The degenerative brain disease known as CTE starts faster and earlier than previously recognized, as jolts to the head trigger abnormalities even in teenagers, according to new research led by Boston University and made public Thursday.
The scientists examined the brains of four deceased teenage athletes and found signs that CTE — chronic traumatic encephalopathy, a disabling condition blamed on blows to the head — had been set in motion days to weeks after a head injury.
They also described experiments in mice subjected to impacts similar to what athletes and soldiers experience, which showed that CTE starts to form right away, after even one hit.
“We see it early, we see it persist, and we see it progress. It’s very alarming,” said Dr. Lee E. Goldstein, the study’s lead author. “Once you get this thing started, you don’t have to have additional injuries to keep it going.”
The report, published Thursday in the journal Brain, also provided what Goldstein called “the best evidence to date” supporting the well-known theory that CTE is caused not just by concussions, but rather by any blow to the head, including mild impacts.
Instead of diagnosing and responding to concussions, he said, coaches would do better to protect children from all hits to the head.
CTE causes progressively worsening difficulties with thinking and planning, impulsive behavior, memory loss, and emotional instability.
The 37-page paper — unusual for combining research in both humans and animals — is the latest effort to understand a condition that has bedeviled the National Football League and worried parents of young athletes.
The sprawling investigation involved 46 researchers from 11 institutions in addition to BU, including the Lawrence Livermore National Laboratory in California and universities in Israel, Canada, and the United Kingdom.
On Thursday, a group cited the study in urging parents to allow children under 14 to play only flag football, and avoid games involving tackles until they are older.
Dr. Julian E. Bailes, director of neurosurgery and codirector of NorthShore University HealthSystem Neurological Institute in Evanston, Ill., called the study an important contribution to the understanding of traumatic brain injury and CTE. But he said it merely corroborates and enhances existing knowledge about the effects of mild impacts.
Bailes, who had no role in the BU study, emphasized that CTE remains a rare phenomenon. Fewer than 300 cases have been documented among tens of thousands of former professional football players and millions of youth athletes. “We don’t have an epidemic,” he said.
CTE has never been diagnosed in someone who played sports only before high school, and then ended their playing days, he said.
“I don’t think this study should call for the abolishment of youth football,” said Bailes, who is chairman of the medical advisory committee of the Pop Warner Little Scholars youth football league, which also offers flag football. “This is a personal choice by athletes, their parents, their coaches. Everybody’s got to decide what’s right for them, and weigh the risk-benefit ratio.”
Michelle McCullough of Salem said the research won’t stop her 9-year-old from playing youth football.
“I’m not going to put my child in a bubble and worry about what could happen,” she said in an interview. “Any physical activity a child is performing, there’s always going to be an injury, a cut, a concussion. There would be no such thing as children being children.”
The BU researchers, with their unique brain bank, have diagnosed CTE in 270 brains, including those of football players such as Aaron Hernandez, the former Patriots tight end who killed himself last year at age 27. Hernandez had the most severe CTE case ever seen in a person younger than 30.
The teenagers in Thursday’s study were nowhere near as severely affected as Hernandez, said Goldstein, a psychiatrist and associate professor at BU’s School of Medicine and College of Engineering.
But they were a decade younger than Hernandez when they died, and Goldstein said he was surprised to find any damage at all in these otherwise healthy young people.
“What we saw is pretty much all the fingerprints that we see in later-stage CTE — only in these cases it’s very early in the course,” he said.
Because CTE can be diagnosed only after death, scientists have been unable to observe its progress within the brain. But with the donations of the teenagers’ brains, the researchers were able to study what happens soon after the injury, rather than years or decades later. The teenagers were injured playing sports one day to four months before death.
The two 17-year-olds and two 18-year-olds were all male athletes who suffered concussions in a variety of sports, including snowboarding, rugby, and football. Two died of suicide and two of rare complications from mild sports-related head injuries.
The four brains showed the blood-vessel damage and inflammation associated with CTE. Two of them also bore the hallmark of CTE — the clumps of malformed proteins know as tau. And one of those two was diagnosed with full-blown CTE. “That’s staggering,” Goldstein said.
The BU group had previously diagnosed CTE in two other teenaged brains. But Goldstein said the four brains in Thursday’s study were significant because the injuries were recent, and because researchers had a control group. For comparison, they examined the brains of four people of the same age who did not have a recent head injury, and found no signs of CTE.
In the mouse experiments, Goldstein and colleagues engineered devices that subject rodents to head motions like those that occur in two different circumstances: sports-related impacts and wartime explosions.
These experiments enabled researchers to glimpse what happens immediately after a hit. They found that direct impacts and blasts both had the same effect in the brain. And they delineated the physiological mechanisms that lead to CTE. In particular, they saw toxic tau proteins clustering around leaky blood vessels, showing that vascular damage plays a major role in triggering CTE.
None of the mice subjected to blasts suffered concussions. They emerged looking as if nothing had happened to them, Goldstein said. But when their brains were examined, all had CTE.
These experiments, Goldstein said, “show that the concussion is not the causal determinant of CTE. It’s the hit — the rapid head motion from the hit. By focusing on the concussion we’re missing people that are hit and hurt and not getting helped.”
Goldstein emphasized that point at news conference Thursday held by the Concussion Legacy Foundation, a Boston-based nonprofit devoted to brain trauma treatment and prevention.
The foundation announced the launch of the Flag Football Under 14 campaign, calling on parents to avoid enrolling children in tackle football until they are 14.
Dr. Allen Sills , a neurosurgeon hired last year as the NFL’s chief medical officer, said in a statement that researchers have yet to explain how and why CTE manifests and who is at risk. Meanwhile, he said, “the NFL has made real strides to try to better protect our players and reduce contact to the head.” He added that youth sports programs have started to take similar measures.
“Ultimately,” Sills added, “being active, getting outside, playing sports, particularly team sports, is important.”
Correspondent Margeaux Sippell contributed to this report.