Abstract
The effects of a synthetic homolog of beta-amyloid (beta 1-42) on the secretion of interleukin-1 (IL-1) and basic fibroblast growth factor (bFGF) from cultures of microglia and astrocytes, cells that surround beta-amyloid-containing plaques in Alzheimer's disease, were examined. Our results show that beta-amyloid not only enhances glial cell secretion of these factors, it stimulates the proliferation and morphological transformation of microglia. Since IL-1 and bFGF are known to elevate the synthesis of the beta-amyloid precursor protein and other plaque components, it is suggested that in this way, cascades may arise that contribute to the process of plaque development.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Alzheimer Disease / metabolism*
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Alzheimer Disease / pathology
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Amyloid beta-Peptides / pharmacology*
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Animals
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Animals, Newborn
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Astrocytes / drug effects
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Astrocytes / metabolism
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Brain / drug effects
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Brain / metabolism*
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Cells, Cultured
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Dose-Response Relationship, Drug
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Fibroblast Growth Factor 2 / biosynthesis*
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Fibroblast Growth Factor 2 / metabolism
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Humans
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Interleukin-1 / biosynthesis*
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Interleukin-1 / metabolism
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Kinetics
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Neuroglia / cytology
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Neuroglia / drug effects
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Neuroglia / metabolism*
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Peptide Fragments / pharmacology*
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Rats
Substances
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Amyloid beta-Peptides
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Interleukin-1
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Peptide Fragments
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amyloid beta-protein (1-42)
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Fibroblast Growth Factor 2