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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)

journal contribution
posted on 2002-06-14, 00:00 authored by J A Hamilton, G Whitty, A R White, M F Jobling, A Thompson, Colin BarrowColin Barrow, R Cappai, K Beyreuther, C L Masters
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 (Abeta) 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.

History

Journal

Brain research

Volume

940

Issue

1-2

Pagination

49 - 54

Publisher

Elsevier Science BV

Location

Amsterdam, The Netherlands

ISSN

0006-8993

Language

eng

Publication classification

C1.1 Refereed article in a scholarly journal

Copyright notice

2002, Elsevier Science B.V.