Fig. 7

Aβ1-42 induces a pro-inflammatory phenotype in primary cultured glia with removal of IFNAR demonstrating a predmoninatly anti-inflammatory response. a Q-PCR of primary wildtype and IFNAR1^−/− glial cultures treated with 10 μM Aβ1-42 for 24–96 h analyzing iNOS, CD11b and CD32 pro-inflammatory glial marker expression levels. b Q-PCR of primary wildtype and IFNAR1^−/− glial cultures treated with 10 μM Aβ1-42 for 24–96 h analyzing ARG1, CCL22, YM1, CD206 and TGFβ anti-inflammatory glial marker expression levels. For Q-PCR all samples were normalized back to the Ct value of the housekeeping gene GAPDH (ΔCt). The mRNA of the Aβ1-42 treatment groups was then expressed relative to their gene-specific vehicle controls (fold change, ΔΔCt). Data are displayed as mean ± SEM (n = 4 (wildtype), n = 5 (IFNAR1^−/−); *p < 0.05, **p < 0.01). See Additional file 2: Table S1 for further analysis