WEDNESDAY, Feb. 3, 2016 (HealthDay News) — Suffering a traumatic brain injury may lead to a buildup of Alzheimer’s-type plaques in the brain, including in regions not typically affected by such plaques, a small new study suggests.
Building on previous research indicating traumatic brain injury (TBI) may be a major risk factor for dementia, researchers found that moderate to severe head injuries led to an accumulation of amyloid plaques in the brains of nine middle-aged study participants over months or years.
A buildup of amyloid plaques in the spaces between nerve cells in the brain is a hallmark of Alzheimer’s disease.
“More and more evidence suggests brain trauma can trigger long-term processes that may be harmful, suggesting the window for treatment after a head injury may be much greater than previously thought,” said study author David Sharp. He is a National Institute for Health Research professor at Imperial College London in the United Kingdom.
“Additional research needs to be done to understand these long-term processes, such as amyloid plaque deposition and persistent brain inflammation, and of course to develop treatments that target these processes,” he added.
The study is published online Feb. 3 in the journal Neurology.
Alzheimer’s disease affects more than 5 million people in the United States, and in 2015, as many as 700,000 deaths will occur in people with the condition, according to the Alzheimer’s Association.
The rate of traumatic brain injury-related emergency department visits soared by 70 percent over the last decade in the United States, the authors of an accompanying journal editorial said. In 2010, 2.5 million emergency visits were due to traumatic brain injury, according to background information in the editorial. In addition, between 3 million and 5 million Americans are estimated to live with a TBI-related disability, said the editorialists, Ansgar Furst of Stanford University and Erin Bigler of Brigham Young University.
Sharp and his team included 28 participants in the study. Nine had a past traumatic brain injury, nine were healthy and 10 had Alzheimer’s disease. The mean age of those with traumatic brain injury was 44 years. The mean age in the other groups was about 20 years older, the study said. The nine with traumatic brain injury experienced a single brain injury between 11 months and up to 17 years before the start of the research.
All of the study volunteers had MRI and PET brain imaging scans for the study. Those with a traumatic brain injury also had MRI scans using so-called diffusion tensor imaging to detect damage to brain cells that occurs after TBI. PET scans used a marker that detects plaques in the brain.
Participants with brain injuries and those with Alzheimer’s had amyloid plaques in an area of the brain known as the posterior cingulate cortex. This area is usually affected early in Alzheimer’s disease. But, only those with traumatic brain injury also had amyloid plaques in the cerebellum, a region in the back of the brain with an important role in motor control, the findings showed.
The researchers also learned that amyloid plaques were more plentiful in study participants with more damage to the brain’s white matter, which is composed of nerve fibers.
“We were surprised to find amyloid plaques in the cerebellum, an area of the brain not usually affected by Alzheimer’s disease,” Sharp said. “This suggests the processes which produce amyloid in brain injury and Alzheimer’s are not the same.”
An animal study released in January complemented the new human findings. Researchers from University of Texas Medical Branch at Galveston learned that a toxic form of protein known as tau that increases after a traumatic brain injury may contribute to the development of dementia symptoms.
Keith Fargo, director of scientific programs and outreach for the Alzheimer’s Association, said that although the new study is small, “it adds a little to our knowledge about TBI … because there appears to be a connection. It’s not clear whether it’s due to Alzheimer’s pathology, although this paper seems to point in that direction.”
Fargo, who wasn’t involved in the new research, agreed with Sharp that more research on the topic is necessary before any conclusions can be drawn.
“I think we need a larger study with a more diverse group of people to see if this holds up over time in larger groups of people, and then we’d want to see what we can do to start slowing this [amyloid buildup] down,” Fargo said.
While brain damage from concussions and other mild head injuries are a growing public health concern, Sharp said, it’s difficult to translate his findings into any recommendations about whether people should avoid contact sports and other scenarios where concussions are frequent.
“A single severe head injury is not the same as many concussions, so extrapolating from our study is difficult,” he said. “However, they do have pathological similarities … and other studies have linked repetitive mild head injuries to the development of chronic traumatic encephalopathy (CTE), a condition which has pathological features that include amyloid plaques.”
CTE has recently received a lot of attention in the news. Researchers have linked the disease to head injuries sustained while playing football and subsequent brain damage observed decades later in retired National Football League players. CTE has been found in the brains of 90 of 94 former NFL players examined at Boston University. The disease can be diagnosed only after death.
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