McKee had prepared a PowerPoint presentation, but she also brought along a box of lantern slides with four-by-five-inch slivers of brain the doctors could hold up to the light. She passed those around first, and it quickly became clear that this was not going to be the academic discussion Perl had anticipated. Members of the MTBI committee seized on the absence of visible bruising to question how football-related head trauma could have caused the disease. If there was no contusion, there was no trauma. But no contusions was the point: Almost all the NFL brains had looked normal from the outside. This wasn't a disease caused by a single blow or even a few. The brain was deteriorating from the inside, McKee believed, as a result of repetitive pounding.
McKee turned to the slides. She pointed out the brown splotches representing neurofibrillary tangles of tau protein that had suffocated the cells. The tangles were indisputable signs of disease, and there was little or no beta-amyloid, which meant it wasn't Alzheimer's. And these were relatively young men with one common trait: All had played football for years. Members of the committee again challenged her. Some wanted to know why the tangles weren't closer to the surface of the brain, where the trauma had occurred. To many in the room, Casson seemed especially combative. "Casson interrupted the most," said Colonel Jaffee. "He was ...at times mocking. These were pretty compelling neuropathological findings, so to outright deny there could be a relationship, I didn't think [Casson] was really making an honest assessment of the evidence."
Hank Feuer, the Colts' physician and a charter member of the committee, sat across from McKee. "I honestly don't think we were any different with her than we were with anybody else," he later said. But the guests were increasingly uncomfortable with the line of questioning.
To Mann, the Columbia suicide expert, it was obvious that McKee had found a serious brain disease in these players. After she finished, Mann presented his own research, describing data that showed how people who had had mild head injuries as children or adolescents were at an increased risk for suicidal behavior. Casson tossed up his hand and interrupted. "It would be impossible to link a disease like CTE to suicide," he asserted.
"It's not just possible," Mann replied, "it's entirely plausible based on what I've seen from Ann McKee."
McKee was asked whether CTE wasn't just a "misdiagnosed case of frontotemporal dementia," a disease of the brain's frontal lobe. She replied, "Well, I was on the NIH committee that defined frontotemporal dementia's diagnostic criteria, so, no."
McKee had experienced heated debate before, but this, she thought, was almost personal. "I felt like they weren't really listening," she said, "like they had their heads in the sand." Casson, Pellman and others bombarded McKee and Perl with alternative theories: steroids, nutritional supplements, high blood pressure, diabetes. Finally McKee threw up her hands. "You are delusional," she told them.
The two-hour meeting ended cordially, with McKee and the others receiving thanks from the MTBI committee but no promises of follow-up discussions. McKee was relieved it was over. "We hadn't made a dent in anybody's opinion," she says.
More than four years later, in a building near McKee's office outside Boston, the largest collection of NFL brains (61) is stored in a freezer at -80º Celsius. By the fall of 2012, McKee had examined the brains of 34 former NFL players. Thirty-three had CTE. Asked what percentage of NFL players probably have the disease, McKee said, "I don't think everybody has it, but I think it's going to be a shockingly high percentage."
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