Traumatic Brain Injury May Contribute to Amyloid Buildup
Axonal Injury After Traumatic Brain Injury May Contribute to Amyloid Buildup
Results from a small study indicate a relationship between the buildup of amyloid plaque in the brains of people who have sustained traumatic brain injury (TBI).
The findings, published in Neurology, suggest that axonal injury produced by TBI may spur the development of amyloid plaques similar to those seen in people with Alzheimer's disease.
“People after a head injury are more likely to develop dementia, but it isn't clear why,” study author Professor David Sharp, PhD, of King's College London, said in a statement. “Our findings suggest TBI leads to the development of the plaques which are a well-known feature of Alzheimer's disease.”
Twenty-eight participants total were included in the study, which utilized structural and diffusion MRI and positron emission tomography (PET) scans to detect the presence of axonal damage and neuropathological signs of dementia. Imaging from 9 participants with moderate to severe TBI (mean age 44.1 ± 4.9 yrs, range 38–54; TBI sustained 11 mo. – 17 yrs prior) was compared to nine healthy aged controls and 10 participants with Alzheimer's disease. Additionally, neuropsychological performance in participants with TBI was compared to 15 age-matched controls.
Following direct comparison, increased levels of amyloid plaque density were found in participants with TBI compared to controls, especially in the precuneus/posterior cingulated cortex (PCC) and cerebellum regions. Plaque density was greater in participants with increased white matter tract damage and increased with time since TBI. Participants with Alzheimer's disease and TBI showed plaques in the PCC; however only participants with TBI showed plaques in the cerebellum. Comparison of neuropsychological testing showed that participants with TBI showed impairments compared to age-matched healthy controls, including poor outcomes for tests of attention, information processing speed, and cognitive flexibility.
“The distinct distribution of 11C-PiB binding in the 2 contexts suggests that amyloid pathology is triggered by a different mechanism after TBI, which is likely to relate to biomechanical forces underlying the distinctive pattern of Aβ plaque pathology seen in cases of chronic traumatic encephalopathy,” the authors write.
Although preliminary, the findings may contribute to the development of prevention and treatment strategies for Alzheimer's dementia if the link between TBI and Alzheimer's is confirmed in larger studies.