For years, studies have revealed the long-term impact of continued head trauma on older athletes, like former NFL players. But now, new research from Boston University is exploring the damage done to high school and college athletes.

The study looked at 152 athletes, all of whom were exposed to repetitive head impacts and died before the age of 30. Researchers found that over 40% of those athletes had neuropathological evidence of chronic traumatic encephalopathy, or CTE, a degenerative brain disease caused by repetitive head impacts. The research also includes the first woman soccer player to have confirmed CTE. 

Dr. Ann McKee, VA Boston Healthcare System’s chief of neuropathy and the director of BU’s CTE center, joined All Things Considered host Arun Rath to discuss the consequences of this disease and the study’s findings. What follows is a lightly edited transcript.

Arun Rath: So I gave just a very brief overview of the study. Can you explain in a bit more detail the findings and how it's distinguished from past studies?

Dr. Ann McKee: Well, I think you phrased it very well. I mean, I think it's become well received by the general public that CTE is a neurodegenerative brain disease that affects older professional football players, ice hockey players and the like. But we've known since the very beginning that some of the individuals that come into the brain bank are very young and show some of the earliest changes of CTE.

And so this study was just putting together our experience over the last 15 years of all the brain donors who were under the age of 30 at the time of death and whose brains were examined by our neuropathy team, and the clinical symptoms were gathered by our clinical team.

What we found was in 41%, they had diagnostic CTE. They had the earliest, often mild changes of CTE, despite their young age. And since we know that CTE is a progressive disease that only gets worse with time, I feel that this is a disturbing finding, given that these are young people and they played — in most cases, 71% of the time — only amateur sports. They played football, ice hockey, rugby, soccer, and some were amateur wrestlers.

Rath: Being familiar with the longer-term effects, were you surprised to see this degree of the disease present in those under 30?

McKee: I was, and I am surprised every time I see it. This is a preventable disease. This is a disease that if we had better guidelines for contact sports if we could eliminate the head impacts in some of these sports or certainly reduce the number and their magnitude, we could prevent this disease. So every time a brain donor comes in who's so young, and I have to speak to the family, the parents, the siblings, it's a tragedy that could be prevented.

Rath: I'm also curious about — because so much of the studies understandably have focused on professional football players. I know that, for instance, we mentioned in the introduction that one of the brains you studied was from a 28-year-old woman who was a [collegiate] soccer player. Can you talk about the trauma involved in soccer, in particular, and what we might not know about that?

McKee: So, in this study, we had a very small representation of females as brain donors. We'd like to make that 50%, but we're not there yet. In this study, only 7% were women. Eleven brain donors were in the study, and of those 11, we did find CTE in one 28-year-old former collegiate soccer player.

We knew it was only a matter of time until we found it in a female athlete, but it's taken us a while to actually demonstrate it. We don't know the relative risk of CTE in women as compared to men. We just don't have the information because we haven't had enough brain donors who are women and contact sports athletes. But it's something we definitely need to find out.

We know that women are more susceptible to concussions and have a longer recovery period from concussions. So we need to know if the long-term effect of repetitive head impacts — the non-concussive injuries — what the effects are of those injuries in women.

Rath: Of the young people that you found that had evidence of CTE, were these individuals showing any behavioral evidence of the trauma, or is this something where [it] only becomes obvious from symptoms later?

McKee: Yeah. So one of the difficulties of a brain donation case series is people have to donate their brains for it to be in the study. And next of kin — the families of these brain donors — are the ones that would pursue brain donation, so all of the individuals in this study were symptomatic; all were referred in by their next of kin because all had some troubling symptoms.

We're limited in the study in that it is a postmortem study that we can only do a retrospective interview with the family. We aren't able to do a physical exam of the individual. We can't do, you know, the very sensitive neuropsych testing or neurobehavioral testing or even a neurologic exam on the living person. Those would be much finer and more comprehensive exams.

So given the limitations, we couldn't find any distinct differences in symptoms between those who had CTE and those who didn't. I think that a lot of it's related to the tools, the methods that we had to use to find those symptoms.

But it also could be that symptoms in this age group are related to non-traumatic things — things like mental health issues, environmental stressors, anxiety — or it could be related to just the repetitive head impacts without it being CTE. Repetitive head impacts over the course of a single season have been shown to cause damage to the white matter in the brain or changes to the small blood vessels, and those changes may produce clinical symptoms as well.

Rath: This is obviously, by definition, a degenerative disease. Do you think it only kind of goes in one direction? Can the brain recover from it in any way if that kind of practice for repetitive head injuries stops?

McKee: In this particular case, with the symptoms being relatively nonspecific and relatively common symptoms, we do feel that there's an urgent need for the individuals that are experiencing these symptoms to come into the clinic to be seen by a medical professional because, in many cases, I'm convinced we could reverse those symptoms with proper symptomatic therapy and management.

We don't have a treatment per se for CTE, but there's a lot of potential therapies on the horizon. Right now, we're limited by the fact that the diagnosis of CTE can only be made after death. In order for us to try these experimental therapies, we need to have a way, a biomarker, to diagnose the disease during life that would enable us to see if the treatment had any efficacy. But right now, we can't diagnose this during life — only after death.

Many centers, including our own, are looking for ways to diagnose CTE during life — blood tests, spinal fluid tests, brain scans — and we're getting closer. We're making tremendous progress. I'm very optimistic that we will be doing this in the clinic in years, maybe five years, hopefully less. And once we're at that point, I think you'll see a dramatic change in attitudes and awareness about CTE, and we also will have the possibility of clinical trials for treatment.