Jan. 22, 2013 at 3:37 PM ET
Like anyone else who is getting a little older, former NFL player Wayne Clark sometimes forgets someone’s name. But unlike most people, Clark has an extra reason to worry -- as a retired football player, he’s had more than his fair share of knocks and is now nervously watching report after report linking concussions with a brain condition known as chronic traumatic encephalopathy (CTE).
“Recalling names, which I recall used to be pretty easy for me, and now I go through stages where I think ‘Why can’t I remember that’? I always wondered are these age-related or are they concussion-related?” Clark, 65, says.
A new study using brain scans might be able to answer that question. The technique may allow scientists to peer into the brains of the living and spot signs of the abnormally tangled clumps of a protein called "tau" that can cause such symptoms as memory loss, impulse control, mood volatility and, eventually, dementia in people with CTE.
Researchers from the University of California, Los Angeles, used the new technique to scan the brains of five former NFL players 45 and older, along with five healthy men of the same age, according to a preliminary report published Tuesday in the American Journal of Geriatric Psychiatry.
The hope is that studies like this will enable scientists to better understand CTE, says Dr. Gary Small, director of the UCLA Longevity Center, who led the study.
“Then maybe we will be able to detect it sooner and possibly come up with a preventive treatment rather than trying to repair what is damaged,” Small says.
A study of five people doesn’t say much about what might be found in a larger population. But Small and his colleagues are encouraged by what they've seen.
Each of the football players in the study had a history of one or more diagnosed concussions and several had cognitive and/or mood symptoms. The players represented a wide range of positions: linebacker, quarterback, guard, center, and defensive lineman.
At the outset, the players were asked to fill out questionnaires designed to detect signs of cognitive decline and mood symptoms.
To look for signs of CTE, Small and his colleagues injected each study volunteer with a newly developed radio tracer that locks on to the tau protein and shows up in bright colors ranging from red to yellow on PET scans.
The scans from the healthy non-players showed no signs of tau build-up, but the images from the players showed a range that correlated with the number of hits they’d sustained during their football careers.
Though the researchers had asked 19 players initially to participate in the study, only five were willing, Small says. And only one was willing to have his name released to the public. That was Clark, a former quarterback for the San Diego Chargers.
Clark, who had sustained only one concussion while playing football, didn’t have much evidence of tau build-up. But he did have some.
“And when I first saw the scan I thought, whoa, that looks pretty extensive,” Clark says in an video interview on UCLA's website.
“Wayne’s scans show the abnormal protein deposits, just like the other football players in the study,” Small says. “Now he's in his mid-60s and he has very minor memory complaints, which could be part of normal aging, but they also could be related to his concussion. When we do further studies, we’ll be able to find out if there’s a solid connection between the two.”
Clark hopes the research will help doctors eventually identify which players might be at risk of developing permanent brain damage. “My hope is that this study will help diagnose the condition before a player dies and is autopsied,” Clark says. "If we can diagnose it when a player is alive, then we can learn how best to intervene and how to improve equipment and rules and practice habits to we can make the game safer.”
It’s not just NFL players. Brain injuries are common among war veterans, victims of accidents and younger athletes.
The researchers don’t completely understand the relationship between tau deposits and jolts to the head. Clark’s scan suggests that one hit might possibly lead to some accumulation of the abnormal protein -- just not enough to lead to symptoms.
“We don’t know how many hits it takes,” says Dr. Joseph Maroon, a professor of neurosurgery at the University of Pittsburgh Medical Center, and team neurosurgeon for the Pittsburgh Steelers. He was not involved in this study. “We don’t know if one severe hit can lead to this progression. Some players can get thousands of hits and never develop CTE. There are millions of football players in high school, college, and pro level who have taken multiple blows to the head and not developed CTE.”
Another unresolved question is whether multiple “sub-concussive” hits, such as those sustained by linemen on every play, can lead to CTE.
Perhaps the biggest question scientists hope to solve with this type of research is what percentage of concussed players end up with CTE.
Many believe that there is a genetic component that can make a person more susceptible and that those with resilient genetics can take a number of jolts to the brain without developing the disease.
Though most of the former NFL players’ brains autopsied up to this point have shown signs of CTE, those brains have come from players who tended to have pronounced symptoms of the disease before their deaths.
Two years ago when former football star Dave Duerson committed suicide, he left a note explaining that he’d decided to shoot himself in the chest, rather than the head, so scientists might examine his brain to see if the concussions he’d suffered in his 11-year NFL career as a hard-hitting safety for the Chicago Bears, the New York Giants and the Phoenix Cardinals could explain the symptoms that were making his life a misery.
Thus far, Boston University’s Center for the Study of Traumatic Encephalopathy has found evidence of CTE in the autopsied brains of 33 former NFL players, including that of Duerson, according to a report published in December in an early online version of the journal Brain.
Some hope that the new research is just the beginning.
“This is a step forward and it emphasizes the importance of what PET scanning might hold as we go forward in trying to diagnose the condition [in living players],” says Maroon.
Maroon and others say they believe that CTE is the result of a normal inflammatory response to brain injury that runs amok. The theory is that the inflammation switch gets turned on and stays on in people with a certain genetic predisposition, Maroon says.
“One might conjecture that it’s like starting a small brush fire in a dry forest,” Maroon said. “If the predisposition is there and the fire is lit, then it may continue inexorably.”
Maroon hopes that new radio tracers will be found that highlight the early signs of inflammation before tau has even begun to accumulate. Then there might be a chance to find therapies that stop CTE from developing, he says.