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Despite the President's claim that football has become soft, the discovery of CTE in Aaron Hernandez's brain renews calls for caution on the field and further study of an insidious disease

AMONG HIS BARRAGE of comments last week about the NFL, President Trump said, "Today if you hit too hard—15 yards! Throw him out of the game! They had that last week. I watched for a couple of minutes. Two guys, just really, beautiful tackle. Boom, 15 yards! The referee gets on television—his wife is sitting at home, she's so proud of him. They're ruining the game! They're ruining the game. That's what they want to do. They want to hit. They want to hit!"

Boston University researchers also made an announcement last week about trauma and football. They revealed that former Patriots tight end Aaron Hernandez, who took his own life this spring while incarcerated for a murder conviction that was pending appeal, died at age 27 with a severe case of chronic traumatic encephalopathy (CTE). Their findings were accompanied by something as central to football in 2017 as X-and-O diagrams: images of a deceased player's brain that had been stained to reveal deposits of abnormal tau protein.

A neurodegenerative disease first recognized by a medical examiner in 1928 among a group of boxers, CTE can only be diagnosed at autopsy. This century its discovery in the brains of more than 100 former NFL players has pushed it to the front page.

Hernandez's diagnosis came just a few months after the researchers at BU's CTE Center, which has been studying this disease, published a sobering picture of some of their findings in The Journal of the American Medical Association: They found CTE in 110 of the 111 deceased NFL players they examined. The study was largely composed of brains donated by players who had shown symptoms of neurological impairment while alive, and thus draws only from an incomplete sample—but the numbers were alarming nonetheless.

There remains much that scientists don't know about CTE. Just two years ago researchers met to define the specific criteria by which CTE should be diagnosed in postmortem exams. And the most recent international consensus statement on concussion in sports—drafted last fall in Berlin during a gathering of the world's leading neuroscientists—stops short of establishing a cause-and-effect relationship between CTE and contact sports.

The public dialogue and public health concerns have outpaced the research. There is no disputing—the President's statements notwithstanding—that repeated blows to the head are damaging to the brain, especially the developing brain. As Ann McKee, the chief neuropathologist at the BU brain bank, once said, "We know there is a problem, but not enough to know how to solve the problem."

Understanding CTE starts with analyzing how degeneration in the human brain occurs. A collision on a football field can damage nerve cells through shearing and stretching. As a result, tau, a protein that stabilizes the structures in nerve cells, may be altered in a way that it aggregates into tangles, which can interfere with brain function. Abnormal tau deposits are a hallmark of Alzheimer's disease as well—but the tangles in the brain manifest in different patterns for each disease, and CTE generally has a much earlier age of onset than Alzheimer's.

It's these specific tau protein patterns in a postmortem examination that determine a diagnosis of CTE, and they are what McKee found in Hernandez's brain: tau protein deposition in the frontal lobes of his brain and microscopic deposition of tau in nerve cells around small blood vessels—"a unique feature of CTE," according to a statement from BU. However, scientists are still trying to unlock how, and to what extent, such neuropathology causes clinical symptoms.

Mike Webster was the first NFL player diagnosed with CTE when Bennet Omalu, then a forensic neuropathologist for the Allegheny County Coroner's Office, performed Webster's autopsy in 2002. Webster had been suffering from dementia for years before his death at age 50. In the years since, as the tally of prominent players diagnosed with CTE has grown, researchers have sought to understand the link between symptoms like memory loss, depression, mood swings and aggression while alive and the abnormalities discovered in the brain after death.

Hernandez's case was notable for its severity; at just age 27 he was diagnosed with Stage 3 CTE, out of four stages, which are determined by how widespread the tau deposits are. Did CTE affect his behavior? We will never be able to say with certainty if tau tangles played any role in a promising young football player's ending his life in a prison cell while incarcerated for murder.

To fully understand a disease that strikes fear in those who love football at every level, more research is needed. How many people have CTE and no symptoms? How many people have CTE and never played a contact sport? How many people played a contact sport and never developed CTE? What role do genetics, substance abuse and performance-enhancing drugs play in the accumulation of abnormal tau? What are the keys to slowing, or stopping, the disease's progression?

The race is on among scientists to find answers and to discover a way to detect CTE in the living—that would be a watershed moment for the disease, and for the sport. For now, football continues, under the specter of a risk we know is real but cannot yet quantify.

Hernandez's case was notable for its severity at just age 27. Did CTE affect his behavior? We'll never know with certainty.



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