reMYND’s TAU[P301L] model

reMYND’s proprietary TAU[P301L] transgenic, modeling a progressive tau-o-pathy and therefore serving as an excellent model for FTD and Alzheimer’s disease.

In reMYND’s single TAU[P301L] transgenic mice, hTAU is expressed under control of the mouse Thy-1 promoter. The observed tau conformational change and age-dependent accumulation of AT8 and AT100 reactive insoluble tau have been proposed to trigger an age-dependent tangle pathology (starting at age 8-9 months) [1]. In parallel, and with a strong correlation in time, the TAU[P301L] mice develop motor deficits like limb clasping and reduced survival, i.e. succumbing before age 12 months [1]. This model has proven very suitable for therapeutic testing of candidate drugs aimed at tau pathology ([1] and unpublished data).

The table below summarizes the key characteristics of reMYND’s proprietary TAU[P301L] Alzheimer transgenic mice, recapitulating important pathological and clinical hallmarks of Alzheimer’s disease and therefore valuable paradigms for evaluating therapeutic candidates.

reMYND's TAU[P301L] model
Summary

Model

Key Characteristics

TAU [P301L]

  • Expression of hTAU driven by the neuron-specific mouse Thy-1 promotor
  • Age-dependent hyperphosphorylation and confirmational change of Tau
  • Onset around 8 months of age
  • Pathology is mainly observed in the brain stem, spinal cord and midbrain and to lesser extent in the cerebral cortex. brain
  • Correlation with motoric impairment (clasping phenotype, motoric testing deficit) and impaired survival
  • Age-dependent increase of CSF pan-Tau
Terwel et al., JBC, 2005

A confidential data package on reMYND’s TAU[P301L] and APP[V717I]xTAU[P301L] model can be obtained upon request. Hereto, and for all other inquiries please contact Bart Roucourt, CRO Manager.

Reference:
[1] Terwel D, Lasrado R, Snauwaert J, Vandeweert E, Van Haesendonck C, Borghgraef P, Van Leuven F. Changed conformation of mutant Tau-P301L underlies the moribund tauopathy, absent in progressive, non-lethal axonopathy of Tau-4R/2N transgenic mice, J. Biol. Chem. 280:3963-3973 (2005).