a peptide binding to the β-site of app improves spatial memory and attenuates aβ burden in alzheimer’s disease transgenic mice肽绑定应用程序改善空间记忆和变弱的β-site aβ负担在阿尔茨海默病转基因老鼠.pdfVIP
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a peptide binding to the β-site of app improves spatial memory and attenuates aβ burden in alzheimer’s disease transgenic mice肽绑定应用程序改善空间记忆和变弱的β-site aβ负担在阿尔茨海默病转基因老鼠
A Peptide Binding to the b-Site of APP Improves Spatial
Memory and Attenuates Ab Burden in Alzheimer’s
Disease Transgenic Mice
1. 1,2. 1 1 1 1,3 1,3
Shi-gao Yang , Shao-wei Wang , Min Zhao , Ran Zhang , Wei-wei Zhou , Ya-nan Li , Ya-jing Su ,
1 2 1,2
He Zhang , Xiao-lin Yu *, Rui-tian Liu *
1Tsinghua University School of Medicine, Haidian District, Beijing, China, 2 National Key Laboratory of Biochemical Engineering, Institute of Process Engineering, Chinese
Academy of Sciences, Beijing, China, 3 School of Life Sciences, Ningxia University, Yinchuan, China
Abstract
Amyloid precursor protein cleaving enzyme 1 (BACE1), an aspartyl protease, initiates processing of the amyloid precursor
protein (APP) into b-amyloid (Ab); the peptide likely contributes to development of Alzheimer’s disease (AD). BACE1 is an
attractive therapeutic target for AD treatment, but it exhibits other physiological activities and has many other substrates
besides APP. Thus, inhibition of BACE1 function may cause adverse side effects. Here, we present a peptide, S1, isolated
from a peptide library that selectively inhibits BACE1 hydrolytic activity by binding to the b-proteolytic site on APP and Ab
N-terminal. The S1 peptide significantly reduced Ab levels in vitro and in vivo and inhibited Ab cytotoxicity in SH-SY5Y cells.
When applied to APPswe/PS1dE9 double transgenic mice by intracerebroventricular injection, S1 significantly improved the
spatial memory as determined by the Morris Water Maze, and also attenuated their Ab burden. These results indicate that
the dual-functional peptide S1 may have therapeutic potential for AD by both reducing Ab gen
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