14 research outputs found

    Tubulin and Tau: Possible targets for diagnosis of Parkinson’s and Alzheimer’s diseases - Fig 3

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    <p><b>Distribution curves of AIAs against tubulin (3A), tau (3B) and the combination of tubulin and tau (3C) in different groups.</b> Curves showed possible differentiation between cases and controls (3A and 3B) and the possibility of identifying profiles specific for PD and AD (Tubulin in blue and Tau in red) (3C).</p

    Histograms showing levels of autoantibodies in different groups (mean ± SEM).

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    <p>Tubulin AIAs show a significant elevation in PD and AD cases compared to control. On the other hands, Tau was elevated in both diseases with higher elevation in AD.</p

    Effects of piericidin A treatment on neuronal cell count and synaptic density.

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    <p>A: Neuronal nuclei (NeuN)-stained sections of the frontal cortex (Cx) of wild-type and P301S<sup>+/+</sup> mice treated with vehicle or piericidin A (left panel). Quantification of NeuN immunoreactive cells in the cortex showed no difference in the four animal groups (right panel). Scale bar 50 µm. B: Sections of the frontal cortex stained with an antibody against synaptophysin as marker for the synaptic density (left panel). The immunoreactivity quantified by optical density measurement was significantly reduced in piericidin A treated P301S<sup>+/+</sup> mice compared to vehicle treated P301S<sup>+/+</sup> (right panel). Scale bar: 10 µm. ## p <0.01, piericidin A treatment vs vehicle treatment at the same genotype. Two-way ANOVA with Fisher LSD post-hoc test.</p

    Histological sections showing the effect of piericidin A treatment on tau pathology.

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    <p>Frontal cortex (Cx) of wild-type and P301S<sup>+/+</sup> mice treated with vehicle or piericidin A. Sections were stained separately with the antibodies AD2 (A), AT 180 (B), AT8 (C), and AT100 (D). The inserts are 2.5-times magnified compared to the overview images. P301S<sup>+/+</sup> mice had significant higher numbers of phospho-tau positive cells in the frontal cortex compared to wild-type animals with the same treatment (lower panels, filled bars). Treatment with piericidin A further increased the number of AD2 immunoreactive cells (A, lower panel) and AT180 immunoreactive cells (B, lower panel). With AT8 immunoreactivity there was the same tendency, however, the difference was not significant (C, lower panel). With the AT100 antibody we only observed immunoreactive cells in piericidin A treated P301S<sup>+/+</sup> mice (D). Scale bars: 20 µm. * p<0.05, ** p<0.01, *** p<0.001, P301S<sup>+/+</sup> vs. wild-type at the same treatment. # p<0.05, ## p<0.01, ### p<0.001, piericidin A treatment vs. vehicle treatment at the same genotype. Two-way ANOVA with Fisher LSD post-hoc test.</p

    Adequacy of the gamma distribution.

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    <p>The gamma distribution provides an adequate fit for multiple types of pedigrees. For example, HRP UT-549917 has <i>k</i> = 4.4 and <i>σ</i> = 3.6 with good visual density (a) and CDF (b) fit, with <i>λ</i> = 0.9. (Goodness of fit was estimated with <i>λ</i>, the median of empirical chi-squared distribution divided by the median of the expected chi-squared distribution.) HRP UT-34955 has <i>k</i> = 2.8 and <i>σ</i> = 2.9 with good visual density (c) and CDF (d) fit, with <i>λ</i> = 1.0.</p
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