Self-Assembly Molecular Chaperone to Concurrently Inhibit the Production and Aggregation of Amyloid β Peptide Associated with Alzheimer's Disease
Self-Assembly Molecular Chaperone to Concurrently Inhibit the Production and Aggregation of Amyloid β Peptide Associated with Alzheimer's Disease
复制标题
自组装分子伴侣同时抑制与阿尔茨海默氏病相关的淀粉样β肽的产生和聚集
DOI：
10.1021/acsmacrolett.8b00495
复制
发表时间：
2018-08-01
影响因子：
7.015
通讯作者：
Shi, Linqi
中科院分区：
文献类型：
--
作者：
Huang, Fan;Qu, Aoting;Shi, Linqi
Amyloid beta peptide (A beta) plays a crucial role in the pathogenesis of Alzheimer's disease (AD). Currently, decreasing A beta production and preventing A beta aggregation are thought to be important strategies in anti-AD therapy. However, inhibiting A beta production or aggregation in isolation is not sufficient to reverse the neurodegenerative process of AD patients in clinical testing. Here, a self-assembly molecular chaperone (SAMC) consisting of gamma-secretase inhibitor DAPT and mixed-shell polymeric micelles is devised, serving as a bifunctional suppressor of AD. This two-in-one combinational system can simultaneously inhibit A beta production and aggregation, which would contribute to enhancing the therapeutic effect by decreasing A beta levels. Decorating a neuron-specific RVG29 peptide onto the surface, the DAPT-incorporated SAMC can specifically target neuronal cells and, thus, will relieve the strong side effect of DAPT on normal cells. Therefore, this combination strategy holds great potential to open up an avenue for AD treatment.
