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<p>Traumatic spinal cord concussion (SCC) can result from motor vehicle accidents, contact sports, falls, and other mild traumatic events. Although clinically significant, the relationship between SCC severity and long‑term outcomes remains unclear. Identifying biochemical biomarkers that reflect post‑injury physiological and molecular changes may improve assessment and guide therapeutic decisions. Similar to advances in traumatic brain injury, integrating biomarkers with imaging and behavioral evaluations could enhance SCC characterization. This study examined biomarkers linked to neuroinflammation and repair mechanisms, ubiquitin C‑terminal hydrolase L1 (UCH‑L1), nitric oxide (NO), glial fibrillary acidic protein (GFAP), and brain‑derived neurotrophic factor (BDNF), and characterized their temporal profiles in a preclinical SCC model. Male Sprague–Dawley rats were assigned to either a blast‑induced SCC group or a sham group. Animals were euthanized at 24&#xa0;h, 72&#xa0;h, or 6 weeks post‑injury for spinal cord culture preparation and blood collection. UCH‑L1 and other neuronal injury markers remained elevated from the acute through chronic phases in spinal cord cultures and ex vivo serum, indicating neuronal damage. NO displayed a biphasic pattern with an early increase at 24&#xa0;h, a decrease at 72&#xa0;h, and renewed elevation at six weeks, suggestive of inflammatory and oxidative stress responses. GFAP levels rose progressively across all time points, consistent with glial activation. In contrast, BDNF levels showed minimal change, suggesting limited neurotrophic support after SCC. Overall, these biomarker expressions on the SCC cell culture and ex vivo serum indicate an ongoing neuronal stress, chronic inflammation, and glial reactivity. UCH‑L1 appears particularly promising for detecting and monitoring SCC‑related injury, while NO and GFAP offers complementary insight into inflammatory response. Combined with clinical assessments, these biomarkers may improve injury stratification and prediction of long‑term outcomes.</p>

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Temporal Biomarker Profiles Following Non-Surgical Spinal Cord Concussion

  • 期刊论文

  • 发表日期：

    2026年4月16日

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  • Taylor M. Dickson,
  • Anastasiya Loos,
  • Malaika Amin,
  • Juliana Vivas Lopez,
  • Susan F. Murphy,
  • Pamela J. VandeVord,
  • Kelly C. S. Roballo

摘要

Traumatic spinal cord concussion (SCC) can result from motor vehicle accidents, contact sports, falls, and other mild traumatic events. Although clinically significant, the relationship between SCC severity and long‑term outcomes remains unclear. Identifying biochemical biomarkers that reflect post‑injury physiological and molecular changes may improve assessment and guide therapeutic decisions. Similar to advances in traumatic brain injury, integrating biomarkers with imaging and behavioral evaluations could enhance SCC characterization. This study examined biomarkers linked to neuroinflammation and repair mechanisms, ubiquitin C‑terminal hydrolase L1 (UCH‑L1), nitric oxide (NO), glial fibrillary acidic protein (GFAP), and brain‑derived neurotrophic factor (BDNF), and characterized their temporal profiles in a preclinical SCC model. Male Sprague–Dawley rats were assigned to either a blast‑induced SCC group or a sham group. Animals were euthanized at 24 h, 72 h, or 6 weeks post‑injury for spinal cord culture preparation and blood collection. UCH‑L1 and other neuronal injury markers remained elevated from the acute through chronic phases in spinal cord cultures and ex vivo serum, indicating neuronal damage. NO displayed a biphasic pattern with an early increase at 24 h, a decrease at 72 h, and renewed elevation at six weeks, suggestive of inflammatory and oxidative stress responses. GFAP levels rose progressively across all time points, consistent with glial activation. In contrast, BDNF levels showed minimal change, suggesting limited neurotrophic support after SCC. Overall, these biomarker expressions on the SCC cell culture and ex vivo serum indicate an ongoing neuronal stress, chronic inflammation, and glial reactivity. UCH‑L1 appears particularly promising for detecting and monitoring SCC‑related injury, while NO and GFAP offers complementary insight into inflammatory response. Combined with clinical assessments, these biomarkers may improve injury stratification and prediction of long‑term outcomes.