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In a Nutshell
- At minimum, nearly one in four NFL players who died between 2016 and 2021 had CTE, the degenerative brain disease tied to repeated head impacts.
- Among players whose brains were studied, almost 60% had dementia before death, but fewer than half of those dementia cases were reflected in the players’ listed causes of death.
- Players with the most severe form of CTE were 44% more likely to have dementia than donors without the most severe form of the disease.
Every Sunday, millions of fans watch football players take thunderous hits and walk back to the huddle. What happens inside those helmets, long after the final whistle, is the subject of a new study that may be the most rigorous accounting of brain disease in professional football to date. At minimum, nearly one in four former NFL players who died between 2016 and 2021 had chronic traumatic encephalopathy, or CTE, a degenerative brain disease linked to repeated blows to the head.
CTE can only be confirmed by examining brain tissue after death, which has made it extraordinarily difficult for scientists to gauge how common the disease really is among those most at risk. The study, published in the medical journal BMJ, drew on data from more than 1,700 former players who died over a 14-year period. Depending on how many unexamined brains carried the disease, the true rate of CTE at death could range anywhere from 18.5% to 98.7%. During the final six years of the study period, when brain donations were most frequent, the minimum rate climbed to nearly 25%.
Beyond measuring how common CTE was, the researchers uncovered something arguably more alarming: the most severe form of the disease was strongly tied to dementia. Among the players whose brains were donated and studied, nearly 60% had dementia before they died. Official death certificates captured barely a fraction of those cases.
What Is CTE, and Why Is It So Hard to Track?
CTE has been linked to repeated hits to the head over time, rather than to any single catastrophic injury. It causes abnormal proteins to build up in the brain, eventually disrupting its function. Because it can only be confirmed through brain examination after death, scientists have long struggled to put reliable numbers on how widespread it truly is.
To build this study, researchers compiled a complete list of all former NFL players who debuted after 1949, the year hard plastic helmets became mandatory, and died between 2008 and 2021. That gave them a pool of 1,712 deceased players. Of those, 338 donated their brains to research, and 93.2% of those donors (315) were found to have CTE.
Specialists who examined the donated brains were kept unaware of each player’s football history and medical records, a standard safeguard to prevent bias. Separately, a team of doctors reviewed medical records and interviews with family members to determine whether each player had dementia before dying. Those clinicians were also kept unaware of each player’s brain diagnosis.
The Dementia Problem Nobody Is Counting
Among the 338 brain donors, 202, or nearly 60%, had dementia. But the findings take a jarring turn against the official record: death certificates captured that dementia diagnosis in only about 40% of those cases. For roughly six out of ten players who had dementia before they died, a neurodegenerative disease was not listed among the causes of death on the official record.
That gap matters well beyond football. Researchers and policymakers often rely on death certificates to track the burden of brain diseases across populations. That finding reinforces a known limitation of death-certificate data: dementia and other neurodegenerative diseases can be undercounted, which can skew estimates that lean on those records.
Among players whose death certificates listed cardiovascular disease as the cause of death, 58.2% actually had dementia according to clinician review. Even among those whose certificates cited injury as a cause of death, more than half had dementia, with the study noting those injuries frequently involved falls inside nursing homes or memory care facilities.
CTE’s Most Severe Stage Carried the Heaviest Toll
CTE is classified into four stages, with stage IV being the most severe. Among the brain donors studied, 104 players, about 31%, had reached that stage by the time they died. Players with stage IV CTE were 44% more likely to have dementia compared to donors without the most severe form of the disease.
Nearly all donors with dementia had some form of brain disease detectable at autopsy. CTE was by far the most common, present in 95.5% of those with dementia. Alzheimer’s disease and Lewy body disease, a condition that causes problems with thinking, movement, and behavior, were also frequently found alongside CTE. In a substantial portion of donors with dementia, CTE was the only neurodegenerative disease found at autopsy.
Longer careers in professional football were tied to more severe CTE, but not to whether a player developed the disease at all. Researchers propose that at this level of the sport, where every player endures enormous cumulative head impact exposure, other factors such as genetics or environment may play a larger role in whether a player develops CTE in the first place. Once it develops, additional time on the field appeared to play a role in how severe it became.
