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Peer-reviewedCC BY 4.0Frontiers in Pharmacology

Omics-guided therapeutic translation in acute traumatic brain injury

  • Logan R. Van Nynatten1,2
  • Enis Cela2
  • Aleah Wilson1
  • Ian Ball1,3,4
  • Douglas D. Fraser2,4,5,6,7,8
8 affiliations
  1. 1Division of Critical Care Medicine, Department of Medicine, Schulich School of Medicine and Dentistry, Western University
  2. 2Physiology and Pharmacology, Western University
  3. 3Epidemiology and Biostatistics, Western University
  4. 4London Health Sciences Centre Research Institute, Western University
  5. 5Division of Critical Care Medicine, Department of Pediatrics, Schulich School of Medicine and Dentistry, Western University
  6. 6Clinical Neurological Sciences, Western University
  7. 7Children’s Health Research Institute
  8. 8GSK Chair in Clinical Pharmacology, Western University
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Abstract

Decades of trials evaluating secondary-injury targeted therapeutics in traumatic brain injury (TBI) have failed almost without exception, typically concluding that the intervention was ineffective. We argue that these failures stem largely from methodological limitations and should be reconceptualized. TBI pathobiology has traditionally been studied, stratified, and treated using single markers, isolated mechanisms, and discrete timepoints, despite being heterogeneous, compartmentalized, and temporally dynamic. High-dimensional omics, interpreted at the level of biological pathways rather than individual analytes, offers a direct means of addressing this complexity. Focusing on the acute phase of moderate-to-severe TBI, we define four recurrent failure modes in TBI therapeutic translation: the wrong patient, the wrong sample, the wrong window, and the wrong mechanism. For each, we identify targeted omics and pathway-level strategies that can mitigate these limitations and summarize what such approaches have revealed about TBI pathobiology. Finally, we argue that pathway-based predictive enrichment, combined with drug repurposing, is a promising near-term strategy that may improve the odds of detecting a real treatment effect where unselected trials have not.

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Cite

BibTeXRIS
BibTeX
@article{nynatten2026omicsguided,
  title = {{Omics-guided therapeutic translation in acute traumatic brain injury}},
  author = {Logan R. Van Nynatten and Enis Cela and Aleah Wilson and Ian Ball and Douglas D. Fraser},
  journal = {Frontiers in Pharmacology},
  year = {2026},
  month = oct,
  doi = {10.3389/fphar.2026.1968318},
  url = {https://www.frontiersin.org/articles/10.3389/fphar.2026.1968318/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Omics-guided therapeutic translation in acute traumatic brain injury
AU  - Logan R. Van Nynatten
AU  - Enis Cela
AU  - Aleah Wilson
AU  - Ian Ball
AU  - Douglas D. Fraser
PY  - 2026
DA  - 2026/10/28
JO  - Frontiers in Pharmacology
DO  - 10.3389/fphar.2026.1968318
UR  - https://www.frontiersin.org/articles/10.3389/fphar.2026.1968318/full
AB  - Decades of trials evaluating secondary-injury targeted therapeutics in traumatic brain injury (TBI) have failed almost without exception, typically concluding that the intervention was ineffective. We argue that these failures stem largely from methodological limitations and should be reconceptualized. TBI pathobiology has traditionally been studied, stratified, and treated using single markers, isolated mechanisms, and discrete timepoints, despite being heterogeneous, compartmentalized, and temporally dynamic. High-dimensional omics, interpreted at the level of biological pathways rather than individual analytes, offers a direct means of addressing this complexity. Focusing on the acute phase of moderate-to-severe TBI, we define four recurrent failure modes in TBI therapeutic translation: the wrong patient, the wrong sample, the wrong window, and the wrong mechanism. For each, we identify targeted omics and pathway-level strategies that can mitigate these limitations and summarize what such approaches have revealed about TBI pathobiology. Finally, we argue that pathway-based predictive enrichment, combined with drug repurposing, is a promising near-term strategy that may improve the odds of detecting a real treatment effect where unselected trials have not.
SN  - 1663-9812
ER  -