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The Journal of Neuroscience, 2001, 21:RC123:1-5

RAPID COMMUNICATION
Amyloid ₄₂ Activates a G-Protein-Coupled Chemoattractant Receptor, FPR-Like-1

Yingying Le¹, Wanghua Gong², H. Lee Tiffany³, Alexei Tumanov¹, Sergei Nedospasov¹, Weiping Shen¹, Nancy M. Dunlop¹, Ji-Liang Gao³, Philip M. Murphy³, Joost J. Oppenheim¹, and Ji Ming Wang¹

¹ Laboratory of Molecular Immunoregulation, Division of Basic Sciences and ² Science Applications International Corporation Frederick, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, Maryland 21702, and ³ National Institutes of Health, Bethesda, Maryland 20892

Amyloid  (A) is a major contributor to the pathogenesis of Alzheimer's disease (AD). Although A has been reported to be directly neurotoxic, it also causes indirect neuronal damage by activating mononuclear phagocytes (microglia) that accumulate in and around senile plaques. In this study, we show that the 42 amino acid form of  amyloid peptide, A₄₂, 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 cells infiltrating senile plaques in brain tissues from AD patients. Thus, FPRL1 may mediate inflammation seen in AD and is a potential target for developing therapeutic agents.

Key words: amyloid ; receptor; FPRL1; monocytes; chemotaxis; Alzheimer's disease

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Copyright © Society for Neuroscience  0270-6474//$05.00/0

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