New research suggests that chronic traumatic encephalopathy (CTE) – the degenerative brain disease associated with football players – is definitively caused by repeated hits to the head. Surprisingly, however, CTE may develop after far more mild injuries than previously thought.
Widely regarded as a health crisis facing professional and even amateur athletes, most people immediately equate the term CTE to concussions. This is because the pioneering research from 2005-2009 that first identified the pathological basis of CTE focused on patients with histories of multiple concussions sustained during football and boxing careers. Moreover, the history of Dr Bennet Omalu's discovery of CTE in football players, and the ensuing media storm were portrayed in a film titled Concussion.
Now, a highly buzzed study published in the journal Brain changes the scope of CTE with the finding that repeated yet seemingly minor injuries in mice can cause changes in the brain that mirror early signs of the condition.
Similar to Alzheimer’s and Parkinson’s diseases, CTE is characterized by an accumulation of abnormal versions of naturally occurring proteins throughout the brain. Through biological pathways we don’t yet fully understand, brain cells of affected individuals overproduce these "tau" proteins in incorrect three-dimensional structures, leading to the development of clumps and tangles that interfere with nerve cell function. This physiological process manifests as a constellation of memory, motor control, and behavioral impairments that worsen to dementia with time.
For an example of the personality changes that can occur with CTE, read the story of NFL player-turned-murderer Aaron Hernandez. After he hanged himself in prison, researchers found alarmingly advanced degeneration in his brain.
"We've had an inkling that subconcussive hits – the ones that don't [show] neurological signs and symptoms – may be associated with CTE," lead author Dr Lee Goldstein of the Boston University School of Medicine told NPR. "We now have solid scientific evidence to say that is so."
Gathering the data required to evaluate their hypothesis took Dr Goldstein and his colleagues seven years. Half of the investigation involved creating head injuries in mice that resemble a human sports injury and then monitoring their behavior and brain physiology. This was performed to establish a direct link between impact injury and development of CTE, as our current understanding hinges upon well-established associations, but lacks certainty.
Mice were whacked hard enough to induce a concussion-like state – transient neurological and behavioral dysfunction – but not hard enough to cause a lasting physical wound like a skull fracture.
Though the same force of impact was used for each mouse, most displayed no response or only a mild response to their first and second injuries. Researchers discovered, however, that malformed tau proteins appeared in the mouse brains as little as 24 hours after injury. Changes in neuron conductivity also began soon after, and then persisted in the long term.
The conditions found in mouse brains matched many of the characteristics that Goldstein’s team observed in brains from young athletes who had died (from unrelated causes) soon after sustaining a traumatic brain injury and showed signs of CTE. This overlap gives proof that impact injuries, independent of signs of a concussion, can lead to the early stages of CTE.
“The results may explain why approximately 20 percent of athletes with CTE never suffered a diagnosed concussion,” said Dr Goldstein in a statement.
Moving forward, this troubling new data could force the medical community to re-evaluate their protocols for head injuries, perhaps making athletes of all ages reconsider the risk and rewards of their activities.
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