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

Article type: Short Communication

Authors: Lou, Guofeng^a | Zhang, Qihao^a | Xiao, Fei^b | Xiang, Qi^a | Su, Zhijian^a | Huang, Yadong^{a; *}

Affiliations: [a] Institute of Biomedicine & Department of Cell Biology, Jinan University, Guangzhou, China | [b] Department of Pharmacology, Jinan University, Guangzhou, China

Correspondence: [*] Correspondence to: Yadong Huang, Institute of Biomedicine & Department of Cell Biology, Jinan University, No. 601, Huangpu Ave., Tianhe District, Guangzhou 510632, China. Tel.: +86 20 85222600; Fax: +86 20 85221865 808; E-mail: tydhuang@jnu.edu.cn.

Abstract: Neurotoxic amyloid-β (Aβ) 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 AβPP/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 Aβ plaques more significantly in AβPP/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.

Keywords: AβPP/PS1, Alzheimer’s disease, haFGF, intranasal administration, TAT

DOI: 10.3233/JAD-151121

Journal: Journal of Alzheimer's Disease, vol. 51, no. 4, pp. 985-990, 2016