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Traumatic brain injury induces tau aggregation and spreading

George Edwards III

University of Texas Health Science Center Houston


The misfolding and aggregation of tau protein into neurofibrillary tangles is the main underlying hallmark of tauopathies. Most of them have a sporadic origin and can be associated to multiple risk factors. Traumatic brain injury (TBI) has been suggested as a risk factor for tauopathies by exacerbating disease onset and progression. TBI is a ubiquitous event and can occur at different severity levels. A moderate to severe TBI is the most violent form of TBI, which can stem from a vehicle accident or hard fall. Several studies indicate that TBI seems to be a risk factor to develop Alzheimer’s disease and chronic traumatic encephalopathy since there is a relationship of TBI severity and propensity to develop these tauopathies. In this study, we evaluated whether moderate to severe TBI could trigger the initial formation of pathological tau that would induce the development of the pathology throughout the brain. To this end, we subjected tau transgenic mice to TBI and assessed tau phosphorylation and aggregation pattern to create a spatial heat map of tau deposition and spreading in the brain. Our results suggest that TBI-induced mice have a more accelerated tau pathology in different brain regions that increases over time compared to sham mice. The appearance of pathological tau occurs in regions distant to the injury area and that are synaptically interconnected, indicating that TBI favors tau aggregates spreading in a prion-like manner. Overall, this work posits TBI as a risk factor for tauopathies through the induction of tau hyperphosphorylation.

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