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Why Can’t We "Cure” Traumatic Brain Injury? Part 2

By: Douglas DeWitt, Ph.D., Director, Moody Center for Traumatic Brain & Spinal Cord Injury Research/Mission Connect  
    The previous column described some of the reasons why, despite the large number of potentially promising treatments identified in animal experiments, few have proven successful in human clinical trials.  We covered the challenges associated with the administration of treatment drugs or techniques soon after brain trauma and the heterogeneous nature of TBI.  This column will focus on the difficulties faced by investigators designing clinical trials of promising new TBI therapies.



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Featured Investigator

Olivera Nesic, Ph.D.

Role of Aquaporins in Spinal Cord Injury
Central nervous system (CNS) injuries such as TBI, stroke and spinal cord injury (SCI) often are associated with edema, the abnormal movement of water from blood vessels into brain tissue (vasogenic edema) or from the extracellular space into brain cells (cytotoxic edema). Since both types of edema can contribute to permanent brain or spinal cord damage, the regulation of water movement in the CNS is critically important.  Water movement across cell membranes is facilitated by a family of proteins called aquaporins (AQP).   Thirteen different AQPs have been identified with the most common in the brain being AQP1, AQP4, AQP5 and AQP9.  Dr. Olivera Nesic has been investigating the effects of contusion spinal cord injury (SCI) on AQP1 and AQP4 production and the role of AQPs in the generation of post-SCI neuropathic pain, chronic and often severe pain that occurs in many patients after SCI.  Dr. Nesic’s research will result in a better understanding of the role of AQPs in SCI and, hopefully, lead to new therapies to reduce permanent neuronal damage and neuropathic pain after SCI.
 

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