Traumatic brain injury (TBI) is a major cause of death and disability in the United States, contributing to about 30 percent of all injury deaths. In 2010, about 2.5 million emergency department visits, hospitalizations or deaths were associated with TBI — either alone or in combination with other injuries.

Those who survive a TBI, about 3.5 million Americans, face a range of outcomes from effects lasting a few days to disabilities that may last the rest of their lives.

Now, a new study published this month in Neurology suggests that suffering a TBI may lead to a buildup of Alzheimer's-type plaques in the brain, including regions not typically affected by such plaques. Building on previous research indicating TBI may be a major risk factor for dementia, researchers found 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, which affects more than 5 million people in the U.S. According the author of the new study, David Sharp, a National Institute for Health Research professor at Imperial College London in the United Kingdom, accumulating evidence indicates brain trauma may trigger long-term processes that may be harmful, suggesting the window for treatment after a head injury may be much greater than previously thought.

Sharp and his team included 28 participants in the study. Nine had a past TBI, nine were healthy and 10 had Alzheimer's disease. The mean age of those with TBI was 44 years. The mean age in the other groups was about 64 years. The study participants with TBI 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. Those with a TBI also had MRI scans using 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 the posterior cingulate cortex area of the brain. This area is usually affected early in Alzheimer's disease. But only those with TBI also had amyloid plaques in the cerebellum, which has an important role in motor control. 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.

The researchers were surprised to find amyloid plaques in the cerebellum, an area of the brain not usually affected by Alzheimer's disease, suggesting the processes producing amyloid in TBI 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 TBI may contribute to the development of dementia symptoms.

Although Sharp's study was small, it adds to our knowledge about TBI in that there appears to be a connection. However, a larger study with a more diverse group of people would enable researchers to note if the connection holds up over time and might lead to research aimed at slowing down the amyloid buildup.

Additional research needs to address and understand these long-term processes, such as amyloid plaque deposition and persistent brain inflammation, and of course to develop treatments that target these processes.