title: Intranasal TAT-haFGF Improves Cognition and Amyloid-β Pathology in an AβPP/PS1 Mouse Model of Alzheimer's Disease.
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.
authors.affiliation: Institute of Biomedicine & Department of Cell Biology, Jinan University, Guangzhou, China.
authors.forename: Guofeng
authors.initials: G
authors.lastname: Lou
authors.affiliation: Institute of Biomedicine & Department of Cell Biology, Jinan University, Guangzhou, China.
authors.forename: Qihao
authors.initials: Q
authors.lastname: Zhang
authors.affiliation: Department of Pharmacology, Jinan University, Guangzhou, China.
authors.forename: Fei
authors.initials: F
authors.lastname: Xiao
authors.affiliation: Institute of Biomedicine & Department of Cell Biology, Jinan University, Guangzhou, China.
authors.forename: Qi
authors.initials: Q
authors.lastname: Xiang
authors.affiliation: Institute of Biomedicine & Department of Cell Biology, Jinan University, Guangzhou, China.
authors.forename: Zhijian
authors.initials: Z
authors.lastname: Su
authors.affiliation: Institute of Biomedicine & Department of Cell Biology, Jinan University, Guangzhou, China.
authors.forename: Yadong
authors.initials: Y
authors.lastname: Huang
mesh_terms: D000281:Administration, Intranasal; D000544:Alzheimer Disease / Q000150:complications* / Q000235:genetics; D016564:Amyloid beta-Protein Precursor / Q000235:genetics; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D003072:Cognition Disorders / Q000188:drug therapy* / Q000209:etiology*; D004195:Disease Models, Animal; D005346:Fibroblast Growth Factors / Q000008:administration & dosage*; D015696:Gene Products, tat / Q000008:administration & dosage; D006801:Humans; D007276:Injections, Intraventricular; D018782:Maze Learning / Q000187:drug effects; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009068:Movement / Q000187:drug effects; D009154:Mutation / Q000235:genetics; D010446:Peptide Fragments / Q000008:administration & dosage; D058225:Plaque, Amyloid / Q000188:drug therapy* / Q000209:etiology; D053764:Presenilin-1 / Q000235:genetics
chemical_list: D016564:Amyloid beta-Protein Precursor; D015696:Gene Products, tat; C508853:PSEN1 protein, human; D010446:Peptide Fragments; D053764:Presenilin-1; D005346:Fibroblast Growth Factors
keywords: Alzheimer’s disease; AβPP/PS1; TAT; haFGF; intranasal administration