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Figure 2 | Molecular Neurodegeneration

Figure 2

From: Fcγ receptors are required for NF-κB signaling, microglial activation and dopaminergic neurodegeneration in an AAV-synuclein mouse model of Parkinson's disease

Figure 2

Effect of α-SYN over-expression on NF-κB activation in wild-type and FcγR-/- mice at four weeks. A-H) SN sections of wild-type and FcγR-/- mice over-expressing human α-SYN or GFP were double stained for NF-κB p65 (red) and SYN/GFP (green). Wild-type mice expressing human α-SYN revealed significantly increased immunoreactivity for NF-κB p65 while no significant enhancement of p65 was observed in FcγR-/- mice. Scale bars: panels A, B, C, D bar = 60 μm; panels E, F, G, H bar = 20 μm. I) Scoring of immunostaining for p65 using a rating scale revealed significant elevated p65 expression in wild-type mice treated with AAV2-SYN compared to AAV2-GFP group. This difference was not observed in FcγR-/- mice expressing SYN or GFP. *p < 0.05, WT-SYN vs WT-GFP, Mann-Whitney U test. J) Immunoblotting and quantification for nuclear NF-κB p65 in WT and FcγR-/- mice. In WT mice, AAV2-SYN treated mice showed significant increase in nuclear p65 level compared with AAV2-GFP controls. No difference was observed between FcγR-/- mice expressing α-SYN or GFP, but FcγR-/- mice have higher baseline levels of nuclear p65 than WT mice. *p < 0.05, WT-SYN vs WT-GFP t-test (N: untreated mice; G: AAV2-GFP mice; S: AAV2-SYN mice).

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