The amyloid beta-protein of Alzheimer's disease is chemotactic for mononuclear phagocytes. |
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Authors: | J B Davis H F McMurray D Schubert |
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Institution: | Salk Institute for Biological Studies, San Diego, CA 92186-5800. |
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Abstract: | The cellular pathology of Alzheimer's disease includes an accumulation of microglia surrounding the amyloid plaques. We report that human amyloid beta-protein is chemotactic for murine resident peritoneal macrophages and rat microglia, which may account for the increased density of microglia in plaques. A maximal chemotactic response was observed at 1-10nM, with a 2.5 fold increase in activity over controls for both classes of mononuclear phagocytes. The neurotoxic peptide fragment (25-35) of amyloid beta-protein is similarly chemotactic, while a control scrambled version and the precursor protein are not chemotactic. These results indicate that beta-protein may influence plaque formation via the recruitment of phagocytes, with consequent implications for the future development of treatments for Alzheimer's disease. |
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