An estimated 75% of former professional football players who died over a 15-year period had signs of chronic traumatic encephalopathy, or CTE, according to a study published Wednesday in JAMA Network Open. The researchers estimated that about 27% of the players had dementia, underscoring both the potential consequences of repeated head impacts and the uncertainty surrounding CTE, which can currently be diagnosed only after death.
The new estimate is the most comprehensive to date. In August, the same research group estimated that about one-quarter of former NFL players who died over a five-year period had CTE.
Not everyone with signs of CTE in the brain experiences cognitive decline or dementia. Some people may not develop symptoms at all.
The findings surprised study leader Yorgos Tripodis, director of statistics and data management at Boston University’s Alzheimer’s Disease and CTE Center. The research used data from the university’s UNITE Brain Bank, which studies the effects of repetitive head trauma on donated brains, including those of athletes and military personnel.
“We had to double-check the numbers,” Tripodis said. He emphasized that the figures remain estimates. “Right now, we don’t know how to diagnose CTE when a person is alive, so we’re just trying to estimate.”
In an emailed statement, an NFL spokesperson said the league “continues to make the game of football safer, including by implementing strategies to reduce concussions and head impacts.”
Repeated blows and diagnostic bias
Dr. Julian Bales, director of neurosurgery at Endeavor Health in the Chicago area, said that when a person’s head moves during a crash, the brain—which is suspended in fluid inside the skull—can strike the skull and twist. Each impact may contribute to the buildup of a protein called tau in the brain.
“If it happens over and over again, the damage accumulates,” said Bales, who was not involved in the study.
CTE affects areas of the brain involved in regulating behavior and emotions. It can cause symptoms including memory loss, depression and severe mood swings, although those symptoms may also result from other illnesses.
Although CTE can produce symptoms resembling those of other neurodegenerative diseases, including dementia and Parkinson’s disease, the changes it leaves in the brain are distinct, Bales said.
One major challenge in estimating the prevalence of CTE is that its subtle changes do not appear on standard brain scans. The condition can currently be confirmed only during an autopsy.
Earlier studies have been criticized as biased because people with cognitive decline, and their families, may be more likely to donate their brains to a brain bank or request an autopsy. In previous research, Boston University scientists found signs of CTE in 99% of donated brains from former NFL players.
To reduce that bias, Tripodis and his colleagues combined UNITE Brain Bank data with national death records for other former NFL players who died between 2008 and 2023.
In total, the researchers examined brain data from 396 people and information about 1,966 other deceased former NFL players. Their analysis accounted for age at death and estimated rates of mild cognitive impairment and dementia among former NFL players over age 50.
About 93% of the donated brains showed signs of CTE, which is associated with structural damage to the brain. The researchers calculated that families of athletes with symptoms of cognitive decline were about five times more likely to donate their relatives’ brains than families of athletes without such symptoms. They used statistical analyses to adjust for that bias.
Based on those adjustments, the researchers estimated that about 75%—approximately 1,760 of the roughly 2,360 former players who died during the 15-year period—had CTE. By comparison, the researchers said, signs of the disease appear in about 1% of brains donated to brain banks in the United States, Austria and Brazil.
However, many people with signs of CTE do not develop symptoms, Tripodis said.
The researchers estimated that 27% of the approximately 2,360 players had dementia.
“Dementia can have any number of causes,” Tripodis said. “However, it is very likely that CTE is causing dementia in this particular population.”
Reducing head impacts
Dr. Jim Kelly, professor emeritus of neurology at the University of Colorado Anschutz Medical Campus, said that until doctors can diagnose CTE during a person’s lifetime, studies estimating how many people have the condition will remain estimates.
“These are all estimates,” said Kelly, who was not involved in the study. “We have not performed autopsies on five times as many dead players as we have autopsied.”
Depending on the autopsy findings, researchers may have identified only one or two lesions associated with CTE, Kelly said. Such limited damage “seems unlikely that it would lead to anything in terms of behavioral changes or dementia.”
Bales agreed that these are difficult studies. Researchers are trying to determine “how many people have this condition, even though they don’t all show symptoms,” he said. The findings also highlight the need for research into diagnosing CTE in living people.
“You can’t really help someone unless you can tell if they have a particular disease until they die,” Bales said.
In the meantime, prevention remains important, Tripodis said: “If we can reduce the number of brain injuries and effects on the brain, the risk is significantly reduced.”
The NFL has taken steps intended to reduce the number of high-impact collisions players face. Those measures include redesigned helmets, Guardian Caps and dynamic kickoff rules, which are intended to reduce collision velocity.
Source: www.nbcnews.com
