Three in four former NFL players died with CTE, even after correcting for bias

About three in every four former NFL players who died over a 16-year span had chronic traumatic encephalopathy, the brain disease linked to repeated blows to the head. That is the first population-level estimate of CTE in professional football, and it holds up after researchers removed the bias that has clouded the field for a decade: the families who donate a player’s brain are usually the families who watched something go wrong.

The correction was expected to shrink the number sharply. It did shrink it, from 93.5% among donated brains to 74.5% across all the players, but nowhere near the level that critics of earlier studies had predicted. In community brain banks, which collect the brains of ordinary people, CTE turns up in fewer than 1% of cases.

The study, published in JAMA Network Open, was led by Julia Gallini, a doctoral candidate in biostatistics at Boston University, with Yorghos Tripodis, a Boston University professor of biostatistics, as senior author. It covers every former NFL player who died in the study window: 2,362 men who had played at least one regular-season or postseason game, of whom 396 had donated their brains to science.

The same analysis estimates that 27.2% of those players lived with dementia before they died. “Providing a precise estimate for the prevalence of CTE among deceased NFL players helps define the scale of the problem,” Gallini said in a statement from Boston University.

How they counted brains nobody examined

CTE can only be confirmed at autopsy. Its signature is a build-up of tau, a protein that normally stabilises the internal scaffolding of nerve cells and in CTE clumps into tangles around small blood vessels deep in the folds of the brain. Standard scans cannot see these deposits, so no one can say who has the disease while they are alive.

The team worked with two sources. The first was the UNITE brain bank at Boston University, the world’s largest collection of brains studied for repetitive head trauma. Of 387 donated NFL brains with a completed examination, 362 showed CTE. The second was the National Death Index, the United States’ federal database of death certificates, which identified the 1,966 players whose brains were never studied.

The key step was to measure how strongly symptoms drove donation. Using a statistical model that compared donors with non-donors on cognitive symptoms, dementia on death records, age at death, playing position and years in the league, the researchers estimated that a player with cognitive problems was about five times more likely to end up in the brain bank. The exact figure was 4.97, with a 95% confidence interval of 4.72 to 5.26.

They then used that ratio to deflate the donor rate. If sick players are five times over-represented among donors, the donor figure overstates the true rate, and the model calculates by how much. The result was 74.5%, with a 95% confidence interval of 69.6% to 78.3%.

Why statistics instead of more autopsies? Examining every deceased player is impossible, and the alternative, following thousands of living players for decades and then studying their brains, would take a generation. The bias correction is the only way to get a population number now.

From 99% to 75%, and why the drop is smaller than expected

An earlier Boston University analysis made headlines by finding CTE in 110 of 111 donated brains of former NFL players. Critics pointed out that this was a sample of the sickest, not a census, and that the real rate could be far lower.

A separate study by the same group, published in The BMJ, tried to bound that uncertainty for more than 1,700 players who died in a five-year window. It could only say the true rate was at least 25% and possibly as high as 97.7%. The new paper narrows that range to a single estimate with a tight margin.

Even a conservative version of the calculation, built to give the lowest plausible answer, lands at 63.7%. Selection bias inflated the donor figure, but it does not explain away the disease.

For scale, previous research has found that NFL players develop dementia at about four times the rate of the general population. “No other environmental or occupational exposure ever studied is known to have increased dementia risk at death by that amount,” Tripodis told Scientific American.

What the number does not tell a living player

The 74.5% figure describes brain tissue at death, not symptoms during life. It counts any CTE pathology, including mild, early-stage changes that may never have caused a problem. The dementia estimate of 27.2% is much lower, which is a reminder that pathology and illness are not the same thing.

There is also no comparison group. Russell Lonser, a neurosurgeon at Ohio State University who was not involved in the work, called it “the best attempt so far to correct for selection bias in CTE brain bank data” but added that “it is an estimate from a model and should be read that way.” Without similar men who never played contact sports, he told Scientific American, no one can say how much of the pathology or the dementia comes from football itself.

The cohort is old. More than four in ten of the players were 80 or older when they died, so most of them played decades ago, before the league’s rule changes on head contact and before padded helmet covers such as Guardian Caps. Kristen Dams-O’Connor, who directs the Brain Injury Research Center at Mount Sinai, told CBS News that the results “cannot and should not be interpreted as being representative of current living athletes.”

The model also leans on death certificates, which often leave dementia off, and on the assumption that symptoms are what push families to donate. If other unmeasured factors shape that decision, the estimate moves. The study says nothing about youth or college football, and nothing about the thousands of former players who are still alive.

Common questions about CTE in football

What is chronic traumatic encephalopathy?

CTE is a degenerative brain disease linked to repeated head impacts, including the many sub-concussive hits in football. Abnormal tau protein builds up in the brain and spreads over time. It has been associated with memory loss, depression, aggression and poor impulse control.

Can CTE be diagnosed in a living person?

Not yet. A definitive diagnosis still requires examining brain tissue after death. Researchers are testing blood markers and specialised brain imaging to detect the disease during life, but none is approved for diagnosis.

Does everyone with CTE develop dementia?

No. In this study, about three in four former NFL players had CTE pathology at death, but an estimated 27.2% had a history of dementia. Early-stage CTE may cause few or no symptoms.

Why did earlier studies find CTE in 99% of NFL brains?

Those studies examined donated brains, and families are far more likely to donate when a player showed symptoms. This study estimates that bias at about five to one and corrects for it, which brings the rate down to 74.5%.

What comes next

The paper covers players who died between January 2008 and December 2023, and the team analysed the data between November 2025 and April 2026. It appeared in JAMA Network Open on October 28, 2026, building on the BMJ estimate published in August and on the 2017 Boston University study of 111 brains. The NFL said in a statement that it “continuously strives to make the game of football safer, including by implementing strategies to reduce concussions and head impacts.”

The next goal for the Boston University group is a diagnosis in living players, through its Diagnose CTE research project, which follows former athletes over time. Tripodis says the core lesson is already clear. “CTE is a preventable disease,” he told Scientific American. “If you reduce exposure to repetitive head impacts, then you reduce the risk of CTE.”

Reference: Gallini et al., “Bias-Adjusted Prevalence of Chronic Traumatic Encephalopathy Among Deceased National Football League Players,” JAMA Network Open, 2026. DOI: 10.1001/jamanetworkopen.2026.40884

Tags: NFL, American football, neuroscience, dementia, Boston University, chronic traumatic encephalopathy