%0 Journal Article %J J Alzheimers Dis %D 2016 %T Intranasal TAT-haFGF Improves Cognition and Amyloid-β Pathology in an AβPP/PS1 Mouse Model of Alzheimer's Disease. %A Lou, Guofeng %A Zhang, Qihao %A Xiao, Fei %A Xiang, Qi %A Su, Zhijian %A Huang, Yadong %K Administration, Intranasal %K Alzheimer Disease %K Amyloid beta-Protein Precursor %K Animals %K Brain %K Cognition Disorders %K Disease Models, Animal %K Fibroblast Growth Factors %K Gene Products, tat %K Humans %K Injections, Intraventricular %K Maze Learning %K Mice %K Mice, Inbred C57BL %K Mice, Transgenic %K Movement %K Mutation %K Peptide Fragments %K Plaque, Amyloid %K Presenilin-1 %X

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.

%B J Alzheimers Dis %V 51 %P 985-90 %8 2016 %G eng %N 4 %1 http://www.ncbi.nlm.nih.gov/pubmed/26890786?dopt=Abstract %R 10.3233/JAD-151121