How can we prevent brain damage during contact sports?

DEAR DOCTOR K:

My kids play contact sports. After all the news about how repeated concussions might cause permanent brain damage, I’m worried. Do doctors understand why the brain damage occurs and how to prevent it?

DEAR READER:

People have known for a long time that boxers could develop difficulty with thinking, remembering, balance and mood following the end of their careers. The term “punch-drunk” was often used. After all, they’re getting hit in the head constantly and are often knocked unconscious.

The revelation that people in contact sports who suffer less frequent head injuries can also develop similar problems has surprised many people. Indeed, the National Football League is supporting research — including here at Harvard — to find out what’s going on.

Traumatic brain injury (TBI) occurs in about 2.5 million people annually in the United States. Moderate to severe TBI — such as occurs during war or in major auto accidents — can lead to the permanent brain damage called chronic traumatic encephalopathy (CTE). That’s no surprise. What has been a surprise is that repeated mild TBI (such as can occur in athletes) also can lead to CTE.

When doctors look through a microscope at the brain of someone with CTE, they see scattered throughout the brain something called “neurofibrillary tangles.” These tangles also are seen in Alzheimer’s disease. However, they are not seen in the brains of people who have recently had TBI.

The tangles are made up of tau protein (also seen in Alzheimer’s disease and some other dementias). Scientists who were studying the results of TBI in mice recently reported a potentially important result. They found that TBI promptly causes the brain to produce a pathologic form of tau protein (I’ll call it “bad tau”). This type of tau protein kills some brain cells and does so quite quickly following the injury.

Worse, this injury to some brain cells slowly leads to the death of nearby brain cells — which leads to the death of other nearby brain cells. In other words, a vicious cycle develops that leads to a spreading wave of dying brain cells.

Having pointed the finger at “bad tau,” the scientists experimented with ways to block its ability to kill brain cells. They created what is called a monoclonal antibody that recognizes and attaches itself to bad tau. To their delight, they found that the antibody blocked the ability of bad tau to kill brain cells in the laboratory. More remarkable, when they injected the antibody into living mice following TBI, it protected against the death of brain cells. In tests of memory and thinking, the mice treated with the antibody did far better than those not treated.

It has not yet been proven that TBI produces the same changes in the human brain. Nor do we know if the same type of antibody might protect humans suffering from TBI from permanent brain damage. But studies in mice often forecast what will be true in humans.

Only a few years after discovering CTE, we may have learned what causes it and even how to prevent it. Only through support of research can we solve medical problems.