Amyloid beta (A beta) is a major contributor to the pathogenesis of Alzheim
er's disease (AD). Although A beta has been reported to be directly neuroto
xic, it also causes indirect neuronal damage by activating mononuclear phag
ocytes (microglia) that accumulate in and around senile plaques. In this st
udy, we show that the 42 amino acid form of beta amyloid peptide, A alpha (
42), is a chemotactic agonist for a seven-transmembrane, G-protein-coupled
receptor named FPR-Like-1 (FPRL1), which is expressed on human mononuclear
phagocytes. Moreover, FPRL1 is expressed at high levels by inflammatory cel
ls infiltrating senile plaques in brain tissues from AD patients. Thus, FPR
L1 may mediate inflammation seen in AD and is a potential target for develo
ping therapeutic agents.