Authors: Alice Weatherston
Extensive research now suggests that head injuries in early to mid-life can increase the risk of dementia later in life, however the mechanism and biological changes underlying this association have remained little understood. New research from Imperial College London (UK), published today in Neurology, however has revealed that amyloid plaques identified in the brains of head injury patients shortly after an incident can remain in the brain for over a decade. The findings offer a possible explanation for the increase in dementia risk in brain injury patients and may help to influence the management and treatment of head injuries to reduce this risk.
“The consequences of a head injury have been called a hidden disability – although patients may seem to have outwardly made a good recovery, when we see them in clinic years later they can have persistent problems which affect their daily life ,” explained lead author Gregory Scott (Imperial College London).
The current study included a group of nine patients aged 38–55 years of age with moderate to severe traumatic brain injuries (TBI), mainly sustained through road traffic accidents between 11 months and 17 years prior to the investigation. Despite not exhibiting any physical disabilities, many of the subjects suffered regularly from problems with memory and concentration.
Researchers utilized C-Pittsburgh compound B PET imaging to identify amyloid plaques within the brains of TBI patients as well as the brains of nine healthy controls and 10 Alzheimer’s patients. Overall, TBI patients exhibited more amyloid plaques than healthy volunteers but fewer then Alzheimer’s patients. Specifically, the amyloid plaques in TBI patients were located in two main brain regions, namely the posterior cingulate cortex and the cerebellum, linking to problems with memory and motor control.
As a next step, damage to the white matter of the brain was also analyzed, indicating that amyloid plaque levels in the posterior cingulate cortex were associated with the extent of white matter damage, highlighting another possible trigger of amyloid plaque formation through traumatic axonal injury.
Scott commented: “This is a preliminary study, and it’s important to stress that these head injury patients didn’t have Alzheimer’s disease. However it supports the idea that the window of treatment for brain injury is potentially months or even years after the initial event. If we can find out exactly what processes are going on in the brain, it may be that we can intervene and improve long-term outcomes for patients.”
Source: Imperial College London press release