LRP1型
载脂蛋白E
淀粉样前体蛋白
早老素
糖基化
血脑屏障
下调和上调
愤怒(情绪)
基因剔除小鼠
阿尔茨海默病
老年斑
脑淀粉样血管病
化学
低密度脂蛋白受体
受体
医学
脂蛋白
内分泌学
疾病
内科学
基因
生物
神经科学
胆固醇
生物化学
痴呆
中枢神经系统
作者
Wei Wei,Hang Sun,Bingwei Yang,Chengyu Zhu,Erqun Song,Yang Song
标识
DOI:10.1021/acs.chemrestox.3c00378
摘要
The increasing nanoparticle (NP) applications in the biomedical field have become an emerging concern regarding human health. NP exposure may play a role in the accelerating Alzheimer's disease (AD) progression; however, the etiology of this disorder is complex and remains largely unclear. Here, we identified that intravenous injection of silica NPs (SiNPs) caused the blood–brain barrier breakdown via downregulating tight junction-related gene expressions. Meanwhile, SiNPs upregulate the transport receptor for advanced glycation end products (RAGE) that govern the β-amyloid (Aβ) influx to the brain; however, low-density lipoprotein receptor-related protein 1 (LRP1) that controls the efflux of Aβ from the brain was not affected. Consequently, an increase in Aβ burden in the brain of SiNP-challenged APP/PS1 mice was found. Intriguingly, plasma apolipoprotein E (ApoE) adsorbed on the surface of SiNPs partially relieves this effect. Using ApoE knockout (ApoE–/–) mice, we confirmed that SiNPs covered with serum without ApoE showed further elevated AD symptoms. Together, this study offered a compilation of data to support the potential risk factors of NP exposure and AD pathology.
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