Journal article
Tat-haFGF14–154 Upregulates ADAM10 to Attenuate the Alzheimer Phenotype of APP/PS1 Mice through the PI3K-CREB-IRE1α/XBP1 Pathway
T Meng, Q Cao, P Lei, AI Bush, Q Xiang, Z Su, X He, JT Rogers, IM Chiu, Q Zhang, Y Huang
Molecular Therapy Nucleic Acids | CELL PRESS | Published : 2017
Abstract
Acid fibroblast growth factor (aFGF) has shown neuroprotection in Alzheimer's disease (AD) models in previous studies, yet its mechanism is still uncertain. Here we report that the efficacy of Tat-haFGF14–154 is markedly increased when loaded cationic liposomes for intranasal delivery are intranasally administered to APP/PS1 mice. Our results demonstrated that liposomal Tat-haFGF14–154 treatment significantly ameliorated behavioral deficits, relieved brain Aβ burden, and increased the expression and activity of disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) in the brain. Tat-haFGF14–154 antagonized Aβ1–42-induced cell death and structural damage in rat primary neuron..
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Awarded by National Natural Science Foundation of China
Funding Acknowledgements
This work was supported by grants from the National Key New Drug Creation of China (2012ZX09103301-034), the National Natural Science Foundation of China (81373313), the Science & Technology Major/Planning Project of Guangdong Province (2012A080201010 and 2013B051000063), the Natural Science Foundation of Guangdong Province (2015A030311010), and the Science & Technology Plan Project of Guangzhou (201508020001).