Penn Team Furthers Understanding of How Concussion Can Cause Permanent Injury
On January 16, 2016 the University of Pennsylvania announced the findings of a unique team studying concussion science, consisting of a professor of materials science and engineering and a professor of neurosurgery (also director of Penn Center for Brain Injury and Repair.)
The team has developed a new mathematical model of how permanent injury can happen on the molecular scale. The model evaluates why axons, the connections that allow brain cells to communicate with each other, can be damaged by a sudden force, even though they are understood to be quite elastic. The researchers note that “microtubules” run down the length of the axons in bundles, linked by a protein known as “tau.” The link between the tau proteins and the microtubules is, however, not permanent – the proteins bind and unbind every few seconds, allowing the microtubules to slide relative to one another without damage and enabling the axon to stretch up to twice its original length. A rapid jolt –a concussive force – does not allow this process to take place. “When you pull [the microtubules] very fast, that bond doesn’t break and the forces get exerted on the microtubule itself. That’s what’s causing the damage in a traumatic brain injury.”
As the researchers note, an interesting aspect of this model is that it shows the tau protein as the center of axon damage in concussion. Aggregation of tau protein is the signature of chronic traumatic encephalopathy, (CTE) the neurodegenerative condition found in some athletes with multiple head traumas. Dr. Omalu, the pathologist played by Will Smith in the new movie “Concussion”, discovered pathological tau protein deposits throughout the brain of Mike Webster and other players who developed symptoms of neurodegeneration following their football careers.
Hello Mr. Luce…I would love to talk with you about your knowledge of brain injury and CTE. I am a Vermont and a writer, and am writing a book about my dad that I began before all of the recent media attention on brain injury. However, media attention is how I learned of your work. I listened to the program “Advancements in Concussion Science” on VPR. I believe you were one of the guests?
My dad was an amateur softball and baseball player. He died in 2009 after three confusing years of cognitive, emotional, and physical decline. His symptoms began after he sustained a line drive to the face at third base in a softball game. The line drive knocked him out cold, and for weeks his face looked like he was bludgeoned. Of course, being a tough guy, he never went to the doctor after.
Part way through his illness, I put two and two together and began to suspect the softball. When I mentioned it to doctors at the time, they said that it wasn’t a factor. This was before the CTE research going on at the time was well-known. Indeed, I knew nothing about CTE; I didn’t even know the condition existed.
In my initial investigation since I started my book project, I’ve uncovered at least 5 significant un-helmeted hits to the head that my father sustained in the last 10 years of his playing. I am sure there were other hits earlier on.
If you are able and interested to talk with me, just email me at the address provided. What I am trying to figure out, is how many hits to the head it takes to develop CTE. I realize that researchers don’t know yet. Nor do they know why some people develop it and some don’t. I also realize that the football players in most of the BU studies and Omalu’s studies sustain hundreds of helmeted hits to the head. So are un-helmeted hits worse? I would suspect they are.
Hope we can chat!