Gary M Fiskum

Publication Detail

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The potential role of mitochondria in pediatric traumatic brain injury.

Courtney L Robertson; Lucian Soane; Zachary T Siegel; Gary Fiskum (Profiled Author: Gary M Fiskum)

Department of Pediatrics, University of Maryland School of Medicine, Baltimore, MD 21201, USA. croberts@peds.umaryland.edu
Developmental neuroscience 2006;28(4-5):432-46.

Mitochondria 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.

2 Originating Grant

• 1.

  MCKENNA, MARY C

  Metabolic &Developmental Aspects of Intellectual Disability

  1 May 1997 - 31 January 2014

  EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT

• 2.

  Zielke, H Ronald

  Metabolic & Developmental Aspects of Mental Retardation

  1 May 1997 - 31 January 2009

  NATIONAL INSTITUTE OF CHILD HEALTH AND HUMAN DEVELOPMENT

Scientific Context

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