Blocking Site-Specific Cleavage of Human Tau Delays Progression of Disease-Related Phenotypes in Genetically Matched Tau-Transgenic Mice Modeling Frontotemporal Dementia

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Figure 9.
Figure 9.

Age-related tau accumulation and AMPAR alteration in PSD of rT2 and rT3 mice. A, Representative WBs showing fl-htau (HT7), phosphorylated tau (PHF-1), GluA1 subunit of AMPAR (anti-GluA1), and PSD95 from a female (F) and a male (M) rT2 and rT3 mice (htau+/− tTA+/−) at 5, 8, and 12 months of age (mo) and their respective, age- and gender-matched non-Tg littermates (htau−/− tTA−/−). Total PSD proteins were also shown to demonstrate equal loading of samples. kDa, kilodaltons. B-M, Scatter plots with bar (individual data plus group mean ± SD) graphs showing levels of fl-htau (B-E), PHF-1-reactive phosphorylated tau (F-I), and GluA1 (J-M), all normalized to levels of PSD95, in rT2 and rT3 mice at 5 (B,F,J), 8 (C,G,K), and 12 (D,H,L) mo. Age-related alterations between rT2 and rT3 mice (E,I,M) were also analyzed. Numbers of animals (for detailed gender distribution, see Table 1) used are shown in parentheses. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, #p = 0.0715, $p = 0.0576, %p = 0.0895, &p = 0.0525. a.u., arbitrary units.

  1. The Journal of Neuroscience vol. 42 no. 23 4737-4754
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