Following the observations that circulating progenitors do not contribute to the microglial pool (Figs. 1 and 2) and that CCR2 deficiency does not modify the inflammatory reaction in prion disease except in the perivascular compartment (Fig. 4), we examined the pathological course of the ME7 model in WT vs. CCR2−/− mice using behavioral techniques (Fig. 5), to address the overall contribution of CCR2 to the disease. This evidence concerns the gene CCR2 and prion disease.