Young contact sports players’ brains can show signs of damage years before symptoms of long-term brain disease appear, a small US study finds.
Researchers found that brain tissues from under-51-year-old sports players had more inflammation, loss of nerve cells, and damage to blood vessels, than those of non-athletes.
The study suggests that repeated head knocks can cause long-term brain damage regardless of whether the athlete goes on to develop the degenerative brain condition Chronic Traumatic Encephalopathy (CTE).
The Science Media Centre asked experts to comment.
Associate Professor Mangor Pedersen, Department of Psychology and Neuroscience, AUT, comments:
“Together, this has important implications for sports safety and beyond. It highlights the need for better monitoring, earlier detection, and stronger protections to reduce the risk of long-term brain injury.”
Dr Helen Murray, Head of the Brain Injury & Neurodegeneration Research Lab at the University of Auckland, comments:
“This study used a powerful tool called single-nucleus RNA sequencing to examine how human brain cells respond to repetitive head impacts. The study authors examined brain cells from postmortem tissue from younger men (aged between 25 and 51) who had played contact sports, comparing three groups: eight healthy controls with little or no history of contact sports, nine athletes with a history of repetitive head impacts but no chronic traumatic encephalopathy (CTE), and eleven athletes who had been diagnosed with early-stage CTE after death.
“Although a small number of subjects were examined as is common for brain donation studies, the research provides valuable insight into the brain’s response to repeated head impacts. The study focuses on the frontal cortex, which is an area often affected early in CTE, but did not look directly at the hallmark CTE lesions that are defined by patchy tau pathology around blood vessels. Therefore, the findings provide an insight into the broader brain changes linked to years of head impact exposure.
“The study shows that the repetitive head impact and CTE brains had fewer neurons within a specific cortical layer deep in the folds of the brain. This is the area most affected by shear stress during a head knock and the area where CTE lesions specifically develop. Importantly, the reduction in neuron number did not correlate with the amount of tau pathology in that region, suggesting that these changes happen early, before the established markers of CTE pathology appear. However, the data also shows that the number of neurons varied a lot between individuals, and it is not yet clear what these changes mean for brain function.
“The study also pointed to inflammation as an early and lasting effect of repeated head impacts. Microglia, the brain’s immune cells, show a shift from a healthy resting state to a more inflamed, active state with increasing years of play. Blood vessel cells and support cells called astrocytes also showed signs of stress and activation. Together, these changes suggest that repetitive head impact alone, even without CTE pathology, is linked to processes of inflammation, blood vessel disruption, and neuron loss. This work supports the findings from our lab group at the University of Auckland Centre for Brain Research, published earlier this year, showing that astrocyte-mediated inflammation is a key feature of the CTE lesions.
“While more work is needed to understand the functional consequences of these findings, this study strengthens the evidence that years of repeated head impacts can induce chronic changes in the brain’s inflammatory cells, even in young athletes who might never develop CTE. The findings of this study emphasise the importance of developing strategies to reduce exposure to head impacts in training and games and to be cautious in our approach to head injury management and return to play.”
Conflict of interest statement: “New Zealand representative in ice hockey. Currently researching the neuropathology of Chronic Traumatic Encephalopathy with funding from the Health Research Council of NZ and the Neurological Foundation of NZ.”
Professor Patria Hume, Professor Human Performance, AUT, comments:
“This research has suggested a new idea: repeated head knocks may first cause other types of brain damage and inflammation, which could be responsible for early symptoms. The known CTE brain changes might only show up later. This is a shift from previous thinking, which focused on a specific brain protein (called p-tau) as the main cause of the disease and its symptoms. The new study opens the door to fresh ways of understanding and tackling CTE.
“One of the biggest challenges in CTE research is that the symptoms people experience, like changes in mood, memory, or behaviour, don’t always match up with the amount of disease found in their brains after death. People without the classic signs of CTE in their brains can have symptoms that look just like those who do have it. The authors of this new study openly admit that the symptoms seen in the people examined weren’t fully explained by the usual brain changes linked to CTE.
“However, the study’s design means we can’t say for sure that head impacts directly cause these changes, or that these changes always lead to CTE. The study did not clearly explain how head injury history was measured, and did not link its findings to real-life symptoms. Without that connection, it’s hard to know what the results mean for athletes or the public. The findings are important, but more research is needed to understand the full story.”
“The research relies on brain samples taken after death, making it impossible to track how these changes develop over time. Without following people during their lives, it’s hard to know if these changes always lead to disease, or if they might be part of a different process altogether. The study’s conclusions may be overstated.
“While the study offers new clues about how head injuries might affect the brain, it doesn’t provide a way to diagnose or treat CTE in living people. Until researchers can reliably identify who has the disease during life, and link brain changes to symptoms, promises of new treatments remain out of reach. The study is a step forward, but it’s not the final answer.”
Conflict of interest statement: “As a sports injury biomechanics expert employed by AUT, I have no conflicts to declare.”
Professor Gisela Sole, School of Physiotherapy, University of Otago, comments:
“This study found signs of damage and inflammation in post-mortem brain tissue of relatively young contact sports athletes (late twenties to fifty years old) who had experienced repeated head impacts, concussions, and in severe cases, CTE. These worrying findings highlight why early diagnosis and treatment are critical for young people, especially when dealing with second or third concussions while the brain is still healing from the first injury.
“Many players don’t report suspected concussions, preferring to keep playing rather than being sidelined for the minimum three-week recovery period. Rest remains crucial after even mild concussions – at least 48 hours of reduced activity, followed by gradual return to learning and sports based on symptoms like dizziness, headaches, fatigue, balance problems, light or noise sensitivity, or concentration difficulties.
“Given these new findings, getting diagnosed by trained healthcare providers (doctors, nurse practitioners, or physiotherapists) is even more important for proper rest guidance and graduated return to activities. The mandatory stand-down period from sports is critical to allow brain inflammation to settle and minimize long-term risks. Players need medical clearance before returning to contact sports, as healthcare providers can detect hidden symptoms not apparent during daily activities.
“Developing brains in children and adolescents are particularly vulnerable and need adequate healing time. Poor concussion management can lead to longer recovery, increased reinjury risk, and lasting problems with memory, concentration, and academic performance. Parents, teachers, and coaches have greater responsibility to ensure players with suspected concussions seek immediate medical assessment.
“Risking long-term disability for one game simply isn’t worth it.”
Conflict of interest statement: “Professor at the School of Physiotherapy, University of Otago; completed Lottery Health funded research project to co-design and implement a framework for management of concussion in NZ secondary schools and a website. Co-investigator on the World Rugby funded ORCHID study, measuring head impacts via instrumented mouthguards during rugby training/games in 2022/2023 (Principal investigator Prof Melanie Bussey).”