• Courtney L Robertson, Lucian Soane, Zachary T Siegel, and Gary Fiskum.
• Department of Pediatrics, University of Maryland School of Medicine, Baltimore, MD 21201, USA. croberts@peds.umaryland.edu
• Dev. Neurosci. 2006 Jan 1; 28 (4-5): 432-46.

AbstractMitochondria play a central role in cerebral energy metabolism, intracellular calcium homeostasis and reactive oxygen species generation and detoxification. Following traumatic brain injury (TBI), the degree of mitochondrial injury or dysfunction can be an important determinant of cell survival or death. Literature would suggest that brain mitochondria from the developing brain are very different from those from mature animals. Therefore, aspects of developmental differences in the mitochondrial response to TBI can make the immature brain more vulnerable to traumatic injury. This review will focus on four main areas of secondary injury after pediatric TBI, including excitotoxicity, oxidative stress, alterations in energy metabolism and cell death pathways. Specifically, we will describe what is known about developmental differences in mitochondrial function in these areas, in both the normal, physiologic state and the pathologic state after pediatric TBI. The ability to identify and target aspects of mitochondrial dysfunction could lead to novel neuroprotective therapies for infants and children after severe TBI.Copyright (c) 2006 S. Karger AG, Basel.

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