Indeed, the amyloid-beta peptide Aβ42 has been shown to be an agonist for FPR-like-1 (FPRL1); FPRL1 is strongly expressed by inflammatory cells infiltrating neuritic plaques in postmortem Alzheimer cerebral tissue and so may be involved in the cerebral inflammatory processes associated with this form of dementia [10]. The gene discussed is FPR2; the disease is dementia.