Tau pathology is significantly reduced in 3xTg-AD^2–18 mice.

<p>(<b>A–F</b>) Representative sections depicting CA1 pyramidal neurons from brains of 3xTg-AD^CTL, 3xTg-AD^15–18 and 3xTg-AD^2–18 mice (n = 8/group) immunostained with the indicated anti-tau antibodies. Note the reduction of AT100- and AT180-positive neurons in the 3xTg-AD^2–18 mice compared to 3xTg-AD^CTL and 3xTg-AD^15–18 mice. (<b>G</b>) Representative Western blots of proteins extracted from 3xTg-AD^CTL, 3xTg-AD^15–18 and 3xTg-AD^2–18 mice (n = 8/group) and probed with the indicated antibodies. (<b>H</b>) Quantitative analysis of the blots shows that rapamycin did not change the steady-state levels of full length tau transgene as measured by the human-specific anti-tau antibody, HT7. In contrast, the levels of tau phosphorylated at the AT100 and AT180 epitopes were significantly reduced in the 3xTg-AD^2–18 mice compared to the 3xTg-AD^CTL and 3xTg-AD^15–18 mice (F = 5.271 and p = 0.018 for AT100; F = 14.25 and p = 0.0003 for AT180). Data are presented as means ± SEM.