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Lipoprotein-Based Nanoparticles Rescue the Memory Loss of Mice with Alzheimer's Disease by Accelerating the Clearance of Amyloid-Beta 期刊论文

编号：

33fa8196-aa09-4b43-8c57-4cd2ca346792
作者：

Song, Qingxiang^[1];Huang, Meng^[1];Yao, Lei^[1];Wang, Xiaolin^[1];Gu, Xiao^[1];Chen, Juan^[2,3];Chen, Jun(陈钧)^[4,5]Huang, Jialin^[1];Hu, Quanyin^[4,5];Kang, Ting^[4,5];Rong, Zhengxing^[1];Qi, Hong^[1];Zheng, Gang^[2,3];Chen, Hongzhuan^[1];Gao, Xiaoling^[1];
语种：

English
期刊：

ACS NANO ISSN：1936-0851 2014 年 8 卷 3 期 (2345 - 2359) ; MAR
收录：
关键词：

reconstituted high density lipoprotein nanomedicine amyloid beta apoliporpotein E clearance Alzheimer's disease
摘要：

Amyloid-beta (A beta) accumulation in the brain is believed to play a central role in Alzheimer's disease (AD) pathogenesis, and the common late-onset form of AD is characterized by an overall impairment in A beta clearance. Therefore, development of nanomedicine that can facilitate A beta clearance represents a promising strategy for AD intervention. However, previous work of this kind was concentrated at the molecular level, and the disease-modifying effectiveness of such nanomedicine has not been investigated in clinically relevant biological systems. Here, we hypothesized that a biologically inspired nanostructure, apolipoprotein E3-reconstituted high density lipoprotein (ApoE3-rHDL), which presents high binding affinity to A beta might serve as a novel nanomedicine for disease modification in AD by accelerating A beta clearance. Surface plasmon resonance, transmission electron microscopy, and co-immunoprecipitation analysis showed that ApoE3-rHDL demonstrated high binding affinity to both A beta monomer and oligomer. It also accelerated the microglial, astroglial, and liver cell degradation of A beta by facilitating the lysosomal transport. One hour after intravenous administration, about 0.4% ID/g of ApoE3-rHDL gained access to the brain. Four-week daily treatment with ApoE3-rHDL decreased A beta deposition, attenuated microgliosis, ameliorated neurologic changes, and rescued memory deficits in an AD animal model. The findings here provided the direct evidence of a biomimetic nanostructure crossing the blood brain barrier, capturing A beta and facilitating its degradation by glial cells, indicating that ApoE3-rHDL might serve as a novel nanomedicine for disease modification in AD by accelerating A beta clearance, which also justified the concept that nanostructures with A beta-binding affinity might provide a novel nanoplatform for AD therapy.
推荐引用方式
GB/T 7714：

Song Qingxiang,Huang Meng,Yao Lei, et al. Lipoprotein-Based Nanoparticles Rescue the Memory Loss of Mice with Alzheimer's Disease by Accelerating the Clearance of Amyloid-Beta [J].ACS NANO,2014,8(3):2345-2359.
APA：

Song Qingxiang,Huang Meng,Yao Lei,Wang Xiaolin,&Gao Xiaoling.(2014).Lipoprotein-Based Nanoparticles Rescue the Memory Loss of Mice with Alzheimer's Disease by Accelerating the Clearance of Amyloid-Beta .ACS NANO,8(3):2345-2359.
MLA：

Song Qingxiang, et al. "Lipoprotein-Based Nanoparticles Rescue the Memory Loss of Mice with Alzheimer's Disease by Accelerating the Clearance of Amyloid-Beta" .ACS NANO 8,3(2014):2345-2359.

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