Ain’t that a kick in the head: A look into CTE
It’s nearly impossible to imagine having your head hit hundreds of thousands of times over the course of your lifetime, but for many football players, military veterans, and boxers — that is reality.
Chronic traumatic encephalopathy (CTE) is a degenerative brain disease caused by repetitive brain trauma over a period of many years. Contrary to popular belief, this brain trauma is more often comprised of patients who have had hundreds of subconcussive impacts on their head, not full concussions. Symptoms are slow-progressing and may not present themselves for anywhere from eight to 30 years post-sport activity.
Because this disease affects the brain, symptoms show in four different categories: behavioral, cognitive, mood, and motor control. They may include changes like impulsiveness, aggression, irritability, impaired memory, muscle weakness, inability to concentrate, and can eventually lead to dementia.
Chronic traumatic encephalopathy (CTE) is a degenerative brain disease caused by repetitive brain trauma over a period of many years.
CTE has become well-known due to football player Aaron Hernandez, the 27-year old New England Patriots tight end who committed suicide in jail in September 2017 while serving time for the murder of his friend, semi-professional football player Odin Lloyd. After Hernandez’ death, researchers were able to identify Stage 3 CTE through brain tissue analysis, the worst case ever seen in someone of his age. The damage was equivalent to a CTE patient in their 60s — parts of his brain were atrophied, others severely damaged and shrunken.
But how does this disease actually work?
In the brain, we heavily rely on the complex nervous system to help us react and interpret everything around us. Brain cells called neurons send signals throughout the brain through electrical stimulation down their axons to other nearby neurons. Axons give each neuron its length, as long and spindly pieces that help reach different parts of the brain. However, because of their structure, they are also very fragile to injuries like concussions. Damaged axons make it more difficult for the brain to send messages and distribute chemicals.
Every nerve cell has microtubules running the length of the cell, that can help axons pass on these messages and chemicals. Their structure is supported by the Tau protein, which sticks on to the outside of the microtubules. In healthy brains, this is an efficient system, with all components working well together. But in brains that have sustained many head injuries, the Tau protein becomes the root of the problem.
The damage was equivalent to a CTE patient in their 60s — parts of his brain were atrophied, others severely damaged and shrunken.
Microtubules are much weaker than the axons, so they are even more vulnerable to both concussions and smaller head injuries that would not damage the axons themselves. As microtubules break down due to these injuries, the Tau proteins begin to float around inside the cell, clumping together and phosphorylating — a chemical process that changes the structure of proteins.
As these clumps form, they begin spreading around the brain and can continue to grow abnormally. This spread of Tau takes many years for enough brain tissue to be affected to alter its function and present symptoms.
There is still much we don’t know about why this disease does not happen to everyone or when it starts developing in the brain. Because it is so slow to develop, it is very difficult to diagnose before death, since it requires analysis of many slices of the brain. However, because of increased awareness about CTE, there is more research occurring and hopefully developments to be made.
In 2005, the Boston University School of Medicine formed the VA-BU-CLF Brain Bank with the Veteran’s Association and the Concussion Legacy Foundation as a research center for CTE, after Pittsburgh Steeler Mike Webster was the first American football player to be found with the disease. They have now studied over 400 brains, 250 of which have been found to have CTE. In 2015, the Brain Bank collaborated with the National Institutes of Health (NIH) to help increase the ability to accurately diagnose CTE by publishing diagnostic criteria for the disease.
There are still many questions to be answered, including more about how the disease actually works, and others on how to diagnose CTE in living people, but ideally as we learn more about this complicated disease, we can either develop better protective gear and technology to prevent and predict damage, or perhaps less people will play these high impact sports which could inevitably lead to their demise.
