Systemic inflammation exacerbates behavioral and histopathological consequences of isolated traumatic brain injury in rats.

Abstract

The proinflammatory cytokine interleukin-1beta (IL-1beta) is induced rapidly after traumatic brain injury (TBI) and contributes to the inflammatory events that lead to neuronal loss. Although an important source of IL-1beta is from the injured brain itself, in patients with multiple organ trauma (polytrauma) IL-1beta is also released into the bloodstream… (More)
DOI: 10.1016/j.expneurol.2008.02.001

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