Not every family chooses to donate a loved one’s brain, and that creates a real statistical challenge. Families dealing with a player who showed obvious signs of memory loss or behavioral changes may have been more motivated to donate, which could skew the sample toward players who were already sicker. To account for this, the researchers used a statistical method that assigned different weights to donors based on how likely they were to donate given characteristics like age at death, position played, and career length. Even after applying those corrections, the link between severe CTE and dementia held strong. Donors also tended to have longer careers and appear in more Pro Bowl games than non-donors, suggesting that higher public profiles may have helped motivate families to come forward.
This study cannot speak to the prevalence of CTE among living players or those who played at lower levels of the sport. The researchers also cannot confirm what fraction of the 1,374 players whose brains were never examined actually had CTE, which is why they offer a range rather than a single number. But even the floor of that range demands serious attention. For families of former players, the findings expose how poorly official records capture the true scope of brain disease in this population. For anyone watching football on a Sunday afternoon, the article puts a human face on what “repetitive head impacts” actually means long after the game is over.
Disclaimer: This article summarizes findings from a peer-reviewed study and is intended for general information only. It is not medical advice. CTE can currently be diagnosed only after death, and the study examined former NFL players who had died — its findings do not establish the rate of CTE among living players, players at other levels of the sport, or the general public. Because brain donation is not random, the authors report prevalence as a range rather than a single figure. Anyone with concerns about brain health or head-injury history should consult a qualified medical professional.
Paper Notes
Limitations
Several important limitations shape how these findings should be interpreted. Brain donation is not random, meaning families of players who showed more obvious symptoms were potentially more likely to donate, which could push the sample toward sicker individuals. Researchers attempted to correct for this using statistical weighting, but acknowledged the method has limits. Informants who provided family history of a player’s behavior and thinking may have had knowledge about CTE and could have unconsciously over-reported or under-reported certain symptoms, though the study notes the direction of that bias is unclear. The study also cannot identify how many of the 1,374 non-donor players had CTE, which is why prevalence is expressed as a range rather than a fixed number. Additionally, findings are specific to NFL players and cannot be generalized to football players at other levels of the sport. Because CTE can only be diagnosed after death, the study is necessarily limited to deceased individuals, which introduces the possibility that sicker or older players were more likely to die and enter the study population. Researchers also note that at least 11 CTE cases diagnosed in NFL players by other brain banks during the study period were not incorporated, and at least 12 additional former players were suspected of having CTE but were never evaluated, meaning the true minimum prevalence is likely higher than what was calculated here.
Funding and Disclosures
This study was supported by the National Institute of Neurological Disorders and Stroke (grant numbers U54NS115266 and U01NS086659), the National Institute on Aging (grant numbers P30AG13846 and P30AG072978), and the Maloney/Carpenter Trauma-Related Neurodegenerative Disease Research Fund. Several authors disclosed a range of financial relationships with outside entities, including expert testimony fees, advisory roles with pharmaceutical and technology companies, consulting arrangements with sports leagues including the NFL and NFL Players Association, and royalties from published works. Full disclosures are listed in the published paper.
Publication Details
Paper Title: Prevalence of chronic traumatic encephalopathy at death in National Football League players: retrospective population-based cohort study, 2008-21
Authors: Daniel H Daneshvar, Christopher J Nowinski, Bobak Abdolmohammadi, Charlotte B Luster, Madeline Uretsky, Brett M Martin, Joseph N Palmisano, Jennifer Weuve, Michael D McClean, Jonathan D Cherry, Brigid Dwyer, Evan D Feigel, Michael J Mastrodicasa, Victor E Alvarez, Gil D Rabinovici, William W Seeley, Lea T Grinberg, John F Crary, Thor D Stein, Lee Goldstein, Douglas I Katz, Ross D Zafonte, Yorghos Tripodis, Robert C Cantu, Robert A Stern, Michael L Alosco, Ann C McKee, Jesse Mez
Journal: BMJ
Citation: BMJ 2026; 394: e100418
Published: August 25, 2026







