Evidence indicates that having a traumatic brain injury greatly increases the risk of developing dementia, but the link between these two conditions has been unclear. Now a new study in the March 2016 issue of Neurology has found a possible explanation: It appears that the brains of people with traumatic brain injury have increased levels of the same amyloid plaque that characterizes the brains of people with Alzheimer’s disease.
This finding suggests that traumatic brain injury may lead to the deposition of the beta-amyloid protein in their brains and that this triggers a cascade of events that causes the cell death that occurs in Alzheimer’s disease.
The study was conducted in 28 participants—9 with moderate-to-severe traumatic brain injury,10 with Alzheimer’s, and 9 controls. Using diagnostic imaging, investigators determined that, compared with controls, participants with traumatic brain injury had higher amyloid plaque density in their brains and that this increased with the amount of time since the traumatic brain injury.
However, investigators saw one major difference: Beta-amyloid deposits were also in the cerebellum (one of the areas of the brain that controls balance) of participants with traumatic brain injury, an area of the brain that typically is not affected until late in Alzheimer’s development. This raises the possibility that different mechanisms trigger amyloid pathology in individuals with Alzheimer’s and with traumatic brain injury.
Whether this means that treatments between the disorders would be different is unknown.
Marian Freedman is a freelance medical editor and writer based in Watchung, NJ. She is a contributing editor to Contemporary Pediatrics, as well as chief editor for MedEdits, a medical education consulting firm.