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RESEARCH

Although spinal cord injury causes complex damage, a surprising amount of the basic circuitry to control movement and process information can remain intact. This is because the spinal cord is arranged in layers of circuitry. Many of the connections and neuronal cell bodies forming this circuitry above and below the site of injury survive the trauma. An important question to research scientists is how much do these surviving neurons "know"? Can they regenerate and make new, correct connections?

Research points to a multiplicity of possible interventions to promote recovery from a spinal injury. Some would be delivered immediately following the injury; others are less time-specific and involve rebuilding and reconnecting the injured cord. Clearly, both approaches are important: Limiting degeneration will enhance the probability of greater recovery, while stimulating regeneration will build upon the remaining system to restore lost connectivity, and perhaps to prevent further degeneration.

To cure the paralysis and loss of function that spinal cord injuries cause, doctors will need a carefully orchestrated series of interventions. Treatments will begin in the emergency room and continue for months. Even new forms of rehabilitation will be part of the therapeutic package. To speed the day when this regimen is available, the Sam Schmidt Paralysis Foundation supports research on a variety of fronts. Individual grants encourage a multi-disciplinary approach to solving the complex medical problems that result from spinal cord injuries, in both the acute and chronic stage.

RESEARCH FUNDING 2006

Katerina Akassoglou, PhD, University of California, San Diego, CA.
Fibrin depletion as a therapeutic strategy to enhance regeneration in the injured spinal cord.
Jaimie Borisoff, PhD, Neil Squire Brain Interface Laboratory, University of British Columbia, Canada.
Sensory substitution for the functional recovery of sexual sensations after SCI.
Jonah Chan , PhD, University of Southern California, Los Angeles, CA.
Identification of the axonal signals that control oligodendrocyte myelination.
Jon Kaas, PhD, Vanderbilt University, Nashville, TN.
Recoveries of forelimb use and somatosensory cortex activation in monkeys with and without treatments to promote axon growth after section of forelimb afferents in the spinal cord.
Richard Bernard Stein, PhD, University of Alberta, Canada.
Feedback control of walking after spinal cord injury.
Jeffery Lewis Twiss, MD, PhD, Alfred I DuPont Hospital for Children, Wilmington, DE.
RNA transport in regenerating axons.
Wee V. Yong, V., PhD, University of Calgary, Alberta, Canada.
Enhancing neuroprotection and regeneration in spinal cord injury by the combination of minocycline and glatiramer acetate.
The Mardian Family Fund to Cure Paralysis of the Sam Schmidt Paralysis Foundation.
John McDonald, PhD, MD; Dr. Monica Perez. International Center for Spinal Cord Injury, Kennedy Krieger Institute, Baltimore, MD.
Inter-CPG communication; harnessing the inherent potential of CPGs for recovery.
Sharon Matheny, PhD, University of Texas, Southwestern Medical School, Dallas, TX.
Molecular mediators of EphA4-induced axon inhibition in the CNS.
Dr. Wise Young, PhD, MD, W.M. Keck Center for Collaborative Neuroscience, The Spinal Cord Injury Project, Rutgers, The State University of New Jersey, Piscataway, NJ.
Dedicated to multidisciplinary collaborative research and to accelerating the transition of scientific discoveries into effective human therapies.

© 2008 Sam Schmidt Paralysis Foundation
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