Co-localization of cholesterol, apolipoprotein E and fibrillar Aβ in amyloid plaques

被引:109
作者
Burns, MP
Noble, WJ
Olm, V
Gaynor, K
Casey, E
LaFrancois, J
Wang, L
Duff', K
机构
[1] Nathan S Kline Inst Psychiat Res, Ctr Dementia Res, Orangeburg, NY 10962 USA
[2] NYU, Dept Psychiat, New York, NY 10016 USA
来源
MOLECULAR BRAIN RESEARCH | 2003年 / 110卷 / 01期
基金
美国国家卫生研究院;
关键词
apolipoprotein E; cholesterol; fibrillar plaque; Alzheimer's disease;
D O I
10.1016/S0169-328X(02)00647-2
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Recent evidence strongly suggests a role for cholesterol and apolipoprotein E in the etiology of Alzheimer's disease. We have demonstrated the co-localization of cholesterol and apolipoprotein E with P-amyloid immunoreactivity and thioflavin S immunofluorescence in AD type plaques of a transgenic mouse model. Cholesterol and apolipoprotein E co-localized to the core of thioflavin S-positive (fibrillar) plaques, but not thioflavin S-negative (diffuse) plaques from an early age. By 18 months of age, there was extensive coverage of fibrillar plaques immunopositive for apolipoprotein E and cholesterol oxidase. These findings support evidence that cholesterol and apolipoprotein E are involved in fibrillar plaque formation or maintenance, and suggest that cholesterol may impact amyloid formation extracellularly, as well as through an intracellular effect. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:119 / 125
页数:7
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