Traumatic Brain Injury Induces Tau Aggregation and Spreading
Open accessAbstract
The misfolding and aggregation of tau protein into neurofibrillary tangles is the main underlying hallmark of tauopathies. Most tauopathies have a sporadic origin and can be associated with multiple risk factors. Traumatic brain injury (TBI) has been suggested as a risk factor for tauopathies by triggering disease onset and facilitating its progression. Several studies indicate that TBI seems to be a risk factor to development of Alzheimer disease and chronic traumatic encephalopathy, because there is a relationship of TBI severity and propensity to development of these illnesses. In this study, we evaluated whether moderate to severe TBI can 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 brain injured tau transgenic mice have an accelerated tau pathology in different brain regions that increases over time compared with sham mice. The appearance of pathological tau occurs in regions distant to the injury area that are connected synaptically, suggesting dissemination of tau aggregates. Overall, this work posits TBI as a risk factor for tauopathies through the induction of tau hyperphosphorylation and aggregation.
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TBI triggers formation of pathological TauO and upregulation of senescence biomarkers in glial cells, establishing links among TBI, TauO, and cellular senescence.
“Importantly, TBI also triggers the formation of pathological TauO 108 , 109 and upregulation of senescence biomarkers in glial cells, thus establishing links among TBI, TauO, and cellular senescence. 108 , 110”
From Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies (2024) · cites this paper as [109]
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Tau Ablation Rewires Brain Cell Programs in Health and Restores Function in Disease
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- Authors
- Edwards, G., Zhao, J., Dash, P. K., Soto, C., & Moreno-Gonzalez, I.
- Affiliations
- The University of Texas Health Science Center at Houston (US)
- Mitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, The University of Texas Health Science Center at Houston, Houston, Texas.
- Venue
- Journal of Neurotrauma
- Publisher
- SAGE Publications
- Published
- 2019-12-11
- Volume
- 37
- Issue
- 1
- Pages
- 80-92
- ISSN
- 0897-7151 (ISSN-L)
- 1557-9042
- PMC
- PMC6921297
- OpenAlex
- W2963219749
- Cited by
- 195
- References
- 70
- Citations by year
- 2026: 19 · 2025: 31 · 2024: 25 · 2023: 42 · 2022: 37 · 2021: 24 · 2020: 14 · 2019: 3
- FWCI
- 13.75
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neurotrauma (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Repositorio Institucional de la Universidad de Málaga (University of Málaga) (acceptedVersion, cc-by)
- Funders
- U.S. Department of Defense (AZ160082, AZ160106)
- Alzheimer's Association (NIRG-394284)
- University of Texas System
- National Institutes of Health
- National Institute of Allergy and Infectious Diseases (P01AI077774)
- National Institute of Neurological Disorders and Stroke (F31NS103499)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- traumatic brain injury, tau protein, tau aggregation, tauopathy, tau propagation, tau phosphorylation, neurofibrillary tangles, Alzheimer's disease, chronic traumatic encephalopathy, tau transgenic mice, risk factors, synaptic connectivity
- MeSH terms
- Brain Injuries, Traumatic, Animals, Mice, Transgenic, tau Proteins, Mice, Protein Aggregation, Pathological
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