Abstract
Phenotypic knockout of nerve growth factor (NGF) activity in transgenic anti-NGF mice (AD11 mice) results in a progressive neurodegenerative phenotype resembling Alzheimer's disease. In this article, we examine whether and how the progressive neurodegenerative phenotype of AD11 mice could be prevented or ameliorated by pharmacological treatments with NGF or the cholinergic agonist galantamine, at a relatively early phase of Alzheimer's disease-like neurodegeneration. We demonstrate that the neurodegeneration induced by the expression of anti-NGF antibodies in AD11 mice can be largely reversed by NGF delivery through an olfactory route.
MeSH terms
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Alzheimer Disease / etiology
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Amyloid beta-Peptides / metabolism
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Amyloid beta-Protein Precursor / metabolism
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Animals
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Antibodies / genetics
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Choline O-Acetyltransferase / metabolism
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Cholinergic Agonists / pharmacology*
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Disease Models, Animal
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Entorhinal Cortex / drug effects
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Entorhinal Cortex / metabolism
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Entorhinal Cortex / pathology
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Galantamine / pharmacology*
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Humans
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Mice
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Mice, Knockout
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Mice, Transgenic
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Nerve Degeneration / drug therapy
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Nerve Degeneration / etiology
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Nerve Degeneration / pathology
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Nerve Degeneration / prevention & control*
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Nerve Growth Factor / antagonists & inhibitors*
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Nerve Growth Factor / immunology
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Nerve Growth Factor / pharmacology*
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Nerve Growth Factor / physiology
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Phenotype
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Phosphorylation
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Recombinant Proteins / pharmacology
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tau Proteins / metabolism
Substances
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Amyloid beta-Peptides
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Amyloid beta-Protein Precursor
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Antibodies
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Cholinergic Agonists
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Recombinant Proteins
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tau Proteins
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Galantamine
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Nerve Growth Factor
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Choline O-Acetyltransferase