Background:
What is Chronic traumatic encephalopathy (CTE)? From the Merck Manual (Professional version).
The midbrain in humans controls “functions such as hearing and temperature regulation.” But, because of its location–in the middle of the brain–this area is “likely to sustain damage” when a person suffers a hit to their head.
A 2019 study that tracked football players (American football) at the University of Rochester in New York (NCAA Division III) found that though only 2 of the 38 subjects were judged to have received an actual concussion, more than 67% of the subjects “showed changes to the integrity of the white matter of their midbrains” from hits to the head that the players received during practices and games over one season.
“Researchers also found the same MRI signature of injury in the midbrain in a separate cohort [of subjects] with diagnosed concussions.”
From: Frederick, Eva (2019). Just one season of playing football—even without a concussion—can cause brain damage: Study suggests midbrain may hide significant injury. Science.
“Repetitive head impacts are common in contact and collision sports, and the potential long term effects of these on brain health have become an important public health concern. Evidence from a cohort of nearly 20 000 former National Football League (NFL) players found neurodegenerative related mortality to be almost four times higher than expected in the general population, despite substantially lower overall mortality.”
From: Kurth, Tobias and Riley, Richard D. (2026). Chronic traumatic encephalopathy in former NFL players. BMJ 394, e100526. [PDF]
What does all this mean?
The research shows that it does not take an actual concussion for a football player to receive damage to their brain–damage similar to that of players who do receive actual concussions. “Normal” hits to the head sustained in practices and games can cause the same damage.
Should anyone be playing American football?
Sources:
*Daneshvar, Daniel H., et al. (2026). Prevalence of chronic traumatic encephalopathy at death in National Football League players: retrospective population based cohort study, 2008-21. BMJ 394, e100418. [PDF]
“Objectives: To determine the range of possible prevalences of chronic traumatic encephalopathy (CTE) at death among National Football League (NFL) players and examine the association between CTE severity and risk of dementia.
Design: Retrospective population based cohort study.
Setting: NFL players from the era of hard-shell helmets (post-1949) in the US, including brain donors to the UNITE (Understanding Neurologic Injury and Traumatic Encephalopathy) and UCSF ADRC (University of California, San Francisco Alzheimer’s Disease Research Center) brain banks.
Participants: 1712 former NFL players who died during 2008-21, of whom 338 donated their brains for neuropathological evaluation. Personal information and causes of death according to the National Death Index (NDI) were obtained for all NFL players who died during the study period. Neuropathologists masked to clinical and playing histories assessed postmortem CTE diagnosis and stage IV CTE. Clinicians, masked to neuropathological status, reviewed donors’ medical records and informant based clinical histories, to adjudicate a dementia diagnosis.
Main outcome measures: The main outcome measures were the minimum (number of donors with CTE/total number of NFL deaths) and maximum (1-(number of donors without CTE/total number of NFL deaths)) CTE prevalence at death during the study period and the six years (2016-21) when brain donation was most frequent. To account for selection pressure of brain donation status, inverse probability weighting was used to estimate the association between stage IV CTE and study clinician diagnosed dementia.
Results: Among 1712 NFL players who died, 338 (19.7%) players’ brains were studied, 315 (93.2%) of whom had a diagnosis of CTE; thus, among all 1712 NFL players who died, the possible CTE prevalence at death ranged between 18.5% and 98.7%. The possible prevalence at death during 2016 to 2021, when brain donation was most frequent, ranged between 24.5% and 97.7%. Among brain donors, 104 (30.8%) had stage IV CTE, 202 (59.8%) had study clinician diagnosed dementia (dementia onset: 63.4 years, standard deviation (SD) 12.5; death: 73.1 years, SD 10.5), and 63 (18.6%) had neurodegenerative disease listed as primary cause of death. In donors, stage IV CTE was associated with study clinician diagnosed dementia (risk ratio 1.44, 95% confidence interval 1.16 to 1.78; P<0.001). Only 40.6% of donors (n=82) with study clinician diagnosed dementia had neurodegenerative disease listed as the primary or secondary cause of death.
