Fig. 6

The type-1 IFN and pro-inflammatory cytokine response to Aβ1-42 is attenuated upon removal of IFNAR1 in primary cultured glia. a Q-PCR of primary wildtype and IFNAR1^−/− glial cultures treated with 10 μM Aβ1-42 for 24–96 h analyzing IFNα, IFNβ, IL-1β, IL-6 and TNFα transcript levels. b Representative immunoblot of primary wildtype and IFNAR1^−/− glial cultures treated with 10 μM Aβ1-42 for 24–72 h using anti-p-NFkB (p65). c Densitometry of p-NFkB (p65) levels in primary wildtype and IFNAR1^−/− glial cultures treated with 10 μM Aβ1-42 for 24–72 h. 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, ∆∆Ct). For densitometry raw intensities of p-NFkB (p65) bands were normalized to β-actin levels. All intensity values of Aβ1-42 treated groups are expressed as fold change relative to the genotype-specific vehicle control (average of which is represented by the dashed line). Immunodetection of β-actin was used to ascertain loading quantities. Data are displayed as mean ± SEM (Q-PCR: n = 4 (wildtype), n = 5 (IFNAR1^−/−); Western blotting: n = 3 per genotype; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001). See Additional file 2: Table S1 for further analysis