Amyloid beta and its naturally occurring N-terminal variants are potent activators of human and mouse formyl peptide receptor 1
Lukas Busch, Zukaa Al Taleb, Yu‐Liang Tsai, Vu Thu Thuy Nguyen, Qi Lu, Christopher V. Synatschke, Kristina Endres, Bernd Bufe
Abstract
evoked cell migration, which argues for a functional selectivity of different Aβ peptides. Together, these findings provide the first evidence that not only hFPR2 but also hFPR1 and hFPR3 may contribute to neuroinflammation in Alzheimer's disease through an interaction with different Aβ variants.
Topics & Concepts
NeuroinflammationPeptideReceptorHEK 293 cellsFormyl peptide receptorChemotaxisAmyloid betaTransfectionCell cultureAmyloid (mycology)Cell biologyCellChemistryHuman brainBiologyBiochemistryPharmacologyInflammationNeuroscienceGeneImmunologyGeneticsInorganic chemistryS100 Proteins and AnnexinsAlzheimer's disease research and treatmentsBone Metabolism and Diseases