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Fig. 5 | Molecular Neurodegeneration

Fig. 5

From: A brain-penetrant triazolopyrimidine enhances microtubule-stability, reduces axonal dysfunction and decreases tau pathology in a mouse tauopathy model

Fig. 5

PS19 mice treated with 51657 show a reduction of insoluble pathological forms of tau. Brains of PS19 mice treated with vehicle (n = 12), or 3 mg/kg (n = 11) or 10 mg/kg (n = 12) of 51657 were sequentially extracted to remove high salt- and RIPA-soluble proteins. The remaining insoluble fraction was solubilized in 2% SDS and analyzed by immunoblotting, utilizing antibodies that recognize (a) total tau (17025 antibody), (b) phospho-tau (AT8 antibody) and (c) tau acetylated at residue K280 (AcTau; tau K280 antibody). The lower dose of 51657 caused a significant reduction of all three forms of insoluble tau, and the higher dose of 51657 dose resulted in a reduction of all insoluble tau species, with a significant reduction of AcTau. After quantification, a Grubb’s test determined there were extreme outliers within some treatment groups, resulting in the removal of a sample (B2) from the 10 mg/kg 51657 group from the AcTub antibody immunoblot (see Additional file 1: Figure S6), and a sample from each treatment group in the 17025 antibody immunoblot. d Soluble tau levels as measured by ELISA within the high salt fractions were unaffected by 51657-treatment. All comparisons consisted on one-way ANOVA with Tukey’s post-hoc analysis of between group differences. Error bars represent SEM

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