| ironjustice@aol.com 2006-03-24, 11:31 am |
| Traumatic injury to the immature brain: inflammation, oxidative injury,
and iron-mediated damage as potential therapeutic targets.
Potts MB, Koh SE, Whetstone WD, Walker BA, Yoneyama T, Claus CP,
Manvelyan HM, Noble-Haeusslein LJ
NeuroRx. 2006 Apr ; 3(2): 143-53
Traumatic brain injury (TBI) is the leading cause of morbidity and
mortality among children and both clinical and experimental data reveal
that the immature brain is unique in its response and vulnerability to
TBI compared to the adult brain. Current therapies for pediatric TBI
focus on physiologic derangements and are based primarily on adult
data. However, it is now evident that secondary biochemical
perturbations play an important role in the pathobiology of pediatric
TBI and may provide specific therapeutic targets for the treatment of
the head-injured child. In this review, we discuss three specific
components of the secondary pathogenesis of pediatric TBI -
inflammation, oxidative injury, and iron-induced damage - and potential
therapeutic strategies associated with each. The inflammatory response
in the immature brain is more robust than in the adult and
characterized by greater disruption of the blood-brain barrier and
elaboration of cytokines. The immature brain also has a muted response
to oxidative stress compared to the adult due to inadequate expression
of certain antioxidant molecules. In addition, the developing brain is
less able to detoxify free iron after TBI-induced hemorrhage and cell
death. These processes thus provide potential therapeutic targets that
may be tailored to pediatric TBI, including anti-inflammatory agents
such as minocycline, antioxidants such as glutathione peroxidase, and
the iron chelator deferoxamine.
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