Role of Non-neuronal Cells in Tauopathies After Brain Injury
Abstract
The purpose of this study is to identify how, after mild repeated traumatic brain injury (TBI), specific inflammatory factors (complement proteins) elevated during long asymptomatic prodromal period are responsible for the eventual onset of cognitive deficits and neurodegeneration. We investigate how inflammation leads to accumulation of aberrant tau aggregates, a common downstream pathway directly causing neurodegeneration in many neurodegenerative disease, including TBI. We use a human Tau Tg mouse that models effects of TBI on normal tau expression. This mouse is bred to mice with novel transgenes associated with complement activation: one lacking the brake of the complement cascade (C1inh KO) and the other overexpressing C5a. During this 2nd year we produced new data demonstrating a robust effect of C1inhKOaffecting the response to TBI in human tau mice, increasing tau and pyknotic neurons as well as a tau kinase which increases tau phosphorylation, supporting a pathogenic role of C1q in tau-dependent injury after TBI.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 2017
- Accession Number
- AD1048135
Entities
People
- Sally A Frautschy
Organizations
- University of California