ArticleFrontiers in neuroscience2026
Article in Frontiers in neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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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.
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction and objective: Populations at high altitude (HA) face a higher incidence and severity of traumatic brain injury (TBI). This pilot study utilized longitudinal Methods: Male C57BL/6J mice were exposed to simulated HA (5,000 m) or sea level (SL) for 12 weeks. Following adaptation, a unilateral mTBI was induced via closed head injury (CHI). Mice were then monitored for an additional 2 weeks at HA (total duration of 14 weeks). Results: Chronic HA exposure induced significant reductions in myo-inositol (Ins) and total choline (tCho) in the hippocampus, establishing a baseline of metabolic fragility that sensitized the brain to subsequent traumatic insult. Post-mTBI, the HA group exhibited a profound "metabolic crisis," characterized by significantly lower tCho and failed recovery of total N-acetylaspartate (tNAA) compared to SL controls. Total creatine (tCr) was the most acutely affected metabolite, underscoring a depletion of the bioenergetic reserve. Conclusion: Chronic hypobaric hypoxia fundamentally alters baseline brain metabolism and impairs the neurochemical recovery from mTBI. These findings suggest that standard recovery protocols may be insufficient for HA-adapted populations and highlight
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