Intranasal TAT-haFGF Improves Cognition and Amyloid-β Pathology in an AβPP/PS1 Mouse Model of Alzheimer's Disease

被引：8
|
作者：
Lou, Guofeng [1 ,2 ]
Zhang, Qihao [1 ,2 ]
Xiao, Fei [3 ]
Xiang, Qi [1 ,2 ]
Su, Zhijian [1 ,2 ]
Huang, Yadong [1 ,2 ]
机构：
[1] Jinan Univ, Inst Biomed, 601 Huangpu Ave, Guangzhou 510632, Guangdong, Peoples R China
[2] Jinan Univ, Dept Cell Biol, 601 Huangpu Ave, Guangzhou 510632, Guangdong, Peoples R China
[3] Jinan Univ, Dept Pharmacol, Guangzhou 510632, Guangdong, Peoples R China
来源：
JOURNAL OF ALZHEIMERS DISEASE | 2016年 / 51卷 / 04期
关键词：
A beta PP/PS1; Alzheimer's disease; haFGF; intranasal administration; TAT; CENTRAL-NERVOUS-SYSTEM; FOCAL CEREBRAL-ISCHEMIA; MEDIATED DELIVERY; MICE; FGF; NEURODEGENERATION; MECHANISMS; PROTEINS; GDNF;
D O I：
10.3233/JAD-151121
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
Neurotoxic amyloid-beta (A beta) peptide causing cognitive function disabilities is one of the most characteristic pathological features in Alzheimer's disease (AD). A novel fusion protein, TAT-haFGF, was administrated to A beta PP/PS1 transgenic mice by intravenous (IV) injection and intranasal (IN) delivery, respectively, for 5 weeks to compare the pharmacodynamics between the two routes of administration. Our results showed that IN administration of TAT-haFGF improved cognition and reduced A beta plaques more significantly in A beta PP/PS1 mice, when compared with IV injection. Our new findings suggest that TAT-haFGF might be a promising new therapy to attenuate AD pathological process.
引用
收藏
页码：985 / 990
页数：6
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