Long term potentiation (LTP) is widely accepted as a cellular model of synaptic plasticity and memory (Lynch et al 2007, Kumar et al 2011).
Aβ and Tau, two major players in Alzheimer’s disease, inhibit long term potentiation and can be modulated by experimental therapies (Shipton et al, 2010, Lasagna-Reeves et al 2012).
In collaboration with E-PHY-SCIENCE, reMYND offers LTP measurements to allow clients to assess the effect of their experimental Alzheimer treatment on synaptic plasticity and memory in a transgenic model of Alzheimer’s Disease.
reMYND’s APP-ld and Tau models have shown to be impaired in LTP in areas such as the CA1 or CA3 region of the hippocampus (Chong et al 2013) and we have shown that a reference compound was able to improve and partially restore LTP in APP-ld transgenic animals (example in Figure 1).
Figure 1: LTP measurements in CA1 region of ~8-month-old vehicle or compound treated APP-Id animals (n=5 per group) (left). Average recording high frequency stimulation of 10-45 min post high frequency sitmulation (right), * p<0.05.
For more information or a confidential data package, please contact Bart Roucourt, CRO Manager.