http://brain.oxfordjournals.org/content/136/1/28.abstract
Summary
A single traumatic brain injury is
associated with an increased risk of dementia and, in a proportion of
patients surviving
a year or more from injury, the development of
hallmark Alzheimer’s disease-like pathologies. However, the pathological
processes
linking traumatic brain injury and
neurodegenerative disease remain poorly understood. Growing evidence
supports a role for
neuroinflammation in the development of Alzheimer’s
disease. In contrast, little is known about the neuroinflammatory
response
to brain injury and, in particular, its temporal
dynamics and any potential role in neurodegeneration. Cases of traumatic
brain injury with survivals ranging from 10 h to 47
years post injury (n = 52) and age-matched, uninjured control subjects (n
= 44) were selected from the Glasgow Traumatic Brain Injury archive.
From these, sections of the corpus callosum and adjacent
parasaggital cortex were examined for microglial
density and morphology, and for indices of white matter pathology and
integrity.
With survival of ≥3 months from injury, cases with
traumatic brain injury frequently displayed extensive, densely packed,
reactive microglia (CR3/43- and/or
CD68-immunoreactive), a pathology not seen in control subjects or
acutely injured cases.
Of particular note, these reactive microglia were
present in 28% of cases with survival of >1 year and up to 18 years
post-trauma.
In cases displaying this inflammatory pathology,
evidence of ongoing white matter degradation could also be observed.
Moreover,
there was a 25% reduction in the corpus callosum
thickness with survival >1 year post-injury. These data present
striking
evidence of persistent inflammation and ongoing
white matter degeneration for many years after just a single traumatic
brain
injury in humans. Future studies to determine
whether inflammation occurs in response to or, conversely, promotes
white matter
degeneration will be important. These findings may
provide parallels for studying neurodegenerative disease, with traumatic
brain injury patients serving as a model for
longitudinal investigations, in particular with a view to identifying
potential
therapeutic interventions.
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