The Hub (SUB II), VIP III
October 07, 2019, 03:00 PM to 05:00 PM
Aging is characterized by a decline in synaptic plasticity and cognitive functions. This is intensified in Alzheimer’s disease by the buildup of plaques and tangles in the brain. The tangles contain a stabilizing protein called tau, that detaches from a collapsing neuron and clump together, thus called tau tangles. There are limited treatments for Alzheimer’s disease, therefore the exploration of new alternatives is warranted. In a recent study, plasma was transfused from young mice to older transgenic mice containing plaques, causing an improvement in new spatial learning and memory tasks and an increase in proteins that support synaptic plasticity of neurons (Middeldorp et al. 2016). Because mice with tau tangles in the brain were not included in this design, we propose to transfuse plasma from young wild-type mice to older transgenic mice that can develop tangles expressing human tau (h-Tau, P301L/CaMKII), followed by an examination of behavioral outcomes and tau pathology of the older mice. Studies conducted in our lab have shown that tau tangles do cause learning and memory impairments in mice. Therefore, this study will be able to fill in the information gaps relating Alzheimer’s disease and young blood transfusion.