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Alzheimer's disease amyloid beta and prion protein amyloidogenic peptides promote macrophage survival,DNA synthesis and enhanced proliferative response to CSF-1 (M-CSF) |
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| Authors: | Hamilton John A Whitty Genevieve White Anthony R Jobling Michael F Thompson Andrew Barrow Colin J Cappai Roberto Beyreuther Konrad Masters Colin L |
| Affiliation: | a Arthritis and Inflammation Research Centre, The University of Melbourne, Department of Medicine, The Royal Melbourne Hospital, Clinical Sciences Building, Royal Parade, Parkville, Victoria 3050, Australia b Department of Pathology, The University of Melbourne, Melbourne, Victoria 3010, Australia c The Mental Health Research Institute, Parkville, Victoria 3052, Australia d School of Chemistry, The University of Melbourne, Melbourne, Victoria 3010, Australia e Centre for Molecular Biology, The University of Heidelberg, IM Neuenheimer Feld 282, 69120 Heidelberg, Germany |
| Abstract: | Microglial cells, macrophage-lineage cells in the brain, are increased in amyloid-containing plaques in Alzheimer’s disease (AD) and in the lesions of prion diseases. Recent studies suggest that microglia have a central role in turnover of amyloid in these diseases. We report here that synthetic amyloid beta (Aβ) 1-42 and prion protein (PrP) 106-126 peptides promote macrophage survival; they also induce macrophage DNA synthesis, particularly in the presence of sub-optimal concentrations of the growth factor, macrophage-colony stimulating factor (M-CSF or CSF-1). These responses are proposed to provide a means to increase brain microglia/macrophage numbers thereby enhancing subsequent inflammatory/immune responses. These fibrillogenic peptides join the list of aggregates having these effects on macrophages, indicating the generality of this type of response. |
| Keywords: | Aβ peptide Prion protein Macrophage M-CSF (CSF-1) Survival DNA synthesis |
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