Neurotoxicity in Alzheimer's disease:: is covalently crosslinked Aβ responsible?

被引：14
作者：
Naylor, Ryan [1 ,2 ]
Hill, Andrew F. [2 ]
Barnham, Kevin J. [1 ]
机构：
[1] Univ Melbourne, Dept Pathol, Mol Sci & Biotechnol Inst Bio21, Parkville, Vic 3010, Australia
[2] Univ Melbourne, Dept Biochem & Mol Biol, Mol Sci & Biotechnol Inst Bio21, Parkville, Vic 3010, Australia
来源：
EUROPEAN BIOPHYSICS JOURNAL WITH BIOPHYSICS LETTERS | 2008年 / 37卷 / 03期
关键词：
Alzheimer; beta-amyloid; A beta; oligomer; covalent crosslinks; metal; neurotoxicity;
D O I：
10.1007/s00249-007-0243-2
中图分类号：
Q6 [生物物理学];
学科分类号：
071011 ;
摘要：
Alzheimer's disease is the most common form of dementia in the elderly, and is characterised by extracellular amyloid plaques composed of the beta-amyloid peptide (A beta). However, disease progression has been shown to correlate more closely with the level of soluble A beta oligomers. Recent evidence suggests that these oligomers are covalently crosslinked, possibly due to the interaction of A beta with redox-active metal ions. These findings offer new avenues for the treatment and prevention of disease, by modulating metal binding or preventing the formation of neurotoxic A beta oligomers.
引用
收藏
页码：265 / 268
页数：4
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