Research Paper Volume 11, Issue 17 pp 6762—6791

Knockout of p75 neurotrophin receptor attenuates the hyperphosphorylation of Tau in pR5 mouse model

Figure 2. Knock out of p75NTR in pR5 mice attenuated human Tau phosphorylation at 6 months. (A) Protein blots for total Tau, and phosphorylated Tau probed at 75 kDa for human and 50 kDa for mouse protein bands in the forebrains of Wt, p75KO, pR5 and pR75KO mice at 6 months. (B) Protein band intensity quantification of phosphorylated human Tau at S262, S396 and S202/T205 (AT8) in pR5 and pR75KO mice normalised with total human Tau and expressed as fold change relative to pR5. Protein band intensity quantification of total human Tau and pTau detected by HT7 (C), total mouse Tau detected by Tau5 (D), and total human Tau detected by sheep-anti human Tau (E) normalised to β-actin and expressed as fold change relative to Wt. (F) Protein blots of cleaved caspase-3, glial fibrillary acidic protein (GFAP) neuronal nuclei (NeuN). Protein band intensity quantification of cleaved caspase-3 (G), GFAP (H), and NeuN (I) normalised with their respective total β-actin and expressed as fold change relative to Wt. Data are represented as the mean ± SEM, n=6. Statistical comparisons were performed using one-way ANOVA and Tukey’s test. For human pTau, two-tailed unpaired t-test was used to compare pR5 and pR75KO mice. Statistical significance: *P<0.05, **P<0.01.