Newswise — American football players develop chronic traumatic encephalopathy, or CTE, after only playing football at the high school level, with higher rates of CTE associated with higher levels of play, according to a new study presented this week at the Association of Academic Physiatrists Annual Meeting in Puerto Rico.
There is a growing concern that football players are at an increased risk for long-term neurological conditions, particularly CTE, a progressive neurodegenerative condition associated with repetitive head trauma.
Researchers at the Boston University School of Medicine CTE Center conducted a study of the brains of deceased American football players to analyze the neuropathological and clinical features of the disease.
“By focusing this study specifically on football players, we were able to ensure that all our donors had a similar type of exposure to repetitive head impacts. The goal of this study was not just characterizing the disease in individuals who passed away, but rather learning as much as possible from our donors in order to apply this knowledge to help the living,” said Daniel Daneshvar, MD, PhD, the study’s author. “Given the millions of contact sport athletes and military service members exposed to repetitive head impacts each year, understanding CTE is a major public health concern.”
Study participants were deceased American football players who donated their brains for research between February 2008 and May 2016. The researchers performed retrospective clinical evaluations using online surveys, and structured and semi-structured post-mortem telephone interviews with people who knew the players.
The researchers who conducted the evaluations and the interview subjects did not know the results of the neuropathological examinations. A team of neuropathologists performed the neuropathological evaluations on the players’ brains, and they were blinded to clinical findings. They made a neuropathological diagnosis of CTE using criteria defined by the 2015 NINDS-NIBIB Consensus Conference, and well-established criteria for other neuropathological diseases, including Alzheimer’s disease, Lewy body disease, frontotemporal lobar degeneration and motor neuron disease.
Prior to January 2014, they asked about the players’ demographics, educational attainment, athletic history, military history and traumatic brain injury history during the telephone interviews. Beginning in January 2014, with funding of a NINDS-NIBIB U01, they conducted these queries using online surveys.
CTE was neuropathologically diagnosed in 177, or 87%, of American football players in the study: 0 of 2 pre-high school (0%), 4 of 14 high school (29%), 46 of 53 college (87%), 10 of 14 semi-pro (71%), 7 of 8 Canadian Football League (88%) and 110 of 111 National Football League players (99%). The researchers found that CTE-related ptau pathology followed an age-dependent evolution from focal cortical lesions in teenagers and young adults, to a severe neurofibrillary neurodegeneration at mid-life that involved the medial temporal lobes and widespread brain regions.
The findings also showed that neurofibrillary degeneration advanced with increased age in the affected individuals. This was in concert with deposition of beta amyloid, alpha-synuclein and TDP-43 in their brains. Based on the interviews and survey results, the players also often presented with cognitive, behavior, mood and motor symptoms during their lifetimes.
Professional football players had a higher frequency of CTE, more frequently died at an advanced stage of CTE, and were more often diagnosed with dementia, compared with college football players, the study’s findings showed.
This study represents over half of the world's documented cases of CTE. Each of these brain donors’ primary exposure to repetitive head trauma was through participation in football. The study’s findings suggest that CTE begins as focal cortical lesions that evolve into a progressive neurodegeneration, and the disease worsens with age even in the absence of additional exposure to head trauma. This evolution in CTE pathology is typically followed a decade or so later by progressive cognitive symptoms.
“Now that we have gathered this large collection of donated tissue from individuals diagnosed with CTE, including brains, spinal cords and eyes, we are well-positioned to understand the risks for CTE. We can begin to determine what genes are involved, whether starting earlier or playing longer affect disease risk, and whether other exposures, such as alcohol, drugs or steroids, accelerate CTE,” Dr. Daneshvar said.
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