APP[V717I]xTau[P301L] model

Key characteristics

  • Beta-amyloid plaques are observed in the cortex, hippocampus and amygdala
  • Tau pathology is observed in the cortex, brainstem, midbrain and at a later age in the hippocampus
  • Progressive motoric impairment
  • Cognitive deficit in the Morris Water Maze, preceded by an impaired synaptic plasticity
     
Quantified Methoxy-X04 and AT100 (pTAU S212/T214)

Quantified Methoxy-X04 and AT100 (pTAU S212/T214) IHC staining of 6-13 months old APP[V717I] x Tau[P301L] animals in a specified area of the frontal cortex.

mice develop age-dependent motoric inabilities

APP[V717I]xTau[P301L] mice develop age-dependent motoric inabilities from ~10 months of age onwards

Quadrant analysis during the probe trial, Morris Water Maze with 9 months

Quadrant analysis during the probe trial, Morris Water Maze with 9 months- old APP[V717I]xTau[P301L] and age-matched non transgenic control animals (N = 22-23 per group, NE = Target Quadrant)

LTP measurements in CA1 region of 4-6 months-old APP[V717I]xTau[P301L]

LTP measurements in CA1 region of 4-6 months-old APP[V717I]xTau[P301L] (biAT) animals compared to wild type animals and other transgenic Alzheimer models (Chong et all, 2011).

Literature

Describing papers

  • Terwel et al., 2008. Amyloid activates GSK-3beta to aggravate neuronal tauopathy in bigenic mice. DOI: 10.2353/ajpath.2008.070904
  • Chong et al., 2011. Synaptic dysfunction in hippocampus of transgenic mouse models of Alzheimer’s disease: A Multi-electrode array study. DOI: 10.1016/j.nbd.2011.07.006