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Role of Nonneuronal Cells in Tauopathies After Brain Injury

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Technical Report,15 Aug 2017,14 Aug 2018

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University of California Los Angeles United States

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This study focuses on the role of inflammatory complement proteins, which are elevated during a prolonged asymptomatic period in mild repeated traumatic brain injury TBI, in chronic traumatic encephalopathy CTE. We propose there is synergism between these proteins and aberrant tau aggregates, a common downstream pathway in many neurodegenerative disease. A central goal of this study is to create and characterize two novel bigenic mouse models that will define the interaction between human tau and these inflammatory proteins, using a repeat lateral mild, head trauma model to recapitulate common injuries suffered in combat or sports. During this third year we have produced approximately 80 percent of the required mice, overcoming obstacles with rederivation, breeding and low yield of bigenics. We have performed most of the TBIs on these mice and are currently analyzing the single transgenic mouse brains both biochemically and histologically. We have identified TBI- and transgene-dependent locomotor disturbances associated with neuroinflammatory pathology. Further we have made progress in the development of GFAP and ER stress markers as brain-derived plasma biomarkers that will be helpful in dissecting the dynamics of neuroinflammation in the complex prodromal sequalae of CTE. Effects of mTBI on tissue contralateral to the injury is also identified, such as increased soluble and insoluble tau aggregates of tau and glia.

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  • Medicine and Medical Research

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