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Published on: February 10, 2020
Traumatic Brain Injury Induces Tau Aggregation and Spreading
George Edwards1, Jing Zhao2, Pramod K Dash2
1Mitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, The University of Texas Health Science Center at Houston, Houston, Texas.
Traumatic brain injury (TBI) accelerates tau pathology in mice, leading to widespread neurofibrillary tangles. This suggests TBI is a significant risk factor for tauopathies, including Alzheimer's disease.
Area of Science:
- Neuroscience
- Neuropathology
- Molecular Biology
Background:
- Tauopathies, characterized by neurofibrillary tangles, are linked to tau protein misfolding and aggregation.
- Traumatic brain injury (TBI) is increasingly recognized as a potential risk factor for neurodegenerative diseases like Alzheimer's disease and chronic traumatic encephalopathy.
- The severity of TBI correlates with the propensity for developing these tau-related illnesses.
Purpose of the Study:
- To investigate whether moderate to severe TBI can initiate pathological tau formation.
- To determine if TBI can induce the spread of tau pathology throughout the brain.
- To establish TBI as a risk factor for tauopathies.
Main Methods:
- Tau transgenic mice were subjected to moderate to severe TBI.
- Tau phosphorylation and aggregation patterns were assessed post-injury.
- A spatial heat map was generated to visualize tau deposition and spreading.
Main Results:
- TBI-injured mice exhibited accelerated tau pathology compared to sham controls.
- Pathological tau appeared in brain regions distant from the injury site.
- The spread of tau pathology was observed to occur via synaptic connections.
Conclusions:
- TBI significantly accelerates tau hyperphosphorylation and aggregation in tau transgenic mice.
- Pathological tau disseminates from the injury site to connected brain regions.
- TBI is posited as a critical risk factor for the development and progression of tauopathies.
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