How different are dogfighting and football?
The stained tissue of Alzheimer’s patients typically shows the two trademarks of the disease—distinctive patterns of the proteins beta-amyloid and tau. Beta-amyloid is thought to lay the groundwork for dementia. Tau marks the critical second stage of the disease: it’s the protein that steadily builds up in brain cells, shutting them down and ultimately killing them. An immunostain of an Alzheimer’s patient looks, under the microscope, as if the tissue had been hit with a shotgun blast: the red and brown marks, corresponding to amyloid and tau, dot the entire surface. But this patient’s brain was different. There was damage only to specific surface regions of his brain, and the stains for amyloid came back negative. “This was all tau,” Ann McKee, who runs the hospital’s neuropathology laboratory, said. “There was not even a whiff of amyloid. And it was the most extraordinary damage. It was one of those cases that really took you aback.” The patient may have been in an Alzheimer’s facility, and may have looked and acted as if he had Alzheimer’s. But McKee realized that he had a different condition, called chronic traumatic encephalopathy (C.T.E.), which is a progressive neurological disorder found in people who have suffered some kind of brain trauma. C.T.E. has many of the same manifestations as Alzheimer’s: it begins with behavioral and personality changes, followed by disinhibition and irritability, before moving on to dementia. And C.T.E. appears later in life as well, because it takes a long time for the initial trauma to give rise to nerve-cell breakdown and death. But C.T.E. isn’t the result of an endogenous disease. It’s the result of injury. The patient, it turned out, had been a boxer in his youth. He had suffered from dementia for fifteen years because, decades earlier, he’d been hit too many times in the head.
McKee’s laboratory does the neuropathology work for both the giant Framingham heart study, which has been running since 1948, and Boston University’s New England Centenarian Study, which analyzes the brains of people who are unusually long-lived. “I’m looking at brains constantly,” McKee said. “Then I ran across another one. I saw it and said, ‘Wow, it looks just like the last case.’ This time, there was no known history of boxing. But then I called the family, and heard that the guy had been a boxer in his twenties.” You can’t see tau except in an autopsy, and you can’t see it in an autopsy unless you do a very particular kind of screen. So now that McKee had seen two cases, in short order, she began to wonder: how many people who we assume have Alzheimer’s—a condition of mysterious origin—are actually victims of preventable brain trauma? (...)
McKee’s laboratory occupies a warren of rooms, in what looks like an old officers’ quarters on the V.A. campus. In one of the rooms, there is an enormous refrigerator, filled with brains packed away in hundreds of plastic containers. Nearby is a tray with small piles of brain slices. They look just like the ginger shavings that come with an order of sushi. Now McKee went to the room next to her office, sat down behind a microscope, and inserted one of the immunostained slides under the lens.
“This is Tom McHale,” she said. “He started out playing for Cornell. Then he went to Tampa Bay. He was the man who died of substance abuse at the age of forty-five. I only got fragments of the brain. But it’s just showing huge accumulations of tau for a forty-five-year-old—ridiculously abnormal.”
She placed another slide under the microscope. “This individual was forty-nine years old. A football player. Cognitively intact. He never had any rage behavior. He had the distinctive abnormalities. Look at the hypothalamus.” It was dark with tau. She put another slide in. “This guy was in his mid-sixties,” she said. “He died of an unrelated medical condition. His name is Walter Hilgenberg. Look at the hippocampus. It’s wall-to-wall tangles. Even in a bad case of Alzheimer’s, you don’t see that.” The brown pigment of the tau stain ran around the edge of the tissue sample in a thick, dark band. “It’s like a big river.”
McKee got up and walked across the corridor, back to her office. “There’s one last thing,” she said. She pulled out a large photographic blowup of a brain-tissue sample. “This is a kid. I’m not allowed to talk about how he died. He was a good student. This is his brain. He’s eighteen years old. He played football. He’d been playing football for a couple of years.” She pointed to a series of dark spots on the image, where the stain had marked the presence of something abnormal. “He’s got all this tau. This is frontal and this is insular. Very close to insular. Those same vulnerable regions.” This was a teen-ager, and already his brain showed the kind of decay that is usually associated with old age. “This is completely inappropriate,” she said. “You don’t see tau like this in an eighteen-year-old. You don’t see tau like this in a fifty-year-old.”
McKee is a longtime football fan. She is from Wisconsin. She had two statuettes of Brett Favre, the former Green Bay Packers quarterback, on her bookshelf. On the wall was a picture of a robust young man. It was McKee’s son—nineteen years old, six feet three. If he had a chance to join the N.F.L., I asked her, what would she advise him? “I’d say, ‘Don’t. Not if you want to have a life after football.’ ”
by Malcolm Gladwell, The New Yorker (Oct. 2009) | Read more:
Photo: Bill Frakes/Sports Illustrated/Getty
