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

Neuropathol Appl Neurobiol. 2013 Oct;39(6):654-66

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 hypothesized 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-h survival through to 47-year 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 with age matched controls, and within the
traumatic brain injury group cases with diffuse traumatic axonal injury were
compared with cases without diffuse traumatic axonal injury.
RESULTS: A major finding was a neuroinflammatory response that develops within
the first week and persists for several months after traumatic brain injury, 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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