New research reveals genetic damage linked to chronic traumatic encephalopathy
Recent findings suggest that chronic traumatic encephalopathy (CTE), a neurologic disease often identified in athletes with histories of repetitive head trauma, also involves genetic damage within the brain, reports BritPanorama.
The latest study analyzed brain tissues from football players and individuals diagnosed with CTE and uncovered genetic damage reminiscent of Alzheimer’s disease. The extent of this damage was significant, correlating to the equivalent of hundreds of years of neurological aging.
CTE typically emerges years after sustained head impacts, manifesting symptoms such as memory decline, impulse control issues, anxiety, and aggression. Although predominantly observed in contact sports like football, hockey, and soccer, CTE has also been detected in soldiers exposed to blasts and victims of domestic violence.
The condition was first documented nearly a century ago among boxers, initially termed “punch-drunk syndrome.” However, many aspects of CTE remain elusive to scientists, particularly why only some individuals with recurrent head trauma develop the ailment.
Dr. Chris Walsh, co-author of the study published in the journal *Science*, emphasizes that the new evidence should counter arguments from those skeptical of CTE’s legitimacy as a disease. “This study helps establish that CTE is distinct from just repetitive head trauma,” he stated, hinting at a more complex pathological process akin to Alzheimer’s disease.
Currently, there is no blood test or imaging technique for diagnosing CTE in living patients. Definitive diagnoses continue to rely on post-mortem examinations looking for tau protein abnormalities associated with the condition. The study’s methodology utilized advanced sequencing and amplification technologies to assess the genetic profiles of single neurons in the brain’s prefrontal cortex.
The research compared brain samples from four groups: 15 diagnosed with CTE, four with head injuries but no CTE, and others without a history of head trauma or signs of CTE, including individuals with Alzheimer’s. Notably, cells exhibiting CTE showed genomic damage consistent with Alzheimer’s pathology, unlike the samples from those with head injuries but without CTE.
Walsh explains, “Cells carry a bar code of their whole developmental history, reflecting environmental influences, and that’s what’s happening in CTE. The abnormal environment created by the repeated trauma damages the genomes of the cells.”
A deeper understanding of the mechanisms underlying CTE may eventually lead to potential treatment avenues, drawing parallels to therapies utilized for Alzheimer’s patients. However, further research is essential before any practical applications can be realized.
There is a growing body of evidence indicating that brain damage may present much earlier than the pronounced tau aggregates typical of advanced CTE. One study highlighted that brain immune cells activate in proportion to the duration of an athlete’s participation in contact sports, suggesting that early cellular damage could set a trajectory for disease progression.
The NFL has taken steps to mitigate head injuries through revised regulations and improved equipment, contributing to a reported decline in concussions, with the 2024 season reflecting the lowest numbers since records began in 2015. Other professional leagues, including the NHL and English Premier League, have adopted similar initiatives.
Experts, however, caution that the dangers extend beyond concussions, stressing that even minor head impacts can result in damage. Recommendations have emerged suggesting a postponement of tackle football participation until later adolescence, paralleling guidelines in soccer that advise against heading the ball before attaining age ten.
As research continues to unfold, the implications of CTE on sports practices and young athletes’ health remain a pressing concern for stakeholders within the sporting community.
