Fig. 3: Nigrostriatal degeneration was more evident in APOE4/4 mice fed with high fat diet.
From: APOE4 promotes nigral tau hyperphosphorylation through cholesterol in atherosclerosis
A Representative TH IF and IHC staining in SNpc and CPu. Bar in upper panel, 40 μm, bar in lower panel, 50 μm. B, C Quantification of TH positive cell number and intensity in SNpc and CPu. n = 6, two-way ANOVA followed by Bonferroni’s post hoc tests. SN, Treatment: F(1, 20) = 69.73, p < 0.001, Genotype: F(1, 20) = 15.89, p < 0.001, Treatment × Genotype: F(1, 20) = 9.962, p = 0.005, CPu, Treatment: F(1, 20) = 106.3, p < 0.001, Genotype: F(1, 20) = 9.964, p = 0.005, Treatment × Genotype: F(1, 20) = 13.74, p = 0.001. D Representative blots and quantification of TH in CPu and SNpc. n = 6, two-way ANOVA followed by Bonferroni’s post hoc tests. CPu TH, Treatment: F(1, 20) = 246.2, p < 0.001, Genotype: F(1, 20) = 4.147, p = 0.055, Treatment × Genotype: F(1, 20) = 21.85, p < 0.001, SN TH, Treatment: F(1, 20) = 324.3, p < 0.001, Genotype: F(1, 20) = 23.13, p < 0.001, Treatment × Genotype: F(1, 20) = 14.58, p = 0.001. E Time to descend in pole test and latency to fall from an rotarod test. n = 6, two-way ANOVA followed by Bonferroni’s post hoc tests. Time to descend, Treatment: F(1, 20) = 265.2, p < 0.001, Genotype: F(1, 20) = 30.16, p < 0.001, Treatment × Genotype: F(1, 20) = 19.55, p < 0.001, Latency to fall, Treatment: F(1, 20) = 151.0, p < 0.001, Genotype: F(1, 20) = 5.171, p = 0.034, Treatment × Genotype: F(1, 20) = 12.55, p = 0.002.
