1. Beta-amyloid plaques in a model for sporadic Alzheimer's disease based on transgenic anti-nerve growth factor antibodies.
- Author
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Capsoni S, Giannotta S, and Cattaneo A
- Subjects
- Aging immunology, Aging pathology, Alzheimer Disease immunology, Alzheimer Disease physiopathology, Amyloid beta-Protein Precursor metabolism, Animals, Autoantibodies immunology, Autoantibodies metabolism, Benzothiazoles, Brain immunology, Brain metabolism, Brain pathology, Cerebellum immunology, Cerebellum metabolism, Cerebellum pathology, Disease Models, Animal, Locus Coeruleus immunology, Locus Coeruleus metabolism, Locus Coeruleus pathology, Mice, Mice, Transgenic, Neostriatum immunology, Neostriatum metabolism, Neostriatum pathology, Nerve Growth Factor genetics, Nerve Growth Factor metabolism, Neurofibrillary Tangles metabolism, Neurons immunology, Neurons metabolism, Neurons pathology, Plaque, Amyloid immunology, Plaque, Amyloid metabolism, Signal Transduction genetics, Signal Transduction immunology, Silver Staining, Thiazoles, Aging genetics, Alzheimer Disease genetics, Amyloid beta-Peptides metabolism, Autoantibodies genetics, Nerve Growth Factor deficiency, Plaque, Amyloid genetics
- Abstract
Cerebral deposition of beta-amyloid (Abeta) is an invariant event of Alzheimer's disease (AD). We recently described that the brain of aged transgenic mice expressing anti-nerve growth factor (NGF) antibodies (AD11 mice) show a dramatic neurodegenerative phenotype, reminiscent of AD, which includes neuronal loss, cholinergic deficit, and tau hyperphosphorylation, associated with neurofibrillary pathology. We now report that brains of aged transgenic mice contain large amounts of beta-amyloid plaques and describe their morphology by a variety of approaches. In conclusion, the chronic deprivation of NGF leads to the formation and deposition of Abeta in AD11 mice, suggesting a direct link between NGF signaling and abnormal processing of amyloid precursor protein.
- Published
- 2002
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