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A Boston University study published Thursday detailed the strongest link yet that repetitive hits to the head — not just those that produce a concussion — can lead to the debilitating brain disease chronic traumatic encephalopathy (CTE). The new research highlights the risks of younger athletes playing contact sports and could lead to questions about the effectiveness of current concussion protocols.
The study, published in the journal Brain, used two methods to come up with its findings: a postmortem examination of four teenaged brains and a study of mice that showed instant changes to the brain after trauma — even without telltale concussion symptoms.
"There are going to be policy implications to this," Lee E. Goldstein, a co-author of the study, physician and associate professor at Boston University School of Medicine and College of Engineering, told USA TODAY. "This is concerning, particularly for kids who are not old enough to make other decisions legally on their own — like to smoke, drink or drive a car. Just like we don't allow kids to do those activities, I think we have a moral obligation to protect them from harm."
The study was led by Boston University and included scientists from other institutions, including the Cleveland Clinic, Lawrence Livermore National Laboratory and VA Boston Healthcare System. It provided insight into why about 20% of the brains found to have CTE came from those who had never reported a concussion.
"We know now there is no question that some of these kids, some of these adults, who are playing through hits are actually in really bad shape," Goldstein said.
Ann McKee, director of Boston University's CTE Center, said there remains only one surefire way to limit risk of CTE. "There must be a reduction in the number of head impacts," McKee said in a statement. "The continued focus on concussion and symptomatic recovery does not address the fundamental danger these activities pose to human health."
Originally, concussions were thought to be the main driver of CTE, which progresses as a certain protein (tau) accumulates in the brain. Impulsive behavior, depression, suicidal thoughts, irritability, sleep disorders and short-term memory loss are all associated with CTE, which, in later stages, appears to lead to dementia and impaired motor function.
The four brains studied were from deceased high school athletes: An 18-year-old male who played football, baseball and basketball; an 18-year-old male who played football, rugby, soccer and in-line hockey; a 17-year-old male who played football and lacrosse; and a 17-year-old football player.
Each suffered closed-head brain injuries between one and 128 days before their deaths, some with notable concussion histories. Two died of suicide, and two died as a direct result of brain trauma. One of the subjects had early stages of CTE, and two others showed signs of the development of the tau protein.
Researchers compared the postmortem examination of those four to four control subjects of near the same ages who did not have a history of head trauma. None of those four showed signs of CTE or similar pathologies.
That's where the mice come in.
Researchers theorized that early CTE might result from damaged blood vessels within the brain. That could trigger brain inflammation and, eventually, the development of proteins such as tau believed to play the key role in CTE.
The hypothesis was tested on adult male mice; Goldstein said their brains possess similar attributes to human brains. Using a special device, the mice were given precise impacts that would lead to mild brain trauma similar to what an athlete would suffer in contact sports. The mice, whose brains were scanned using a specialized MRI, immediately showed changes to the electrical functions of their brains.
"What we found with this CTE that we can induce with our animal models has absolutely no correlation — zero — with the presence or severity of concussion symptoms," Goldstein said. "Some of our most-affected animals (in terms of the development of CTE) showed the least amount of concussion signs after injury."
Computer simulations confirmed the study on mice.
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