What this means
Traumatic brain injury (TBI) evolves through time-dependent secondary injury, but whether seawater (SW) immersion merely amplifies pathology or reshapes the temporal trajectory of post-traumatic biology remains unclear. Here, we applied time-resolved proteomics to mouse brains after controlled cortical impact (CCI) with or without artificial SW immersion at 1, 3, 7, and 28 days post-injury.
A plain-English summary is on its way. Until then, this is the start of the authors' own summary.
- Who it was tested in
- Animals or cells
- Kind of research
- Research in animals or cells
The science
- Original title
- Seawater immersion reshapes the temporal dynamics of traumatic brain injury and reveals mitochondrial oxidative stress as a modifiable therapeutic target.
- Authors
- Li W, He R, Xie S et al.
- Journal
- Experimental neurology
- Published
- Aug 14, 2026
- Study type
- Lab or animal study · indexed as animal research
- PMID
- 42600764 ↗
Abstract
Traumatic brain injury (TBI) evolves through time-dependent secondary injury, but whether seawater (SW) immersion merely amplifies pathology or reshapes the temporal trajectory of post-traumatic biology remains unclear. Here, we applied time-resolved proteomics to mouse brains after controlled cortical impact (CCI) with or without artificial SW immersion at 1, 3, 7, and 28 days post-injury. Trajectory-based proteomic analysis revealed that SW immersion altered the direction, magnitude, timing, persistence, and recovery of protein responses, rather than simply intensifying TBI-induced changes. This remodeled trajectory exhibited phase-specific patterns, including SW-dominant, synergistically enhanced, and attenuated responses, highlighting mitochondrial oxidative stress, inflammatory activation, complement/coagulation disturbance, and impaired structural repair. Phenotypic validation confirmed phase-specific deficits, including acute inflammatory-redox injury, impaired neuronal survival, chronic axon-myelin disruption, and incomplete behavioral recovery. SS-31 partially mitigated selected inflammatory, redox, neuronal, and white matter abnormalities, supporting mitochondrial oxidative stress as a modifiable node rather than the sole driver of trajectory remodeling. These findings identify seawater immersion as a temporal modifier of secondary injury and emphasize that environmental trauma may require trajectory-informed, phase-specific therapeutic interventions.
Li W, He R, Xie S et al. Seawater immersion reshapes the temporal dynamics of traumatic brain injury and reveals mitochondrial oxidative stress as a modifiable therapeutic target. Experimental neurology. 2026. doi:10.1016/j.expneurol.2026.115979. PMID: 42600764. https://pubmed.ncbi.nlm.nih.gov/42600764/
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