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Murine Model of Controlled Cortical Impact for the Induction of Traumatic Brain Injury
Published on: August 16, 2019
Exploring Pericontusional Temporal Metabolomic Changes after Controlled Cortical Impact in Mice
Amanda M Dave1,2, Helena C Oft3,4, Sambodh Sinha5,6
1Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Journal of Neurotrauma
|August 12, 2026
Summary
Traumatic brain injury (TBI) causes metabolic changes, including energy failure and impaired fat breakdown. Upregulated tryptophan metabolism suggests neuroinflammation, offering potential therapeutic targets.
Area of Science:
- Neuroscience
- Biochemistry
- Metabolomics
Background:
- Traumatic brain injury (TBI) is a major cause of death and disability.
- Metabolic alterations in the injured brain are not fully understood.
- Identifying biomarkers and therapeutic targets requires understanding acute-phase metabolic responses.
Purpose of the Study:
- To investigate time-dependent metabolic changes in the pericontusional tissue after TBI.
- To identify potential biomarkers and therapeutic targets by analyzing metabolites.
- To test the hypothesis of mitochondrial dysfunction and impaired beta-oxidation post-TBI.
Main Methods:
- Controlled cortical impact (CCI) model in mice.
- Targeted metabolomic analysis of TCA cycle intermediates, amino acids, and acylcarnitines.
- Liquid chromatography-high resolution mass spectrometry at 2, 6, 24, and 72 hours post-TBI.
Main Results:
- Two distinct metabolic phases: acute (2-6h) and subacute (24-72h).
- Progressive depletion of TCA cycle and glycolytic metabolites indicating energy failure.
- Accumulation of acylcarnitines and altered amino acid profiles, including upregulated tryptophan metabolism via the kynurenine pathway.
Conclusions:
- TBI induces significant, time-dependent metabolic alterations in pericontusional tissue.
- Impaired mitochondrial function and fatty acid oxidation are key features.
- Upregulated kynurenine pathway suggests a role for neuroinflammation, presenting potential therapeutic avenues.
