Mitochondrial damage and dysfunction in traumatic brain injury

Jonathan Lifshitz, Patrick G. Sullivan, David A. Hovda, Tadeusz Wieloch, Tracy K. McIntosh

Research output: Contribution to journalArticle

134 Scopus citations

Abstract

The enduring cognitive deficits and histopathology associated with traumatic brain injury (TBI) may arise from damage to mitochondrial populations, which initiates the metabolic dysfunction observed in clinical and experimental TBI. The anecdotal evidence for in vivo structural damage to mitochondria corroborates metabolic and physiologic dysfunction, which depletes substrates and promotes free radical generation. Excessive calcium pathology differentially disrupts the heterogeneous mitochondrial population, such that calcium sensitivity increases after TBI. The ongoing pathology may escalate to include protein and DNA oxidation that impacts mitochondrial function and promotes cell death. Thus, in vivo TBI damages, if not eliminates, mitochondrial populations depending on injury severity, with the remaining population left to provide metabolic support for survival or repair in the wake of cellular pathology. With a considerable understanding of post-injury mitochondrial populations, therapeutic interventions targeted to the mitochondria may delay or prevent secondary cascades that lead to long-term cell death and neurobehavioral disability.

Original languageEnglish (US)
Pages (from-to)705-713
Number of pages9
JournalMitochondrion
Volume4
Issue number5-6 SPEC. ISS.
DOIs
StatePublished - Sep 2004
Externally publishedYes

Keywords

  • Brain injury
  • Metabolism
  • Mitochondria

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology
  • Cell Biology

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  • Cite this

    Lifshitz, J., Sullivan, P. G., Hovda, D. A., Wieloch, T., & McIntosh, T. K. (2004). Mitochondrial damage and dysfunction in traumatic brain injury. Mitochondrion, 4(5-6 SPEC. ISS.), 705-713. https://doi.org/10.1016/j.mito.2004.07.021