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Traumatic brain injury: a disease process, not an event.
If the chronic nature of TBI is recognized by government and private funding agencies, research can be directed at discovering therapies that may interrupt the disease processes months or even years after the initiating event.
Traumatic cerebral vascular injury: the effects of concussive brain injury on the cerebral vasculature.
A more thorough understanding of the direct and indirect effects of trauma on the cerebral vasculature will lead to improvements in current treatments of brain trauma as well as to the development of novel and, hopefully, more effective therapeutic strategies.
Rapid Accumulation of Endogenous Tau Oligomers in a Rat Model of Traumatic Brain Injury
- B. E. Hawkins, Shashirekha Krishnamurthy, R. Kayed
- BiologyThe Journal of Biological Chemistry
- 30 April 2013
The results suggest that targeting Tau oligomers may be useful for the prevention of dementia following TBI and diagnostic tools and therapeutics that target only toxic forms of Tau may provide earlier detection and safe, more effective treatments for tauopathies associated with repetitive neurotrauma.
Enduring suppression of hippocampal long-term potentiation following traumatic brain injury in rat
The effects of traumatic brain injury on cerebral blood flow and brain tissue nitric oxide levels and cytokine expression.
TBI-induced expression of mRNAs for interleukin-1 alpha (IL-1alpha), IL-1beta, IL-6, and tumor necrosis factor-alpha (TNFa) and cytokine expression was unchanged after TBI and brain tissue NO levels remained constant in the sham-injured rats but decreased significantly after moderate TBI.
The effects of traumatic brain injury on regional cerebral blood flow in rats.
In rats, the most prominent cerebral circulatory changes following fluid percussion injury were early reductions of CBF and an increasingly heterogeneous CBF pattern and the traumatized group exhibited heterogeneous decreases in CBF following trauma.
L-arginine and superoxide dismutase prevent or reverse cerebral hypoperfusion after fluid-percussion traumatic brain injury.
- D. Dewitt, T. G. Smith, D. Deyo, K. Miller, T. Uchida, D. Prough
- Biology, MedicineJournal of neurotrauma
- 1 April 1997
It is indicated that L-arginine but not D-arg inine administered after TBI prevents posttraumatic hypoperfusion and that pretreatment with SOD will restore CBF after a brief period of hyp operfusion.
Enhanced vulnerability to secondary ischemic insults after experimental traumatic brain injury.
Although numerous mediators may be involved in increased tissue sensitivity, those that particularly merit investigation include oxygen free radicals, glutamate, arachidonate metabolites, calcium ions, and protein kinase C.
Challenges in the development of rodent models of mild traumatic brain injury.
- D. Dewitt, R. Perez-Polo, C. Hulsebosch, P. Dash, C. Robertson
- Biology, PsychologyJournal of neurotrauma
- 1 May 2013
TBI in humans is associated with acute symptoms such as loss of consciousness and pre- and/or posttraumatic amnesia, and many mTBI patients experience long-term effects, including deficits in speed of information processing, attention and concentration, memory acquisition, retention and retrieval, and reasoning and decision-making.
Inflammatory consequences in a rodent model of mild traumatic brain injury.
There are inflammatory consequences to mTBI that persist over time and, in part, are responsible for resultant pathogenesis and clinical outcomes, as well as evidence of heightened cellular stress and blood-brain barrier dysfunction.