Evidence map›Paper›PMID 41989634›Full record

ArticleJournal of molecular neuroscience : MN2026

Temporal Biomarker Profiles Following Non-Surgical Spinal Cord Concussion.

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

Abstract read
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Article in Journal of molecular neuroscience : MN, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Taylor M DicksonDeparment of Biomedical Research, Edward Via College of Osteopathic Medicine, Blacksburg, VA, USA.
Anastasiya LoosDeparment of Biomedical Research, Edward Via College of Osteopathic Medicine, Blacksburg, VA, USA.
Malaika AminDeparment of Biomedical Research, Edward Via College of Osteopathic Medicine, Blacksburg, VA, USA.
Juliana Vivas LopezDepartment of Biological Sciences, Virginia Tech, Blacksburg, VA, USA.
Susan F MurphyDepartment of Biomedical Engineering, Virginia Tech, Blacksburg, VA, USA.
Pamela J VandeVordDepartment of Biomedical Engineering, Virginia Tech, Blacksburg, VA, USA.
Kelly C S RoballoDeparment of Biomedical Research, Edward Via College of Osteopathic Medicine, Blacksburg, VA, USA. kroballo@vcom.edu.

Funding

REAP ICTAS years 2023, 2024 and 2025 23: 1038626; 23-0041-A0001, 22-0046-A0001, 25-0034-A0002
6 · The paper itself

Abstract

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.

Indexed as

Spinal Cord InjuriesUbiquitin ThiolesteraseAnimalsBiomarkersBrain-Derived Neurotrophic FactorGlial Fibrillary Acidic ProteinMaleNitric OxideRatsRats, Sprague-DawleySpinal CordBdnf protein, ratBiomarkersBrain-Derived Neurotrophic FactorGfap protein, ratGlial Fibrillary Acidic ProteinNitric OxideUbiquitin ThiolesteraseUCHL1 protein, ratBack painBiomarkersConcussionSpinal cord injury

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Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.