首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >Increased amyloid beta-peptide deposition in cerebral cortex as a consequence of apolipoprotein E genotype in late-onset Alzheimer disease.
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Increased amyloid beta-peptide deposition in cerebral cortex as a consequence of apolipoprotein E genotype in late-onset Alzheimer disease.

机译:迟发性阿尔茨海默病中载脂蛋白E基因型导致大脑皮质淀粉样蛋白β肽沉积增加。

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摘要

Amyloid beta-peptide (A beta) deposition in senile plaques and cerebral vessels is a neuropathological feature of Alzheimer disease (AD). We examined the possibility that commonly observed variability in A beta deposition in late-onset AD might be related to apolipoprotein E genotype (APOE gene; the two most common alleles are 3 and 4), since APOE4 is a susceptibility gene for late-onset AD and apolipoprotein E interacts strongly with A beta in vitro. In an autopsy series of brains of late-onset AD patients, we found a strong association of APOE4 allele with increased vascular and plaque A beta deposits. Late-onset AD patients with one or two APOE4 alleles have a distinct neuropathological phenotype compared with patients homozygous for APOE3.
机译:老年斑和脑血管中的淀粉样β肽(A beta)沉积是阿尔茨海默病(AD)的神经病理特征。我们检查了以下可能性:由于APOE4是迟发性AD的易感基因,因此通常观察到的迟发性AD中Aβ沉积的变异性可能与载脂蛋白E基因型(APOE基因;两个最常见的等位基因为3和4)有关。载脂蛋白E在体外与A beta强烈相互作用。在一系列迟发性AD患者的大脑解剖中,我们发现APOE4等位基因与增加的血管和斑块Aβ沉积密切相关。与纯合子APOE3的患者相比,具有一或两个APOE4等位基因的晚期AD患者具有明显的神经病理学表型。

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