APP[V717I]xTau[P301S] model

Key characteristics

  • β-amyloid plaques are observed in the cortex, hippocampus and subiculum from an age of 8 months
  • Tau pathology is observed in the cortex, hippocampus, subiculum and brainstem from an age of 8 months
  • Astrocytosis and microgliosis are observed in the cortex and subiculum from an age of 9 months
  • Cognitive impairment in Morris water maze paradigm from an age of 6.5 months
  • Progressive motoric impairment from an age of 9 months
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Progressive accumulation of plaque deposition (LOC), hyperphosphorylated Tau (AT100 = pThr212/pSer214 Tau), astrocytosis (GFAP) and microgliosis (CD45) in the cortex as measured by IHC (mean ± SEM, n = 8, no data for WT at 11.2 months). Statistics: One-Way ANOVA, Tukey’s multiple comparison.

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Adjacent brain section of a single mouse at 13 months of age of Aβ, Tau and inflammatory markers.

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Progressively lower Aβ42/40 in plasma correlates with Aβ plaques in the cortex (mean ± SEM, n = 7 or 8). Plasma Aβ concentration were measured using MSD-technology (kit K15200E). A significant negative correlation is observed between the plasma Aβ42/40 ratio and Aβ pathology in the cortex. Statistics: One-Way ANOVA, Tukey’s multiple comparison and Pearson’s r correlation coefficient.

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