Conclusions: At minimum, nearly a quarter of all former NFL players who died during 2016-21 had CTE neuropathology at death. Among NFL player brain donors, dementia diagnosed based on records before death was common and associated with stage IV CTE.”
*Hirad, A. A., Bazarian, J. J., Merchant-Borna, K., Garcea, F. E., Heilbronner, S., Paul, D., Hintz, E. B., van Wijngaarden, E., Schifitto, G., Wright, D. W., Espinoza, T. R., & Mahon, B. Z. (2019). A common neural signature of brain injury in concussion and subconcussion. Science Advances, 5(8), eaau3460. [PDF] [Cited by]
“The midbrain is biomechanically susceptible to force loading from repetitive subconcussive head impacts (RSHI), is a site of tauopathy in chronic traumatic encephalopathy (CTE), and regulates functions (e.g., eye movements) often disrupted in concussion. In a prospective longitudinal design, we demonstrate there are reductions in midbrain white matter integrity due to a single season of collegiate football, and that the amount of reduction in midbrain white matter integrity is related to the amount of rotational acceleration to which players’ brains are exposed. We then replicate the observation of reduced midbrain white matter integrity in a retrospective cohort of individuals with frank concussion, and further show that variance in white matter integrity is correlated with levels of serum-based tau, a marker of blood-brain barrier disruption. These findings mean that noninvasive structural MRI of the midbrain is a succinct index of both clinically silent white matter injury as well as frank concussion.”
Questions? Please let me know (engelk@grinnell.edu).
**this is an update of a post that originally appeared on August 18, 2019**
Future of Tackle Football
I grew up loving the sport (and played one year of tackle after being asked by the coaching staff at my high school), but don’t think it [football] has much of a future. Dropping participation and lawsuits at the lowest level will continue the trend of awareness for the general public. Ultimately this will lead insurance companies to drop sport coverage at the high school and college level. The NFL will survive the longest, but the quality of athlete it procures will slowly decay. The cultural fanaticism the sport has maintained over the past 80 years is about to be challenged/changed.
It would seem that the 7% drop in football participation over the past ten years isn’t a big deal, but a closer look at the numbers suggests it might be. Football doesn’t have to hit true zero for the sport to evaporate or at least start to decline at an increasing rate. As the rate of players drops (people buying pads/helmets) and the expenses related to the pads/equipment increases (as demanded by new safety requirements), we are likely to see a huge inflationary period within the sport where it becomes unaffordable for small middle or high schools to even offer the sport. Analogous to falling dominos, once smaller schools start to drop, bigger schools will start to fall as well as they will not have teams to play, nor will they have the side of the majority supporting its inclusion in the school curriculum.
Furthermore, the sport needs at least 11 players to even field a squad. For arguments sake, let’s assume that a team needs 22 (one for each position offense/defense) to be a viable “team.” If a high school averages a 50-man roster that leaves us with 28 players to be reduced before the sport hits its floor. Assuming it loses one player per year (1-3-5% / year) the sport of tackle football will not be played in 28 years, at least at the lower levels.
This model excludes one potential catalyst to the collapse – a live test for the disease.
Science’s silver bullet: If scientists develop a test for CTE in the living (expected to come in about 5 years) we might see football go away before 2030 at the lowest levels. No way a middle school or high school can ethically justify giving its students brain damage. I am under the impression that a governmental school is intended to educate students minds, first and foremost. As science advances one will hypothetically be able to say, “this athlete got brain damage during this calendar year on school grounds.” This cannot withstand the litmus test (at least for very long). As with anything where a lot of money is stake, politicians and pseudo-scientist will emerge to try to discredit and disavow what science is informing the public. We are already seeing that in California with the “Save Youth Football Campaign”.
I foresee economic challenges related to football’s closure impacting many major Universities who have overspent and over allocated resources during the past couple decades. My alma mater, Clemson University, may be on the most adverse offenders. Sure, we are excelling at the sport, but we are relying on the sport to do most of our advertising, we have invested hundreds of millions of dollars in a sport that doesn’t look to have moral leg to stand on. Eventually the truth will bear out.
Great points–thank you for posting! Kevin