INCREASED AMYLOID BETA-PEPTIDE DEPOSITION IN CEREBRAL-CORTEX AS A CONSEQUENCE OF APOLIPOPROTEIN-E GENOTYPE IN LATE-ONSET ALZHEIMER-DISEASE
INCREASED AMYLOID BETA-PEPTIDE DEPOSITION IN CEREBRAL-CORTEX AS A CONSEQUENCE OF APOLIPOPROTEIN-E GENOTYPE IN LATE-ONSET ALZHEIMER-DISEASE
复制标题
DOI：
10.1073/pnas.90.20.9649
复制
发表时间：
1993-10-15
影响因子：
11.1
通讯作者：
ROSES, AD
中科院分区：
文献类型：
--
作者：
SCHMECHEL, DE;SAUNDERS, AM;ROSES, AD
淀粉样β肽（Abeta）沉积在老年斑和脑血管是阿尔茨海默病（AD）的神经病理特征。由于APOE4是迟发性AD的易感基因，且载脂蛋白E在体外与Abeta有强烈的相互作用，我们研究了在迟发性AD中普遍观察到的Abeta沉积变异性可能与载脂蛋白E基因型（APOE基因；最常见的两个等位基因是3和4）有关。在对迟发性阿尔茨海默病患者大脑的一系列尸检中，我们发现APOE4等位基因与血管和斑块β沉积增加有很强的关联。与APOE3纯合子的患者相比，携带一个或两个APOE4等位基因的晚发性AD患者具有明显的神经病理表型。
Amyloid beta-peptide (Abeta) deposition in senile plaques and cerebral vessels is a neuropathological feature of Alzheimer disease (AD). We examined the possibility that commonly observed variability in Abeta 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 Abeta 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 Abeta deposits. Late-onset AD patients with one or two APOE4 alleles have a distinct neuropathological phenotype compared with patients homozygous for APOE3.