Study finds chronic brain damage in retired football players
Doctors have discovered a way for professional football players to see how much damage their brains have suffered through a bruising career before it’s too late, according to a new study.
UCLA researchers led a team of scientists that used a chemical marker called FDDNP to measure the degree of brain damage in five retired football players. That marker latches onto the tau proteins that build up in the brain when someone suffers from Alzheimer’s or other cognitive impairments like chronic traumatic encephalopathy. Doctors can then perform a routine positron emission tomography (PET) scan to see those chemical markers, highlighting how many tau proteins there are and where they end up.
Chronic traumatic encephalopathy, also known as CTE, is caused by repeated head trauma. In the case of football players, CTE can be brought on by helmet-to-helmet collisions and hard tackles. The condition can lead to memory loss, depression, suicidal behavior and dementia, among other symptoms.
Over the last few years, doctors and football players have become particularly concerned about the risk for CTE among athletes. Players who have had three or more concussions are three times more likely to be diagnosed with depression and five times more likely to show mild cognitive impairment, said Dr. Gary Small, UCLA’s Parlow-Solomon Professor on Aging and lead author of the new study. Retired NFL players have a higher-than-average risk of developing Alzheimer’s disease, according to a 2012 study of 3,400 retired players by the Centers for Disease Control and Prevention.
In addition, a study last year of former San Diego Chargers linebacker Junior Seau’s brain showed that he was suffering from CTE when he killed himself in May.
“Early detection of tau proteins may help us to understand what is happening sooner in the brains of these injured athletes,” he said. “Our findings may also guide us in developing strategies and interventions to protect those with early symptoms, rather than try to repair damage once it becomes extensive.”
Doctors realized that tau proteins played a role in CTE after they were discovered during autopsies in the brains of players who had the disease. Until then, scientists had only used the FDDNP markers to track them in Alzheimer’s patients. Small and his colleagues wondered whether the marker could also be useful for studying the brains of retired football players, he said.
The team recruited five former NFL players who were at least 45 years old — a quarterback, a linebacker, a guard, a center and a defensive lineman. Each of the players went through a battery of tests, including exams measuring their degree of depression and cognitive ability.
On the whole, the players were more depressed and showed more cognitive loss, such as a loss of short-term memory, than other men of comparable age, education and stature, researchers found. The tau proteins seen in the five volunteers were located in the same areas of the brain as they were in the brains of deceased players who had CTE.
“My hope is that this study will allow us to diagnose conditions much easier, learn which interventions are the best and have a better understanding on how to improve our equipment and the rules to make the game as safe as possible,” said study volunteer Wayne Clark, who was a quarterback in the NFL for five seasons.
Though Clark had more tau proteins in his brain than some of the others, he was the only one who did not show symptoms of CTE. That led researchers to suggest genetics also play a role in the progression of the disease, Small said.
Clark said his results have made him consider working out more and changing his diet, two lifestyle changes that have been shown to help keep the brain healthy and active.
Small said the NFL Players Assn. is looking into how it can help fund further research.
The study was published online Tuesday in the Journal of American Journal of Geriatric Psychiatry.
The study was funded by the Brain Injury Research Institute, the Fran and Ray Stark Foundation Fund for Alzheimer’s Disease Research and the Ahmanson Foundation and the Parlow-Solomon Professorship.
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