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- David N Loy, Angela E Sroufe, Jennifer L Pelt, Darlene A Burke, Qi-Lin Cao, Jason F Talbott, and Scott R Whittemore.
- Kentucky Spinal Cord Injury Research Center, and Department of Neurological Surgery, University of Louisville School of Medicine, Louisville, Kentucky 40292, USA.
- Neurosurgery. 2005 Feb 1; 56 (2): 391-7; discussion 391-7.
ObjectiveWe evaluated whether serum levels of neuron-specific enolase (NSE) and S-100beta protein are biomarkers for traumatic injury in an animal model of spinal cord injury (SCI).MethodsEnzyme-linked immunosorbent assay serum measurements of NSE and S-100beta and assays of serum protein were compared at 6 and 24 hours after a graded contusive SCI (150 or 200 kdyn IH impactor injury (Infinite Horizons, L.L.C., Lexington, KY) or sham laminectomy at T9 in 30 female Sprague-Dawley rats. Serum from control animals was also analyzed.ResultsIncreases in serum levels of NSE were observed for 200-kdyn (3.1-fold, P < 0.001) and 150-kdyn (2.3-fold, P < 0.001) injury groups at 6 hours after injury, which decreased by 73.7% (P < 0.001) and 65.2% (P < 0.001) at 24 hours after SCI, respectively; the levels were still greater than in sham animals (P < 0.001, P = 0.001). The 200- and 150-kdyn injury groups were not different at either time point. S-100beta serum levels increased at 6 hours in the 200-kdyn injury group (P < 0.05), and no differences from sham levels were seen at 24 hours. No differences in total protein concentrations were observed between the injury and control groups.ConclusionPresent data suggest that NSE and S-100beta serum levels may be useful experimental tools for the acute measurement of tissue loss after SCI. Despite significant shortcomings, NSE and S-100beta serum measurements in acute SCI patients with clinically defined functional deficits should allow comparisons with well-characterized SCI animal models. Future efforts to develop biomarkers that predict functional outcomes in the acute phase should focus on axon-specific proteins as markers of secondary axonal loss and regeneration.
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