Intranasal TAT-haFGF Improves Cognition and Amyloid-β Pathology in an AβPP/PS1 Mouse Model of Alzheimer's Disease
Intranasal TAT-haFGF Improves Cognition and Amyloid-β Pathology in an AβPP/PS1 Mouse Model of Alzheimer's Disease
复制标题
鼻内 TAT-haFGF 改善阿尔茨海默病 A beta PP/PS1 小鼠模型的认知和淀粉样蛋白病理学
DOI：
10.3233/jad-151121
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发表时间：
2016-01-01
影响因子：
4
通讯作者：
Huang, Yadong
中科院分区：
文献类型：
--
作者：
Lou, Guofeng;Zhang, Qihao;Huang, Yadong
神经毒性淀粉样β肽（A β）引起的认知功能障碍是阿尔茨海默病（AD）最具特征性的病理特征之一。将一种新型融合蛋白TAT-haFGF分别通过静脉内（IV）注射和鼻内（IN）递送给予A β PP/PS1转基因小鼠5周，以比较两种给药途径之间的药效学。我们的结果表明，与IV注射相比，IN给予TAT-haFGF在A β PP/PS1小鼠中更显著地改善了认知并减少了A β斑块。我们的新发现表明TAT-haFGF可能是一种有希望的减轻AD病理过程的新疗法。
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.