Role of Non neuronal Cells in Tauopathies After Brain Injury
Technical Report,15 Aug 2015,14 Aug 2016
University of California, Los Angeles Los Angeles United States
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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.