| Title | Intranasal TAT-haFGF Improves Cognition and Amyloid-β Pathology in an AβPP/PS1 Mouse Model of Alzheimer's Disease. |
| Publication Type | Journal Article |
| Year of Publication | 2016 |
| Authors | Lou, G, Zhang, Q, Xiao, F, Xiang, Q, Su, Z, Huang, Y |
| Journal | J Alzheimers Dis |
| Volume | 51 |
| Issue | 4 |
| Pagination | 985-90 |
| Date Published | 2016 |
| ISSN | 1875-8908 |
| Keywords | Administration, Intranasal, Alzheimer Disease, Amyloid beta-Protein Precursor, Animals, Brain, Cognition Disorders, Disease Models, Animal, Fibroblast Growth Factors, Gene Products, tat, Humans, Injections, Intraventricular, Maze Learning, Mice, Mice, Inbred C57BL, Mice, Transgenic, Movement, Mutation, Peptide Fragments, Plaque, Amyloid, Presenilin-1 |
| 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. |
| DOI | 10.3233/JAD-151121 |
| Alternate Journal | J. Alzheimers Dis. |
| PubMed ID | 26890786 |
