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Head Injury

New scan reveals proof of brain damage in living, retired NFL players

  • College Football

     (AP)

  • UCLA NFL brain scan.JPG

    The left image shows a normal brain scan and middle and right images show scans of pro football players from the study. The green and red colors demonstrate the higher level of tau protein found in the brain. Note the higher levels (more red and green) in the players’ scans. (UCLA)

  • Junior Seau.jpg

    New England Patriots linebacker Junior Seau (AP)

Concern has recently been on the rise for young athletes – especially football players – as increasingly compelling evidence points to the potential long-term health dangers of playing contact sports.

More and more, researchers have speculated a connection between sports-related concussions and mild traumatic brain injuries with the development of degenerative brain diseases later in life – most notably chronic traumatic encephalopathy (CTE) and even Alzheimer’s disease.

Even with more than 1,600 players in the National Football League (NFL) and countless more involved in contact sports worldwide, the only way to confirm a connection between repetitive brain injury and these debilitating brain conditions is through an autopsy.  

But now, there may be a new way to identify or track the progression of these brain diseases while a current or former athlete is still alive.

For the first time, researchers from the University of California Los Angeles (UCLA) have utilized positron emission tomography (PET) scans and a newly developed chemical marker called FDDNP to do brain imaging tests on five retired NFL players.  The new imaging technique ultimately revealed the buildup of the abnormal tau protein, which has been associated with repetitive head trauma, as well as the onset of Alzheimer’s.

“This is the first time we have done these PET scans in NFL players who are retired,” lead author Dr. Gary Small, UCLA’s Parow-Solomon Professor on aging and a professor of psychiatry and biobehavioral sciences at the Semel Institute for Neuroscience and Human Behavior at UCLA, told FoxNews.com.  “So it’s the first time to show what we think are these tau protein deposits. What’s extraordinary about that is the patterns of the deposits were identical to patterns in CTE, which is only diagnosed through autopsy. The logical conclusion is that’s what we’re seeing – suggestive this is the first time we’re visualizing CTE.”

A new kind of brain imaging

CTE is a condition that has commonly been described in many head trauma victims, military personnel and professional athletes.  The disease is characterized by a cluster of behavioral symptoms, including depression, suicidal thinking and behavior, cognitive decline, memory loss and dementia, just to name a few.

Recently, CTE was in the news when it was confirmed through autopsy that renowned NFL linebacker Junior Seau, who committed suicide in May 2012, suffered from the degenerative brain disease.

In order to conduct their brain imaging scans, Small and his colleagues used the chemical biomarker FDDNP, which they had previously developed to better assess changes with Alzheimer’s.  The FDDNP was injected into the brains of the five former athletes, where it temporarily attached itself to deposits of amyloid beta “plaques” and neurofibrillary tau “tangles” – notable markers of Alzheimer’s disease.  Then through PET scans, they were able to highlight areas of the brain with the most FDDNP accumulation.

Compared to healthy non-athletes, the NFL players had increased levels of FDDNP in the amygdala and subcortical regions of the brain – areas responsible for learning, memory, behavior, emotions and more. Ultimately the FDDNP binding patterns – or the locations FDDNP appeared in the brain – were nearly identical to the patterns of tau protein in CTE, observed through autopsy.  And the more concussions the football player had, the more buildup of tau protein appeared in the PET scans.

Each player was also given a clinical assessment to determine their depression symptoms, as well as a Mini-Mental State Examination (MMSE) to determine cognitive ability.  Generally the players had more depressive symptoms than the healthy control subjects, and three of the players had mild cognitive impairment, one had dementia, and one had normal cognitive function.  

Small said their research ties into a much larger body of research surrounding the long-term health of football players – as well as those who have suffered head trauma in general.

“There are other connections here that are relevant,” Small said. “Recent studies have found that NFL players have a four times greater probability of dying from Alzheimer’s than the general population.  In other studies, if you look at people, not just athletes, but people in general who’ve had a concussion that has led to an hour of unconsciousness – it doubles their risk of Alzheimer’s.”

The future of football

One of the five NFL players involved in the study, Wayne Clark, 65,  a former quarterback who played for the San Diego Chargers from 1970 to 1973, was the player who exhibited the least amount of cognitive decline and least depressive symptoms of the group.  Clark felt he was unique because of his limited lack of play.

“I was in the NFL for six years, and I really didn’t play all that much,” Clark, who also played for the Cincinnati Bengals and Kansas City Chiefs, told FoxNews.com. “I was a backup quarterback, so I didn’t get into that many games and certainly didn’t sustain the constant impacts my teammates did.  I think part of the uniqueness of my situation is that I did not sustain those constant hits, but nevertheless, I did have a concussion and that was enough to qualify me.”

However, Small maintained that Clark – who did have a large build-up of tau proteins in his brain – represents the need for continued research, as the accumulation of tau protein may not be the only reason NFL players suffer from depression and cognitive decline.

“What we’re seeing is yes, tau protein is important, but there has to be other things we don’t understand contributing to this, like genetic factors,” Small said. “Why is it Wayne is OK, but all the players have tau protein in their brains?”

Until new research can more accurately determine how tau protein and other genetic factors contribute to the development of CTE and Alzheimer’s, Small said there are numerous lifestyle changes athletes and others can do to better protect their brain from too much inflammation.  Athletes can make positive changes by doing regular physical conditioning, eating a healthy diet, managing stress and much more.

But Small ultimately hopes this new PET imaging can become a routinely used tool by athletic managers and doctors to better understand when athletes can go back to playing – or when they ought to wait it out.

“Clearly with professional athletes, there’s an issue with exposure,” Small said. “You have to give your head rest, because we know the brain can repair itself.  But if it’s repetitive injury, it’s going to get worse.  If you sprain an ankle or hurt your knee, you have to heal your injury before you go back in the game.  The same is true with your brain.”

As for Clark, he is grateful for the opportunity to have aided his former teammates and future athletes, hoping he can participate in future studies.  For him and other athletes, Clark said the threat of long-term cognitive decline is a strong concern.

“It was relevant to me before, because I knew I had a concussion and so many of my teammates were having these conditions and passed away because of it,” Clark said, referencing his friend John Mackey, a former NFL tight end who died of frontotemporal dementia in July 2011.  “So yes, I’ve been very interested in this.  These were good people and men, and I was there teammate and friend…We all share a history, all the ex-players do, and we’re all anxious about this.”

Added Clark: “Hopefully we’ll make the game safer for athletes in all sports for all ages, and maybe change some rules for the safety of players.”