beta-amyloid is different in normal aging and in Alzheimer disease.
beta-amyloid is different in normal aging and in Alzheimer disease.
复制标题
β-淀粉样蛋白在正常衰老和阿尔茨海默病中是不同的。
DOI：
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发表时间：
2005
影响因子：
4.8
通讯作者：
M. Tabaton
中科院分区：
文献类型：
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作者：
A. Piccini;C. Russo;A. Gliozzi;A. Relini;A. Vitali;R. Borghi;L. Giliberto;A. Armirotti;C. D'Arrigo;A. Bachi;A. Cattaneo;C. Canale;S. Torrassa;T. Saido;W. Markesbery;P. Gambetti;M. Tabaton
阿尔茨海默病中β -淀粉样蛋白引起神经退行性变的机制存在争议。神经元毒性主要由不同种类的可溶性β -淀粉样蛋白低聚物发挥作用，这些低聚物的N端和c端结构域不同。然而，在没有明显神经元功能障碍的情况下，认知正常的老年人大脑中也会出现大量的β -淀粉样蛋白积累。我们假设神经元毒性取决于可溶β -淀粉样蛋白低聚物的分子组成，而不是数量。在这里，我们表明，在阿尔茨海默病中积累的可溶性β -淀粉样蛋白聚集体在组成、聚集和毒性特性方面与正常衰老的聚集体不同。
The mechanism of neurodegeneration caused by beta-amyloid in Alzheimer disease is controversial. Neuronal toxicity is exerted mostly by various species of soluble beta-amyloid oligomers that differ in their N- and C-terminal domains. However, abundant accumulation of beta-amyloid also occurs in the brains of cognitively normal elderly people, in the absence of obvious neuronal dysfunction. We postulated that neuronal toxicity depends on the molecular composition, rather than the amount, of the soluble beta-amyloid oligomers. Here we show that soluble beta-amyloid aggregates that accumulate in Alzheimer disease are different from those of normal aging in regard to the composition as well as the aggregation and toxicity properties.