Fig. 8

Blockade of LRRK2 kinase inhibits α–synuclein propagation in mice. a Representative immunohistochemical analysis of α-synuclein in the neocortex (Nctx), striatum (Str), and corpus callosum (C.C) of non-transgenic (non-tg) and α-syn tg mice. Age-matched mice were injected with either vehicle (Veh) or LRRK2 inhibitor (LKI) for 4 weeks. Scale bars, 250 μm (low magnification) and 25 μm (high magnification). b–e Optical analysis of α-synuclein deposition in non-tg and α-syn tg mice (b) Optical density analysis of α-synuclein immunoreactivity in neocortex. Treatment F(1,20)=6.601, Genotype F(1,20)=276.8, Interaction F(1,20)=6.919, **** p < 0.001, ## p < 0.01. c The number of α-synuclein inclusion positive cells in neocortex. Treatment F(1,20)=4.034, Genotype F(1,20)=99.61, Interaction F(1,20)=4.034, **** p < 0.001, # p < 0.05. d Optical density analysis of α-synuclein immunoreactivity in striatum. Treatment F(1,20)=3.88, Genotype F(1,20)=96.22, Interaction F(1,20)=9.303, **** p < 0.001, ## p < 0.01. e The number of α-synuclein-positive axons in corpus callosum. Treatment F(1,20)=17.66, Genotype F(1,20)=58, Interaction F(1,20)=17.66, **** p < 0.001, #### p < 0.001. f Representative immunohistochemical analysis of phosphorylated (pSer129)- and Proteinase K (PK)-resistant α-synuclein in the neocortex and corpus callosum of non-tg and α-syn tg mice. Brain sections were immunostained against either phosphorylated- α-synuclein (pSer129) or α-synuclein following PK treatment. Scale bars, 250 μm (low magnification) and 25 μm (high magnification). g Optical density analysis of phosphorylated α-synuclein immunoreactivity in neocortex. Treatment F(1,20)=2.064, Genotype F(1,20)=476.2, Interaction F(1,20)=2.064, **** p < 0.001. h The number of phosphorylated α-synuclein-positive axons in corpus callosum. Treatment F(1,20)=8.75, Genotype F(1,20)=40.18, Interaction F(1,20)=8.75, **** p < 0.001, ### p < 0.005. i Optical density analysis of PK-resistant α-synuclein immunoreactivity in neocortex. Treatment F(1,20)=20.97, Genotype F(1,20)=269.3, Interaction F(1,20)=20.97, **** p < 0.001, #### p < 0.001. j The number of PK-resistant α-synuclein-positive axons in corpus callosum. Treatment F(1,20)=17.4, Genotype F(1,20)=55.61, Interaction F(1,20)=17.4, **** p < 0.001, #### p < 0.001. All analyses were done with N = 6 mice per group. All data were analyzed by using two-way ANOVA with Tukey’s post hoc test