Research Reports - Inflammation and white matter degeneration persist for years after a single traumatic brain injury

Brain. 2013 Jan;136(Pt 1):28-42

Johnson VE, Stewart JE, Begbie FD, Trojanowski JQ, Smith DH, Stewart W

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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