Abstract
In Alzheimer's disease, microglia cluster around beta-amyloid deposits, suggesting that these cells are important for amyloid plaque formation, maintenance and/or clearance. We crossed two distinct APP transgenic mouse strains with CD11b-HSVTK mice, in which nearly complete ablation of microglia was achieved for up to 4 weeks after ganciclovir application. Neither amyloid plaque formation and maintenance nor amyloid-associated neuritic dystrophy depended on the presence of microglia.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Alzheimer Disease / genetics
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Alzheimer Disease / metabolism*
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Alzheimer Disease / pathology*
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Amyloid beta-Peptides / metabolism*
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Amyloid beta-Protein Precursor / genetics
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Animals
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Antigens, CD / metabolism
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Antigens, Differentiation, Myelomonocytic / metabolism
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Antiviral Agents / adverse effects
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Antiviral Agents / pharmacology
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CD11b Antigen / genetics*
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Disease Models, Animal
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Enzyme-Linked Immunosorbent Assay / methods
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Female
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Ganciclovir / adverse effects
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Ganciclovir / pharmacology
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Gene Expression Regulation / drug effects
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Gene Expression Regulation / genetics
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Green Fluorescent Proteins / genetics
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Humans
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Injections, Intra-Articular / methods
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Male
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Mice
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Mice, Transgenic
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Microglia / drug effects
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Microglia / physiology*
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Microscopy, Immunoelectron / methods
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Mutation
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Neuroaxonal Dystrophies / etiology
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Neuroaxonal Dystrophies / metabolism
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Neuroaxonal Dystrophies / pathology
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Plague / pathology*
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Presenilin-1 / genetics
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Thymidine Kinase / genetics
Substances
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Amyloid beta-Peptides
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Amyloid beta-Protein Precursor
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Antigens, CD
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Antigens, Differentiation, Myelomonocytic
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Antiviral Agents
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CD11b Antigen
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CD68 antigen, human
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Presenilin-1
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enhanced green fluorescent protein
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Green Fluorescent Proteins
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Thymidine Kinase
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Ganciclovir