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:
Alzheimer’s disease; AβPP/PS1; TAT; haFGF; intranasal administration.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Administration, Intranasal
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Alzheimer Disease / complications*
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Alzheimer Disease / genetics
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Amyloid beta-Protein Precursor / genetics
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Animals
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Brain / drug effects
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Brain / metabolism
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Brain / pathology
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Cognition Disorders / drug therapy*
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Cognition Disorders / etiology*
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Disease Models, Animal
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Fibroblast Growth Factors / administration & dosage*
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Gene Products, tat / administration & dosage
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Humans
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Injections, Intraventricular
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Maze Learning / drug effects
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Mice
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Mice, Inbred C57BL
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Mice, Transgenic
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Movement / drug effects
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Mutation / genetics
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Peptide Fragments / administration & dosage
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Plaque, Amyloid / drug therapy*
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Plaque, Amyloid / etiology
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Presenilin-1 / genetics
Substances
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Amyloid beta-Protein Precursor
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Gene Products, tat
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PSEN1 protein, human
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Peptide Fragments
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Presenilin-1
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Fibroblast Growth Factors