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Fig. 5 | Acta Neuropathologica Communications

Fig. 5

From: Carboxyl truncation of α-synuclein occurs early and is influenced by human APOE genotype in transgenic mouse models of α-synuclein pathogenesis

Fig. 5

CNS accumulation of αSyn inclusion pathology in APOE ε4+/+/M83+/− and APOE ε3+/+/M83+/− mice after intramuscular inoculation with PFFs. (a) Representative images of immunostaining with an antibody specific for αSyn phosphorylated at serine 129 (81A). Brains and spinal cord from APOE ε3+/+/M83+/− and APOE ε4+/+/M83+/− mice were assessed for relative pathological burden in M83+/−mice. Scale bar = 100 μm. (b) Semi-quantification of 81A (pSer129) immunoreactivity in the spinal cord, medulla, pons, midbrain, hypothalamus, thalamus, cortex and striatum of PFF-injected M83+/−, APOE ε4+/+/M83+/− and APOE ε3+/+/M83+/− mice were scored by 3 independent observers. Results were analyzed using 1-way ANOVA and corrected for multiple comparisons using Tukey’s test. Data represents means +/− SEM*p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. (c) Kaplan–Meier analysis of motor phenotype development in PFF-injected M83+/− (n = 8; median survival, 123 days after injection), APOE ε3+/−/M83+/− (n = 12; median survival, 112 days after injection), and APOE ε4+/−/M83+/− mice (n = 12; median survival, 115 days after injection) see Table 2. Overall Log-rank (Mantel–Cox) p = 0.4904

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