Chronic traumatic neurodegenerative disease can start early and without any signs of concussion, according to a study published Thursday.
Alzheimer's disease has been most commonly associated with professional soccer players, but it has also been detected in military veterans, including many who have been exposed to roadside bombs and other types of military explosions.
Previous studies have shown that repetitive head trauma, even without concussion, can cause CTE. But the scientists said that this is the most definitive study to date to find this connection.
"Now we have both the scientific evidence, the pathologies to support it, and all the evidence to show that concussion is not linked to long-term neurological disease," said Dr. Lee Goldstein, one of the authors of the study. study, published in the journal Brain.
Goldstein and his colleagues at Boston University evaluated the brains of four deceased athletes, ages 17 to 18. The four had died from one day to four months after receiving some type of head injury related to the sport and had a history of playing football.
Brain changes detected in 24 hours
In all four brains, there were already changes in the brain that could be an indicator of CTE, including leaky blood vessels and abnormal accumulation of tau protein.
Some of these changes in the brain occurred 24 hours after the injury. Goldstein said one of the cases could be diagnosed as early-stage CTE.
What the researchers found under the microscope was surprising, Goldstein said. "We are seeing the earliest pathology soon after one of these injuries," he said.
All four samples were compared to the brains of four other athletes of similar age who had not experienced any recent head trauma prior to death. The brains of this group did not have changes in their pathology.
Concussion "does not tell you anything about the brain"
Although it seems likely that recent head injuries could be the source of brain changes, Goldstein said: "we can infer it, but we can not prove it".
To try to understand the source of the changes, Goldstein and his colleagues imitated the experiences of human brains in mouse models, exposing mice to repeated head trauma. as well as in football, and a single explosive head trauma, similar to military combat.
The researchers found similar pathologies in both the mouse and human brain, regardless of the type of exposure to the outbreak they had experienced. Goldstein and his colleagues also measured the mice for concussion-like symptoms by testing their excitement and balance. They discovered that even without a concussion, mice exposed to head trauma still had changes in the brain.
Concussion "not only is not correlated, we can uncouple it," Goldstein said. He said that the concussion itself is not the injury, but the symptoms experienced by an injury, such as impaired memory or loss of balance.
But not everyone experiences these symptoms, so "when looking at the concussion, it does not tell you anything about the brain or CTE," he added.
Using animal models and computer models, Goldstein and his associates could see the progression of the disease, finding that as Tau developed, it began to work its way through the brain.
Currently, the only way to diagnose CTE is with an autopsy after death. Researchers are working on the search for biomarkers and other indicators to help detect it in life, with the hope that such findings can help possible treatments.
Goldstein said that while the new work made progress in understanding the underlying mechanisms of CTE, it is not clear how often people experience these kinds of changes in the brain. "We do not know how to weigh the information," he said.
But the risk of CTE is worrisome enough that kids do not play tackle football, said Nick Buoniconti, a member of the professional soccer Hall of Fame. The legendary Miami Dolphins player suffers from dementia and has been diagnosed with probable CTE.
"Now, CTE took my life, youth soccer is a risk without reward," he said.
Buoniconti and Goldstein joined other former players and researchers to launch the Flag Football Under 14 initiative of the Concussion Legacy Foundation on Thursday. The campaign aims to warn parents about the dangers of football's repeated successes.
& # 39; Start early. Persists & # 39;
"I think [this research] really reinforces, as we have suspected, [the idea] that concussion is not per se, it is exposure to multiple impacts on the head," said Dr. Julian Bailes, director of neurosurgery and co-director of NorthShore University HealthSystem Neurological Institute, who was not involved in the study. Bailes was one of the first researchers to connect repeated cranial trauma to neurological damage in soccer players.
A recent evaluation of the Boston University CTE Center found that 110 of 111 former NFL players had been diagnosed with the disease. However, there is a potential bias, since many of the brains studied come from players who experienced clinical symptoms of CTE during their lifetime, such as memory loss, anger and mood swings.
In addition, scientists are also trying to unravel the role factors that influence the disease: factors such as genetics, how early someone is exposed to a traumatic brain injury and how long they were exposed to trauma.
Although it is not clear how common the CTE is, Goldstein said that the brains examined in the new study is a warning.
"CTE develops early, soon after the injury, it does not take years or decades, it starts early, it persists, and all our evidence to date shows that it is progressive."
Goldstein expects policy makers, professional players and parents to heed the warning that CTE may develop early, and that the focus on concussions does not reduce the risk. Instead, he said it was important to focus on ways to reduce the total total exposure to repeated hits, such as limiting face-to-face contact.
"Most of the blows to the head are not touching … but no one is paying attention to them," Goldstein said.
But, he remains optimistic for the future of football.
"You can play football differently, there are all kinds of ways to do it more safely," he said.