Neurotoxic tau oligomers after single versus repetitive mild traumatic brain injury
Open accessAbstract
Mild traumatic brain injury accounts for the majority of head injuries and has been correlated with neurodegeneration and dementia. While repetitive mild traumatic brain injury is highly correlated to neurodegeneration, the correlation of a single mild traumatic brain injury with neurodegeneration is still unclear. Because tau aggregates are the main form of mild traumatic brain injury induced pathology, toxic forms of tau protein most likely play a role in the development of post-mild traumatic brain injury neurodegeneration. Therefore, it becomes crucial to characterize the properties of soluble tau aggregates in single versus repetitive mild traumatic brain injury. Herein, we isolated tau oligomers from wild-type mice exposed to single or repetitive mild traumatic brain injury and characterized the tau aggregates at functional, biochemical and biophysical levels. We demonstrated that single versus repetitive mild traumatic brain injuries frequencies lead to the formation of different tau oligomeric polymorphisms. These polymorphisms express different long-term potentiation impairment potencies, toxicity potentials, morphologies and strain indicating properties. To our knowledge, this is the first evidence that soluble tau oligomers derived from single versus repetitive mild traumatic brain injuries form distinct polymorphisms that possibly correlate with the risk of neurodegeneration after mild traumatic brain injury.
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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 [108]
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- Authors
- Bittar, A., Bhatt, N., Hasan, T. F., Montalbano, M., Puangmalai, N., McAllen, S., Ellsworth, A., Carretero Murillo, M., Taglialatela, G., Lucke-Wold, B., Logsdon, A., Rosen, C., Turner, R. C., & Kayed, R.
- Affiliations
- The University of Texas Medical Branch at Galveston (US)
- Louisiana State University Health Sciences Center Shreveport (US)
- Department of Neurology, The Mitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, TX 77555-1045, USA
- Baylor College of Medicine, Houston, TX 77030, USA
- University of Florida (US)
- University of Washington (US)
- Central Illinois Neural Health Sciences, Bloomington, IL 61701, USA
- West Virginia University (US)
- Corresponding author
- Kayed, Rakez
- ORCID
- Venue
- Brain Communications
- Publisher
- Oxford University Press (OUP)
- Published
- 2019-01-01
- Volume
- 1
- Issue
- 1
- Pages
- fcz004-fcz004
- ISSN
- 2632-1297 (ISSN-L)
- PMC
- PMC6777515
- OpenAlex
- W2965540189
- Cited by
- 60
- References
- 54
- Citations by year
- 2026: 6 · 2025: 11 · 2024: 9 · 2023: 10 · 2022: 13 · 2021: 3 · 2020: 7 · 2019: 1
- FWCI
- 4.11
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Brain Communications (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Gillson Longenbaugh foundation
- National Institutes of Health (AG054025, RFA1AG055771)
- 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
- mild traumatic brain injury, repetitive mild traumatic brain injury, tau oligomers, neurodegeneration, long-term potentiation, tau toxicity, traumatic brain injury
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