reMYND’s Tau.P301S transgenic model is an agressive tau-o-pathy model with minor variability, a strong behaviour-pathology correlation and an apparent forebrain pahology and therefore serves as an excellent model for efficacy testing of Alzheimer treatments.
In the single Tau.P301S transgenic mice, hTau (4R0N) is expressed under control of the mouse Thy-1 promoter. The Tau.P301S model is characterized by progressive hyperphosphorylation of Tau with age leading to a profound NFT-like pathology in the brainstem, spinal cord, cortex and hippocampus regions. The Tau-pathology strongly correlates with the motoric deficit observed in these mice as measured by rotarod and clasping an shows managable inter-mouse variability.
In addition, with age, neuronal loss, astrocytosis and activation of microglia is observed (Bellucci et al 2004, Hampton et al 2010). More information on inflammatory markers.
Allen et al, 2002,
In recent years the Tau.P301S model has been proven to be a pivotal model for generating proof-of-concept data. In a paper published in PLOS ONE, Ozelik and colleagues demonstrate a profound effect of short and long term rapamycin treatments on various pathological read-outs in the brainstem and cortex of Tau.P301S mice (AT8, AT100, GFAP, …) (Ozelik et al 2013).
In another paper published in the Journal of Biological Chemistry, Chai and coworkers show that short term passive immunization with Tau-directed antibodies lead to a preservation of motor function and strong effects on Tau pathology in the Tau.P301S model (Chai et al 2011).
A proprietary data package on the Tau.P301S model can be obtained upon request. Hereto, and for all other inquiries please contact Bart Roucourt, CRO Manager.