While it has been shown (i) that different formyl peptides, such as fMLF, NfMA, or NfM can induce the release of the pro-inflammatory, inflammasome-associated cytokine IL-1β from macrophages [50], (ii) that Aβ1-42 can activate macrophages in a FPR2-dependent manner, and (iii) that FPRL1 is expressed at high levels by inflammatory cells infiltrating senile plaques [25], to the best of our knowledge no data are available regarding the effect of Fpr deletion in AD mice. Here, FPR2 is linked to Alzheimer disease.