Publications by authors named "Toufik Taib"

Article Synopsis
  • Traumatic brain injury (TBI) can cause serious inflammation in the brain by activating special cells called microglia.
  • A study looked at how a specific protein (TSPO) helps track this activation using special imaging and tests on mice with mild TBI.
  • The results showed that while microglia do increase after injury, they're not the only cells affecting the TSPO levels, suggesting that TSPO might not be the best way to track microglial activity alone.
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Traumatic brain injury (TBI) is a leading cause of death and disability all over the world. TBI leads to (1) an inflammatory response, (2) white matter injuries and (3) neurodegenerative pathologies in the long term. In humans, TBI occurs most often in children and adolescents or in the elderly, and it is well known that immune responses and the neuroregenerative capacities of the brain, among other factors, vary over a lifetime.

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Traumatic brain injury (TBI) is a chronic pathology, inducing long-term deficits that remain understudied in pre-clinical studies. In this context, exploration, anxiety-like behavior, cognitive flexibility, and motor coordination were assessed until 5 and 10 months after an experimental TBI in the adult mouse, using two cohorts. In order to differentiate age, surgery, and remote gray and white matter lesions, three groups (unoperated, sham-operated, and TBI) were studied.

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Traumatic brain injury (TBI) results in white matter injury (WMI) that is associated with neurological deficits. Neuroinflammation originating from microglial activation may participate in WMI and associated disorders. To date, there is little information on the time courses of these events after mild TBI.

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