Role of Non neuronal Cells in Tauopathies After Brain Injury

Abstract

The main purpose of this study is to identify how, after mild repeated traumatic brain injury, specific inflammatory factors (components of the complement cascade) 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 down streampathway directly causing neurodegeneration in many neurodegenerative disease, including TBI. We use a human Tau Tg mouse with its native promoter to model effects of injury on normal tau expression, an unstudied response that may be critical to understanding this elusive delay in onset of symptoms.

Open PDF

Document Details

Document Type
Technical Report
Publication Date
Sep 01, 2016
Accession Number
AD1033294

Entities

People

  • Sally A Frautschy

Organizations

  • University of California

Tags

DTIC Thesaurus Topics

  • Brain Injuries
  • Breeding
  • Cells
  • Chronic Encephalopathy
  • Department Of Defense
  • Diseases And Disorders
  • Inflammation
  • Medical Personnel
  • Neurodegeneration
  • Neurodegenerative Diseases
  • Neuroglia
  • Students
  • Tauopathy
  • Vulnerability

Fields of Study

  • Biology
  • Medicine

Readers

  • Molecular Biology and Genetics
  • Molecular and Cellular Biology
  • Traumatic Brain Injury (TBI) and Cognitive Aging in the Guam and Border Populations Affected by Alzheimer's Disease and Tau-Associated Dementias.