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Axonal pathology in traumatic brain injury
Widespread Tau and Amyloid‐Beta Pathology Many Years After a Single Traumatic Brain Injury in Humans
It is demonstrated that widespread NFT and Aβ plaque pathologies are present in up to a third of patients following survival of a year or more from a single TBI, which suggests that a one TBI induces long‐term neuropathological changes akin to those found in neurodegenerative disease.
Inflammation and white matter degeneration persist for years after a single traumatic brain injury.
- V. Johnson, J. Stewart, F. Begbie, J. Trojanowski, Douglas H. Smith, W. Stewart
- Biology, MedicineBrain : a journal of neurology
Findings may provide parallels for studying neurodegenerative disease, with traumatic brain injury patients serving as a model for longitudinal investigations, in particular with a view to identifying potential therapeutic interventions.
Axonal Damage in Traumatic Brain Injury
Future advancements in the prevention and treatment of traumatic axonal injury will depend on the collective understanding of the relationship between the biomechanics and pathophysiology of various phases of axonal trauma.
Diffuse Axonal Injury in Head Trauma
Diffuse axonal injury is one of the most common and important pathologic features of traumatic brain injury and is poorly defined as clinical syndrome, but future advancements in the diagnosis and treatment will be dependent on the collective understanding of injury biomechanics, temporal axonal pathophysiology, and its role in patient outcome.
Chronic neuropathologies of single and repetitive TBI: substrates of dementia?
Little consensus currently exists on specific features of these post-TBI syndromes that might permit their confident clinical and/or pathological diagnosis, and the mechanisms contributing to neurodegeneration following TBI largely remain unknown.
Multiple proteins implicated in neurodegenerative diseases accumulate in axons after brain trauma in humans
Traumatic brain injury and amyloid-β pathology: a link to Alzheimer's disease?
The mechanistic underpinnings of the link between TBI and AD are explored, focusing on the hypothesis that rapid Aβ plaque formation may result from the accumulation of amyloid precursor protein in damaged axons and a disturbed balance between Aβ genesis and catabolism following TBI.
FINITE ELEMENT MODELING APPROACHES FOR PREDICTING INJURY IN AN EXPERIMENTAL MODEL OF SEVERE DIFFUSE AXONAL INJURY
This study clearly demonstrated that the modeling approach which represented the relative motion between the skull and cerebral cortex as a frictional interface best predicted the resulting injury pattern in a 5th axial plane animal experiment.
Biomarkers of mild traumatic brain injury in cerebrospinal fluid and blood
The need for biomarkers of injury to different structures and cell types in the CNS that can be detected in body fluids in young individuals to prevent long-term neurological sequelae due to concussive or subconcussive blows to the head is focused on.