VEGF-induced angiogenesis ameliorates the memory impairment in APP transgenic mouse model of Alzheimer's disease

被引:89
|
作者
Wang, Ping [1 ]
Xie, Zhao-Hong [1 ]
Guo, Yu-Ji [2 ]
Zhao, Cui-Ping [1 ]
Jiang, Hao [1 ]
Song, Yan [1 ]
Zhu, Zheng-Yu [1 ]
Lai, Chao [1 ]
Xu, Shun-Liang [1 ]
Bi, Jian-Zhong [1 ]
机构
[1] Shandong Univ, Hosp 2, Dept Neurol, Jinan 250033, Peoples R China
[2] Shandong Univ, Sch Med, Dept Histol & Embryol, Key Lab,Minist Educ Expt Teratol, Jinan 250012, Peoples R China
基金
中国国家自然科学基金;
关键词
Alzheimer disease; Vascular endothelial growth factor; Angiogenesis; Cerebral hypoperfusion; Cognitive impairment; ENDOTHELIAL GROWTH-FACTOR; BRAIN; NEUROGENESIS; MECHANISMS; MICE;
D O I
10.1016/j.bbrc.2011.07.003
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Vascular endothelial growth factor (VEGF) was investigated in the present study to see whether it could provide a therapeutic opportunity for the treatment of Alzheimer's disease (AD). PDGF-hAPP(v7171) transgenic mice were treated with VEGF or PBS by intraperitoneal injection for three consecutive days. The results showed that VEGF ameliorated the memory impairment of mice, accompanied by CD34(+) cells increasing in peripheral blood, vWF(+) vessels increasing in hippocampus, and CD34(+)/VEGFR2(+), vWF(+)/VEG-FR2(+) and BrdU(+)/vWF(+). cells expressing in hippocampus. Furthermore, the level of choline acetyltransferase (ChAT) was considerably enhanced and AB deposition was decreased in the brains of mice upon VEGF treatment. These observations suggest that VEGF should be pursued as a novel therapeutic agent for treatment of AD. (C) 2011 Elsevier Inc. All rights reserved.
引用
收藏
页码:620 / 626
页数:7
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