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traumatic-brain-injury
9 studies tagged traumatic-brain-injury, dated 2010-05-01 to 2023-08-31. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- Application of P7C3 Compounds to Investigating and Treating Acute and Chronic Traumatic Brain Injury 2023-08-31
- Traumatic brain injury (TBI) in collision sports: Possible mechanisms of transformation into chronic traumatic encephalopathy (CTE) 2019-11-01
- Linguistic and Cultural Acceptability of a Spanish Translation of the Ohio State University Traumatic Brain Injury Identification Method Among Community-Dwelling Spanish-Dominant Older Adults 2019-09-06
Studies
9 studies carry this tag.
Date range
2010 to 2023
Top journals
- Journal of neurotrauma 2
- Archives of rehabilitation research and clinical translation 1
- Brain : a journal of neurology 1
- Frontiers in neurology 1
- Metabolism: clinical and experimental 1
8 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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40/100
Traumatic brain injury (TBI) is a leading worldwide cause of disability, and there are currently no medicines that prevent, reduce, or reverse acute or chronic neurodegeneration in TBI patients.
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TBI arising from closed head trauma (CHT) significantly increases the risk of developing Alzheimer's disease (AD), Parkinson's disease (PD) and chronic traumatic encephalopathy (CTE).
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This linguistically optimized Spanish translation of the OSU TBI-ID is recommended for use as a semistructured interview among Spanish-dominant older adults.
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Traumatic brain injuries (TBI) are an important public health challenge.
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Traumatic brain injury (TBI) may be a significant risk factor for development of neurodegenerative disorders such as chronic traumatic encephalopathy (CTE), post-traumatic epilepsy (PTE), and Alzheimer's (AD) and Parkinson's (PD) diseases.
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Moderate-to-severe traumatic brain injury is one of the strongest environmental risk factors for the development of neurodegenerative diseases such as late-onset Alzheimer's disease, although it is unclear whether mild traumatic brain injury, or concussion, also confers risk.
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Increasing evidence suggests that the calcineurin (CN)-dependent transcription factor NFAT (Nuclear Factor of Activated T cells) mediates deleterious effects of astrocytes in progressive neurodegenerative conditions.
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Ascorbate, LMWT, and protein thiols were reduced at 2 and 24 h; by 24 h, HNE was increased.
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Traumatic brain injury (TBI) has devastating acute effects and in many cases seems to initiate long-term neurodegeneration.