Long term potentiation (LTP), a reflection of dendritic spine density and synaptic plasticity, is gaining importance as a functional ex-vivo or even in-vivo read-out related to learning and memory.
Aβ and Tau, two major players in Alzheimer’s disease, have been shown to influence or interfere with LTP. After introducing the LTP read-out in our APP models, we can offer you now also the LTP read-out in our Tau.P301L and Tau.P301S models in collaboration with E-PHY-SCIENCE. LTP is robustly impaired in reMYND’s Tau models in a pre-tangle stage and can serve as an excellent tool for efficacy testing of experimental Alzheimer treatments. Below you can find the robust LTP deficit as measured in the CA1 region of Tau.P301S animals whereas Chong et al (2011) has published similar results in reMYND’s Tau.P301L model.
Figure 1: LTP measurements in CA1 region of 3-month-old Tau.P301S animals (n=5 per group) (left). Average recording high frequency stimulation of 10-45 min post high frequency stimulation (right), * p<0.05, ** p<0.01.
For more information on reMYND’s transgenic mouse models or LTP, please contact us at firstname.lastname@example.org.