My research interests are primarily in spinal cord and brain injury. My work in biomarker discovery and inflammation led me to evaluating autoantibody production after human spinal cord injury (SCI). Studies using experimental models of SCI have shown that the release of CNS proteins into the circulation can trigger B-cell and T-cell responses leading to the production of autoantibodies. In rodent models of SCI, these autoantibodies have been shown to exacerbate tissue injury and impede functional recovery. I evaluated plasma autoantibodies after human SCI and discovered autoantibodies reactive to GFAP and CRMP2 present in the plasma within 2 weeks after injury. The presence of one or both of these autoantibodies increased the odds by 9.5 times of subsequently developing neuropathic pain within 6 months of SCI (p=0.006). Neuropathic pain is an adverse consequence of SCI that occurs in 40-70% of patients, markedly decreasing quality of life. It is unknown why one patient with SCI develops neuropathic pain while another with a similar injury does not. My ongoing collaborative work in a rat model is evaluating whether a causal link can be established between these autoantibodies and the development of neuropathic pain. Furthermore, I am evaluating additional potential autoantigens in order to expand the panel of autoantibodies, improving sensitivity and specificity for predicting the development of neuropathic pain in humans. The utility of this panel may be to identify patients for potential preventive treatments and potential new targets for therapy.
Publications/Creative Works
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