In July 2025, a man killed four people in a New York City building that houses the National Football League (NFL) headquarters before turning the gun on himself. His suicide note blamed the NFL for concealing the dangers of American football, which he had played through high school. He asked that his brain be evaluated for chronic traumatic encephalopathy (CTE), which is primarily associated with extensive exposure to repetitive head impacts (RHI). Results of an autopsy released in September 2025 confirmed that his brain had ‘low stages’ of CTE. The media pounced, and this tragedy became another missed opportunity to transparently communicate current scientific knowledge to all athletes and their communities. It is both possible and necessary to convey established risks and advocate for safer play without fuelling fear and hopelessness that inspires avoidable tragedy. The media has played an important role in raising awareness and supporting culture change to improve safety in sports. Now, we can all contribute to leveraging popular press platforms to translate science for broad audiences. Clinicians and researchers who interact with athletes need to be equipped with a balanced and nuanced understanding of what is known, what is not yet known and the extent to which current knowledge can answer the most pressing questions.
What is CTE?
CTE is a neuropathological diagnosis. It is defined by the accumulation of hyperphosphorylated tau protein in neurons, with or without this protein in astrocytes, and this tau in neurons is located around small blood vessels in the depths of the sulci in the brain. CTE can only be diagnosed postmortem by searching the brain under a microscope for pathognomonic lesions1 that distinguish CTE from other pathological processes. Some investigators use a four-stage system to characterise pathology burden, but pending consensus-based validation, the terms ‘low’ and ‘high’ have been adopted. CTE is often described as progressive, though some argue that this is difficult to establish definitively through brain autopsy, which is a cross-sectional investigation.
The prevalence of CTE is unknown
CTE is very rare (0.62–2.83%) in autopsy cohorts unselected for head trauma exposure or clinical symptomatology. In contrast, 99% of NFL players whose families donated their brains to a CTE brain bank had CTE.4 In this same study, 14 donors had played at high school level and 3 had CTE. This has been translated in popular media as ‘over 20% of high school football players have CTE’—a grave misrepresentation of a finding from a small, biased sample.5 Autopsy studies suffer from selection bias, such that those with greatest RHI exposure and concerning symptoms may be more likely to participate, thereby inflating estimates of association between exposures (RHI) and outcomes (CTE). Increasingly sophisticated efforts are being made to account for selection bias in CTE studies,6 but the reality is that people with lower levels of RHI exposure, and those who are asymptomatic, are under-represented in athlete samples.
CTE cannot be diagnosed during life
Provisional consensus-based research criteria for traumatic encephalopathy syndrome (TES),7 the proposed but as yet unvalidated clinical manifestation of CTE neuropathology, are being tested. Current TES criteria are too broad: the core clinical criteria (cognitive impairment and/or neurobehavioural dysregulation, and progressive symptom course) are not uncommon in the general population, especially in men with serious mental health symptoms—many of whom never played contact sports. The constellation of clinical symptoms associated with CTE neuropathology remains uncertain at this time and is still being elucidated. Worldwide, researchers are seeking clinical and biological markers to identify the earliest signs of accumulating neuropathology, determine whether the neuropathology is associated with clinical symptoms and to inform novel therapies. A central goal is to more accurately distinguish individuals whose brains have CTE from those whose clinical symptoms are related to other conditions—many of which are treatable with existing interventions.
Inaccurate use of standard terminology contributes to misinformation
CTE is almost exclusively associated with extensive exposure to RHI, that is, blows or jolts to the head or neck sustained over a prolonged period, most commonly through participation in collision, contact and combat sports. These impacts often have no acute clinical sequelae, which means they may or may not meet diagnostic criteria for traumatic brain injury (TBI). A TBI, the mildest form of which is often called a concussion, is an isolated injury that can be diagnosed per consensus criteria.8 TBI is diagnosed when a biomechanically plausible injury results in: (1) ≥1 clinical sign (eg, loss of consciousness, altered mental status, gap in memory or acute neurological signs such as motor incoordination); (2) ≥2 acute symptoms (eg, feeling dazed/confused, headache, nausea, changes in vision or balance) and (if available) clinical/laboratory results; and/or (3) neuroimaging evidence of TBI.8 Simply put, RHI may include one or more TBIs, but a TBI is not RHI. The terms should not be used interchangeably. This nomenclature is important for understanding the head trauma exposure profiles that may be associated with CTE risk. Growing evidence suggests RHI and TBI have different clinical and biological sequelae. Although there are rare reports of CTE in cases without known RHI,9 most evidence suggests that CTE results from RHI—not from single isolated TBI. Misuse of these terms in both media and professional publications results in misleading assertions that ‘CTE is associated with TBIs’ or ‘TBI causes CTE’. Ironically, an entire discussion of the need for rigorous methods to study CTE misused the term TBI throughout.10 One harmful consequence of misusing these terms is that 20–30%11 of Americans who have sustained a TBI may inaccurately believe they are at risk for developing CTE; another is poorly designed studies.
Causality is complex
The Manhattan shooter believed he had CTE, and per media reports, he drove across the country to seek revenge. 2 months later, we learnt he had ‘low stage’ CTE, and the dominating narrative quickly became: CTE causes violent behaviour and suicide. This oversimplification of complex human behaviour defies logic and ignores the likely contributions of demographics, psychiatric and medical conditions and other co-pathologies. It also assumes perfect alignment between clinical diagnosis and postmortem pathology, which is not supported by research. In our programme, when a brain donor with RHI exposure is not found to have CTE, the families are often confused and upset—there is an expectation that CTE, and nothing else, causes clinical deterioration in contact sport athletes. Too often, if a person had not exclusively attributed their struggles to RHI and CTE, many of their symptoms that may be related to other factors such as mental health disorders could have been treated during life. It is also worth considering the extent to which fear that one has CTE (irrespective of CTE status) contributes to clinical symptom progression, self-medication, self-destruction and despair.
Translating what is known, and what is not known, is our responsibility
We do not know the true prevalence of CTE in unselected samples with a range of head trauma exposures and clinical symptom profiles, or what factors influence the strength of associations, if any, between CTE pathology, TES symptoms and whether and how they progress. We know precious little about CTE in RHI contexts other than American football, or in women in general. We do not know if there is a ‘safe’ level of RHI exposure, or if some individuals are more susceptible to develop CTE following exposure to RHI. It is essential to invest in research that will hasten diagnosis during life and identify targeted treatments. Sports medicine clinicians across disciplines can play a pivotal role in educating athletes and their families about the current state of science. It is dangerously reckless to amplify the notion that CTE is a very common cause of mental illness underlying tragic decisions in current and former athletes. Most of the millions of athletes reading news headlines will never develop a degenerative brain disease caused by RHI. However, one study reported over one-third of former professional American football players suspect they have CTE—a quarter of whom report suicidal thoughts or behaviours.12 These athletes deserve evaluation for treatable conditions.
Every effort should be made to reduce head contact in sports, especially for young athletes. For those experiencing changes in mood, cognition, behaviour or any symptoms linked to CTE, the most prudent course is to seek evidence-based care. As we navigate uncertainty, we must remind ourselves that it is our collective ethical responsibility to transparently share facts and to educate—not to entertain.
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Acknowledgments
Thank you to the brain donors and their families whose generosity supports the advancement of science.
