyo Metropolitan Institute for Neuroscience, Tokyo, Fuchu-shi
关键词
CULTURE; HIPPOCAMPUS; IRON; ZINC; CROSS-LINK;
D O I
10.1620/tjem.174.263
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The aggregation of amploid beta-protein has been suggested to enhance its neurotoxicity in cultured hippocampal neurons. We found that aluminum, an epidemiologic risk factor for Alzheimer's disease, promoted the aggregation of synthetic amyloid beta-protein (beta 1-40) using immunoblotting and centrifugation. There were no significant changes by Ca or Mg. Other metals including Zn, Fe caused the small degree of aggregation compared to Al. Furthermore, beta 1-40 which was aggregated by aluminum was applied on cultured rat hippocampal neurons, and the characteristic deposition of amyloid fibrils was observed on cultured neurons. These results suggested that the degeneration of neurons and the deposition of amyloid beta-protein were enhanced by aluminum.
引用
收藏
页码:263 / 268
页数:6
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