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Fig. 5 | Molecular Neurodegeneration

Fig. 5

From: Toll-like receptor 4 stimulation with monophosphoryl lipid A ameliorates motor deficits and nigral neurodegeneration triggered by extraneuronal α-synucleinopathy

Fig. 5

Systemic MPLA treatment of PLP-α-syn mice ameliorates the MSA-like phenotype. a Pole test showed significant improvement of the motor performance of PLP-α-syn after MPLA 100 μg treatment as compared to vehicle treated mice – both Tturn and Ttotal were significantly reduced. MPLA 50 μg and LPS treatment reduced T total but had no significant effect on Tturn. Data are means ± SEM, nvehicle = 14, nLPS = 7, nMPLA50 = 17, nMPLA100 = 16. b TH-immunohistochemistry was used to visualize dopaminergic neurons in SNc. c Stereology counts identified significant rescue of dopaminergic neurons in SNc after MPLA treatment (Data are means ± SEM, nvehicle = 11, nLPS = 3, nMPLA50 = 9, nMPLA100 = 7.* p < 0.05, ** p < 0.01 compared to vehicle treated mice). A historical healthy control group of age-, sex- and background-matched mice (n = 6) was added here to demonstrate the normal level of TH-positive neurons in SNc in non-tg mice (***p < 0.001 compared to vehicle treated PLP-α-syn mice, ##p < 0.01 compared to LPS treated PLP-α-syn mice). d The lower number of dopaminergic neurons in the transgenic SNc significantly correlated with the higher disability (increased Ttotal) in the pole test. e DARPP-32 immunoreactivity was used to define the number of GABAergic medium spiny neurons in the striatum (ce, capsula externa; Str, striatum. f Stereological analysis significant rescue of DARPP-32 neurons in the striatum after MPLA treatment (Data are means ± SEM, nvehicle = 4, nLPS = 3, nMPLA50 = 4, nMPLA100 = 4.* p < 0.05, compared to vehicle treated mice)

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