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Don’t get your taus in a tangle

Hours after Derek Boogaard was found dead, a researcher from Boston called his parents to ask for the hockey enforcer's brain. Boogaard, a notorious fighter and enforcer, played first for the Minnesota Wild and then the New York Rangers.
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Hours after Derek Boogaard was found dead, a researcher from Boston called his parents to ask for the hockey enforcer's brain.

Boogaard, a notorious fighter and enforcer, played first for the Minnesota Wild and then the New York Rangers. He died in May, 2011, of an overdose of prescription pain medication after a night of drinking, joining a growing list of hockey and football players whose lives came to tragic ends.

But back to Boogard's brain. The researchers wanted to study it, along with 84 other brains of people who had been repeatedly hit on the head. Most were athletes in contact sports: hockey and football players, and boxers.

The goal was to learn more about a disease called Chronic Traumatic Encephalopathy, or CTE. This is the name for the accumulated brain damage that people used to call "punch drunk," because it often showed up in boxers. The trauma in the name refers to the jolting of the brain that causes the short-term symptoms of concussion.

The hope is that knowing more about the effects of repeated mild blows to the head will help develop treatments for CTE patients, as well as better equipment and smarter rules that keep players safer.

It seems that even softer hits that don’t cause concussion contribute to CTE.

Athletes who have CTE show different symptoms depending on the severity of the brain damage. For example, those with Stage 1 CTE suffer from headaches and difficulty concentrating. Stage 2 comes with depression and memory problems. By Stage 4, dementia sets in.

The researchers wanted to compare these clinical symptoms with physical changes in the brain.

CTE is caused by misbehaving tau (rhymes with cow) proteins. Brain cells have long, skinny tubes called microtubules that act as train tracks for the cells to move nutrients around.

Tau proteins are supposed to hold these microtubules together, but repeated head trauma makes them let go of the microtubules and clump together in a glob. This effectively derails the track, killing the cells.

In Boogaard's 28-year-old brain, the tau tangles and cell loss were in the cerebral cortex — the outer layer of the brain which helps us control emotion, predict consequences and make choices.

Over the years, as the tau problem spreads to other areas of the brain, symptoms become more severe. Researchers predict that if Boogaard lived on and the CTE progressed, he probably would have developed dementia in middle-age.

Thirty-five of the brains in the study were from football players who had CTE. Interestingly, it didn't matter how many concussions the player had suffered, just how long the athlete had been playing.

This seems to indicate that it's all the smaller hits that add up to more serious CTE.

The researchers also found the longer it had been since the players retired, the more damage their brain showed. This suggests the damage continues to worsen even after someone with CTE stops taking hits to the head.

Once the tau pathology starts, it spreads slowly. On average, it takes a bit more than a decade to go from one stage to the next.

Now that we know what CTE is doing, the next step is to figure out exactly what it takes to cause it. How many blows to the head? How bad do they have to be? Does the age of the person matter?

Unfortunately, researchers may have to make many more difficult phone calls to find the answers.

Ben Williamson is a graduate student in the Laurentian University – Science North program in Science Communication where he needs every one of his taus to behave to perfection. Have a burning science question? Send it to editor@northernlife.ca.


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