TBI-Induced Formation of Toxic Tau and Its Biochemical Similarities to Tau in AD Brains
Abstract
The goal of the current study is to demonstrate that blast-induced traumatic brain injury (TBI) and Alzheimers 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 worked on the first point of the hypothesis. We have found that administration of tau purified from shockwave-exposed mice onto wild-type mice markedly reduces 1) memory including contextual fear memory and spatial memory, and 2) long-term potentiation, a type of synaptic plasticity thought to underlie learning. Additional, planned behavioral and electrophysiological experiments are ongoing that will allow us to complete our test of the hypothesis and provide new insights into the similarities in tau changes between TBI and AD.
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 01, 2016
- Accession Number
- AD1034544
Entities
People
- Ottavio Arancio
Organizations
- Columbia University