Co-localization of cholesterol, apolipoprotein E and fibrillar Aβ in amyloid plaques
Co-localization of cholesterol, apolipoprotein E and fibrillar Aβ in amyloid plaques
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DOI：
10.1016/s0169-328x(02)00647-2
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发表时间：
2003-01-31
期刊：
影响因子：
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通讯作者：
Duff', K
中科院分区：
文献类型：
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作者：
Burns, MP;Noble, WJ;Duff', K
最近的证据有力地表明胆固醇和载脂蛋白E在阿尔茨海默病的病因学中的作用。我们已经证明了胆固醇和载脂蛋白E与p -淀粉样蛋白免疫反应性和硫黄素S免疫荧光在AD型斑块转基因小鼠模型中的共定位。胆固醇和载脂蛋白E共同定位于硫黄素s阳性（纤维状）斑块的核心，而不是早期的硫黄素s阴性（弥漫性）斑块。到18个月大时，广泛覆盖载脂蛋白E和胆固醇氧化酶免疫阳性的纤维斑块。这些发现支持了胆固醇和载脂蛋白E参与纤维斑块形成或维持的证据，并表明胆固醇可能影响淀粉样蛋白在细胞外的形成，以及通过细胞内的作用。(C) 2002 Elsevier Science B.V.版权所有
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.