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Multiple proteins implicated in neurodegenerative diseases accumulate in axons after brain trauma in humans
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.
Traumatic Axonal Injury Induces Proteolytic Cleavage of the Voltage-Gated Sodium Channels Modulated by Tetrodotoxin and Protease Inhibitors
Results suggest a unique “feed-forward” deleterious process initiated by mechanical trauma of axons, where initial increases in [Ca2+]i and subsequent proteolysis of the NaCh α-subunit are triggered by initial influx through NaChs resulting from axonal deformation.
Long-Term Accumulation of Amyloid-β, β-Secretase, Presenilin-1, and Caspase-3 in Damaged Axons Following Brain Trauma
Long-term accumulation of amyloid-beta, beta-secretase, presenilin-1, and caspase-3 in damaged axons following brain trauma.
- Xiao-Han Chen, R. Siman, A. Iwata, D. Meaney, J. Trojanowski, Douglas H. Smith
- BiologyThe American journal of pathology
Plaques composed of amyloid beta (Abeta) have been found within days following brain trauma in humans, similar to the hallmark plaque pathology of Alzheimer's disease (AD). Here, we evaluated the…
Intravascular coagulation: a major secondary insult in nonfatal traumatic brain injury.
The authors found a strong association between the severity of coagulopathy and the density of IC, suggesting that IC is a universal response to TBI and an important secondary cerebral insult.
Mild traumatic brain injury and diffuse axonal injury in swine.
A model of head rotational acceleration in swine is adapted to produce mTBI by scaling the mechanical loading conditions based on available biomechanical data on concussion thresholds in humans, and demonstrates that surprisingly overt axonal pathology may be present, even in cases without a sustained loss of consciousness.
A Lack of Amyloid β Plaques Despite Persistent Accumulation of Amyloid β in Axons of Long‐Term Survivors of Traumatic Brain Injury
- Xiao-Han Chen, V. Johnson, K. Uryu, J. Trojanowski, Douglas H. Smith
- BiologyBrain pathology
- 1 April 2009
These findings fail to support the premise that progressive plaque pathology after TBI ultimately results in AD, and a potential mechanism for Aβ plaque regression was suggested by the post‐injury accumulation of an Aβ degrading enzyme, neprilysin.
Amyloid beta accumulation in axons after traumatic brain injury in humans.
The results of this study indicate that damaged axons can serve as a large reservoir of Abeta, which may contribute to Abeta plaque formation after TBI in humans.
Association between Intravascular Microthrombosis and Cerebral Ischemia in Traumatic Brain Injury
Data support a strong link between intravascular microthrombosis and neuronal death after brain trauma in humans and may have important implications for new therapeutic approaches.