The goal of the current study is to demonstrate that blast-induced traumatic brain injury (TBI) and Alzheimer's disease(AD) lead to similar biochemical changes in tau that increase its toxicity and contribute to cognitive and electrophysiological impairments. Specifically we will test the hypothesis that 1) blast-induced TBI leads to the production of a toxic form of tau that contributes to cognitive and electrophysiological impairments; 2) the formation of soluble tau aggregates contributes to cognitive impairments associated with both blast-exposure and AD; 3) an increase in tau phosphorylation contributes to cognitive impairments associated with both blast-exposure and AD. During the last year we have completed experiments related to the first point of the hypothesis, and started working on the second point. Specifically, we have found that the presence of tau is necessary for a preparation from shockwave-exposed mice to reduce1) memory including contextual fear memory and spatial memory, and 2) long-term potentiation, a type of synaptic plasticity thought to underlie learning. We have also performed a dose response curve for the toxic effect of blasted tau onto memory and LTP.