Aaron Hernandez — the former football star charged with murder in 2013 — suffered from a severe case of the degenerative brain disease chronic traumatic encephalopathy (CTE), researchers at Boston University revealed at a medical conference this week.
Hernandez was 27 years old when he committed suicide in prison. Since CTE can only be diagnosed post-mortem, his brain offered researchers at BU’s CTE Center the rare opportunity to study the disease in a young person.
Ann McKee, MD, who presented the findings, could not say whether his brain was representative of other young NFL players, because her team has received few brains from people in Hernandez’s age group. McKee also emphasized that she could not make a connection between the brain’s pathology and his behavior.
The findings still raise obvious questions about the risks associated with football and repeated blows to the head. But what exactly is CTE? And how is science moving toward understanding, diagnosing and treating repetitive brain trauma?
Ramesh Raghupathi, PhD, is a professor of neurobiology and anatomy at Drexel University College of Medicine, who is investigating the wide spectrum of traumatic brain injuries, as well as their effects on cognition and emotions. He weighed in about the Hernandez findings and what they mean for football’s concussion crisis.
What is chronic traumatic encephalopathy (CTE)?
CTE is a neurodegenerative disease, like Alzheimer’s, Parkinson’s and Huntington’s. It has been found in the brains of athletes, military veterans, and others who have experienced repeated brain trauma. We don’t know if non-trauma conditions can lead to CTE. Symptoms like depression, anger, anxiety, memory loss and impulsivity have been associated with CTE, which are also common across the span of neurodegenerative diseases.
What sets CTE apart, the hallmark of the disease, are the deposits of the tau protein in the brain, particularly around blood vessels. Tau is a protein that stabilizes a cell’s microtubules – important parts of the cytoskeleton that provide structure and shape to the cell. If tau is removed from the microtubules, then the cells will die or become dysfunctional. Instead of getting cleared away in the brain, the tau protein forms complex structures called tangles. This is also what happens in diseases like frontotemporal dementia. But unlike in that disease, where most of the tangles are found in the frontal lobe, evidence of tau tangles can be seen in multiple regions within the brains of people with CTE.
What we don’t know is whether the changes to the tau protein are actually causing the problems, or whether the tau protein deposits are like “grave stones,” after the cell has already died. Is it the causality or the consequence of the dysfunction? There might be changes in tau that makes the problems worse, or the tau could be a structural manifestation of the functional problems.
The team that examined Hernandez’s brain made clear that they could not make a definitive connection between CTE and Hernandez’s behavior. However, his brain shows a severe deposition of the tau protein in the frontal lobe. What is the frontal lobe and how might a tau deposit in this area be connected to Hernandez’s crime?
The frontal lobe has two major functions associated with it: One is executive function, or the ability to organize, process and act on information. The other part is emotional processing and social interactions. With damage to the frontal lobe, you might find yourself losing your temper at the drop of a hat, experiencing anxiety, not being able to control impulses, or making bad decisions. It’s also the very front part of the head, so it’s going to get hit a lot – with or without a helmet. Wearing a helmet reduces the likelihood of skull fractures, but it doesn’t eliminate concussions.
What is known and unknown about how repeated head trauma affects the brain?We know that getting hit in the head multiple times, starting from when a player is very young, can lead to serious brain damage. It doesn’t mean that every time you are hit in the head that you will suffer from a concussion. You might have a small bruise and recover, but you’re still changing the function of your brain cells. We call those small hits sub-concussions. What we don’t know is how many sub-concussions it takes to manifest into greater brain damage. Is CTE the cumulative effect of all those smaller concussions, or do they set the brain up to push it over the edge?
Why is CTE difficult to diagnose and study?
The biggest issue right now is that you cannot diagnose a person with CTE based on the behavior alone, and we don’t have the ability to detect CTE in a living person. However, we’re not that far away from being able to, with advances in tau-specific tracers for positron emission tomography (PET) scanning. The hard part in studying CTE scientifically, is that the type of tau pathology we see in human brains cannot be replicated in a rat or a mouse.
What are the limitations of the current CTE research?
The brains at the CTE Center represent a biased population – they are the brains of football players that were donated because of concerns over behaviors and CTE. One of the biggest paradigms in science is that correlation does not equal causation, and the BU researchers are clear about saying that. Before we can say that football causes CTE and CTE causes these clinical symptoms, researchers need to study a population of football players who did not exhibit behavioral or cognitive problems. If 70 players studied exhibit the tau deposits and 30 do not, then those numbers also have to match the clinical diagnoses. That’s when you can make correlations.
Finally, we are hearing a lot lately about the connection between football and CTE, but less about military veterans. Are military veterans just as much at risk for this disease?
We know that not only if a soldier is close to the vicinity of an IED blast he or she will suffer from a severe injury, but also that the sound generated from a blast can push you and cause you to land on your head. It is likely the brain moves within the skull as a consequence of the sound wave and the impact. We also know that more than 60 percent of traumatic brain injuries that military personnel suffer from are actually not from blasts. They are suffered during motor vehicle accidents or while they are playing sports. For these men and women on the front lines, it’s not like they can get a concussion and then decide to stay out of the game while they heal. So CTE in military veterans is certainly something that needs to be investigated.
For media inquiries, contact Lauren Ingeno at lingeno@drexel.edu or 215.895.2614.
