Beta amyloid peptide (Abeta42) is internalized via the G-protein-coupled receptor FPRL1 and forms fibrillar aggregates in macrophages.

@article{Yazawa2001BetaAP,
  title={Beta amyloid peptide (Abeta42) is internalized via the G-protein-coupled receptor FPRL1 and forms fibrillar aggregates in macrophages.},
  author={Hiroshi Yazawa and Zhiya Yu and Takeda and Yingying Le and Wanghua Gong and V{\'i}ctor J. Ferrans and Joost J Oppenheim and Connie C Li and Ji ming Wang},
  journal={FASEB journal : official publication of the Federation of American Societies for Experimental Biology},
  year={2001},
  volume={15 13},
  pages={2454-62}
}
The 42 amino acid form of beta amyloid (Abeta42) plays a pivotal role in neurotoxicity and the activation of mononuclear phagocytes in Alzheimer's disease (AD). Our recent study revealed that FPRL1, a G-protein-coupled receptor, mediates the chemotactic and activating effect of Abeta42 on mononuclear phagocytes (monocytes and microglia), suggesting that FPRL1 may be involved in the proinflammatory responses in AD. We investigated the role of FPRL1 in cellular uptake and the subsequent fibrillar… CONTINUE READING

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