A new study, published in Neurology, finds plaques in the brains of middle-aged people who have experienced head injuries. These amyloid plaques match those found in Alzheimer’s, but their spatial distribution differs.
According to an editorial that is published alongside the present research, visitors to the emergency department for traumatic brain injuries (TBI) have risen 70% in the last 10 years.
Today, between 2 and 5 million Americans are estimated to live with a TBI-related disability.
According to the National Institute of Neurological Disorders and Stroke, a TBI occurs:
“When a sudden trauma causes damage to the brain.”
TBIs can be generated in any number of ways, from a sporting incident to a workplace calamity. They are caused when the head strikes a solid mass, or by an object penetrating the skull.
The impact of brain injuries
Individuals who experience a TBI can have a multitude of medical issues, varying in gravity. Prognosis depends on a number of factors, including the severity of the injury, where in the brain the impact occurs and the age of the patient.
Around half of TBIs will require surgery to repair ruptured blood vessels or bruised brain tissue. Some individuals will face cognitive problems or difficulties processing sensory information. Others still might have difficulty communicating or display mental health issues such as anxiety or depression.
Another long-term risk for TBI patients is dementia. The mechanisms behind this relationship are unclear, but the current research makes some headway into understanding how this might occur.
Brain injury and Alzheimer’s
Researchers at Imperial College London in the UK, led by Prof. David Sharp, took an in-depth look at the brains of middle-aged individuals who had suffered a TBI.
The study took brain scans of nine individuals with moderate to severe TBIs. The average age of the group was 44, and their brain injuries had occurred between 11 months and 17 years previously.
The researchers utilized two types of scan: PET scans (positron emission tomography) and MRI scans (magnetic resonance imaging). The PET scans detected amyloid plaques in the brain and the MRI scans searched out evidence of cellular damage resulting from the trauma.
The TBI group’s scans were compared with 10 people with Alzheimer’s and 9 healthy control subjects. Commenting on the results, Prof. Sharp says:
“The areas of the brain affected by plaques overlapped those areas affected in Alzheimer’s disease, but other areas were involved.
It suggests that plaques are triggered by a different mechanism after a traumatic brain injury. The damage to the brain’s white matter at the time of the injury may act as a trigger for plaque production.”
The team found that both the Alzheimer’s and the brain injury groups had amyloid plaques in the posterior cingulate cortex. This highly connected and metabolically active brain region is known to be involved in the early stages of Alzheimer’s progression.
Interestingly, the TBI group, but not the Alzheimer’s group, also showed plaques in the cerebellum.
Future research possibilities
To date, medications for Alzheimer’s can only minimize certain symptoms and slow its progression. This is not adequate; hundreds of research teams are investigating better solutions on a global scale.
A vital aspect of Alzheimer’s research is the creation of reliable animal models. Medical News Todayrecently asked Dr. Gregory Scott, the study’s first author, whether his research could be useful in this regard:
“Potentially, however, a well-established challenge is that many animals do not generate amyloid in the same way as humans after a brain trauma.
As you say, there are already animal models of Alzheimer’s disease, of course, and in fact we are involved in a study looking at TBI in animal models of Alzheimer’s disease.”
The team cautiously notes that the current study is a relatively small-scale trial, however, Prof. Sharp holds out hope that it could lead to more. He believes that if a substantial link can be found between brain injury and the onset of Alzheimer’s disease, it might help neurologists uncover treatment and prevention strategies to reduce the progression of Alzheimer’s at an earlier stage.
When asked about future research, Dr. Scott told MNT that he is currently looking at novel ways to reduce inflammation after TBI, and investigating the relationship between brain inflammation and white matter damage:
We have completed another PET study recently looking at neuroinflammation after TBI and the effect of the antibiotic minocycline on the signal. We are also looking at other biomarkers of chronic injury.”
TBIs can be serious and life-changing events. Research will, no doubt, lead to significant improvements in the way brain injury is treated. MNT recently covered research that found a link between ADHD and traumatic brain injury.