Research Reports - The neuroinflammatory response in humans after traumatic brain injury

Neuropathol Appl Neurobiol. 2012 Dec 11

Smith C, Gentleman SM, Leclercq PD, Murray LS, Griffin WS, Graham DI, Nicoll JA

AIMS: Traumatic brain injury is a significant cause of morbidity and mortality
worldwide. An epidemiological association between head injury and long-term
cognitive decline has been described for many years and recent clinical studies
have highlighted functional impairment within 12 months of a mild head injury. In
addition chronic traumatic encephalopathy is a recently described condition in
cases of repetitive head injury. There are shared mechanisms between traumatic
brain injury and Alzheimer's disease, and it has been hypothesised that
neuroinflammation, in the form of microglial activation, may be a mechanism
underlying chronic neurodegenerative processes after traumatic brain injury.
METHODS: This study assessed the microglial reaction after head injury in a range
of ages and survival periods, from <24 hours survival through to 47 years
survival. Immunohistochemistry for reactive microglia (CD68 and CR3/43) was
performed on human autopsy brain tissue and assessed "blind" by quantitative
image analysis. Head injury cases were compared to age matched controls, and
within the traumatic brain injury group cases with diffuse traumatic axonal
injury were compared to cases without diffuse traumatic axonal injury. RESULTS: A
major finding was a neuroinflammatory response which develops within the first
week and persists for several months after TBI, but has returned to control
levels after several years. In cases with diffuse traumatic axonal injury the
microglial reaction is particularly pronounced in the white matter. CONCLUSIONS:
These results demonstrate that prolonged microglial activation is a feature of
traumatic brain injury, but that the neuroinflammatory response returns to
control levels after several years.

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