Amyloid (beta)42 activates a G-protein-coupled chemoattractant receptor, FPR-like-1.

Y. Le, W. Gong, H. L. Tiffany, A. Tumanov, S. Nedospasov, W. Shen, N. M. Dunlop, J. L. Gao, P. M. Murphy, J. J. Oppenheim, J. M. Wang

Research output: Contribution to journalArticlepeer-review

207 Scopus citations

Abstract

Amyloid beta (Abeta) is a major contributor to the pathogenesis of Alzheimer's disease (AD). Although Abeta 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 beta amyloid peptide, Abeta(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 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.

Original languageEnglish (US)
Pages (from-to)RC123
JournalThe Journal of neuroscience : the official journal of the Society for Neuroscience
Volume21
Issue number2
DOIs
StatePublished - Jan 15 2001

ASJC Scopus subject areas

  • Neuroscience(all)

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