Aaron Hernandez suffered the most severe case of chronic traumatic encephalopathy ever discovered in a person his age, damage that would have significantly affected his decision-making, judgment and cognition, researchers at Boston University revealed at a medical conference Thursday.

Ann McKee, the head of BU’s CTE Center, which has studied the disease caused by repetitive brain trauma for more than a decade, called Hernandez’s brain “one of the most significant contributions to our work” because of the brain’s pristine condition and the rare opportunity to study the disease in a 27-year-old.

Hernandez, a former New England Patriots tight end, hanged himself with a bedsheet in April in a Massachusetts prison while serving a life sentence for the murder of Odin Lloyd in 2013.

In a diagnosis that linked one of football’s most notorious figures with the sport’s most significant health risk, doctors found Hernandez had Stage 3 CTE, which researchers had never seen in a brain younger than 46 years old, McKee said. The extent of that damage represents another signpost in football’s ongoing concussion crisis, which has seen professional players weigh early retirements and parents grapple with whether to allow their young sons to take up the sport. The findings released Thursday only will heighten those concerns.

Because the center has received few brains from people Hernandez’s age, McKee could not say whether his brain was representative of a 27-year-old who had played as much football. But she found the advanced stage of CTE alarming.

[The NFL studied every concussion over two seasons. What happens next may be up to manufacturers.]

“In this age group, he’s clearly at the severe end of the spectrum,” McKee said. “There is a concern that we’re seeing accelerated disease in young athletes. Whether or not that’s because they’re playing more aggressively or if they’re starting at younger ages, we don’t know. But we are seeing ravages of this disease, in this specific example, of a young person.”

At Thursday’s conference, McKee flipped through slides comparing sections of Hernandez’s brain with a sample without CTE. Hernandez’s brain had dark spots associated with tau protein and shrunken, withered areas, compared with immaculate white of the sample. His brain had significant damage to the frontal lobe, which impacts a person’s ability to make decisions and moderate behavior. As some new slides appeared on the projectors, some physicians and conference attendees gasped.

“We can’t take the pathology and explain the behavior,” McKee said. “But we can say collectively, in our collective experience, that individuals with CTE — and CTE of this severity — have difficulty with impulse control, decision-making, inhibition of impulses for aggression, emotional volatility, rage behaviors. We know that collectively.”

McKee said Hernandez had a genetic marker that makes people vulnerable to certain brain diseases and could have contributed to how aggressively he developed CTE.

“We know that that’s a risk factor for neurogenerative disease,” McKee said. “Whether or not that contributed in this case is speculative. It may explain some of his susceptibility to this disease.”



Normal 27-year-old's brain and Aaron Hernandez's brain. (Boston University School of Medicine)

The condition of Hernandez’s brain, pristine because of his age and the adept handling of medical examiners, could lead to future breakthroughs and better understanding of CTE. For example, researchers could better study the interaction of inflammation and tau pathology through the use of fluorescent stains. It gave researchers their best view yet of a marker associated with CTE.

“We are able to understand this disease at the scientific level in a way that’s very rarely presented,” McKee said. “We’re very grateful to the family for making this donation. We’re hoping this will advance medical science in a very significant way. . . . This will really accelerate and advance our research going forward.”

BU researchers say they have discovered CTE in more than 100 former NFL players, a handful of whom have committed suicide. Medical examiners delivered Hernandez’s brain, weighing 1,573 grams, to BU’s labs in April. From the outside, it looked like a typical brain — no lesions, no bruises, no abnormalities. When researches sliced the brain into sections, they discovered startling damage.

Ventricles were dilated, in response to the brain shrinking. Researchers determined Hernandez had lost brain tissue. Membranes that were supposed to be firm had grown “thin and gelatinous,” McKee said. There were abnormal, large holes in parts of Hernandez’s brain.

The hippocampus, which plays a key role in memory, had shrunk.

The fornix, which also contributes to memory function, had atrophied.

The frontal lobe, which is responsible for problem-solving, judgment, impulse control and social behavior, had been pockmarked with tau protein.

The amygdala, which produces emotional regulation, emotional behavior, fear and anxiety, had been severely affected.

The temporal lobes, which process sights and sounds, showed significant damage.

Together, they were “very unusual findings in an individual of this age,” McKee said. “We’ve never seen this in our 468 brains, except in individuals some 20 years older.”

The physical damage inside Hernandez’s brain provides another layer to the catastrophic and tragic downfall of Hernandez, a gifted player who caught a touchdown pass from Tom Brady in the 2012 Super Bowl.

Hernandez grew up a football star in Connecticut and fell in with a rough crowd at age 15, after his father died unexpectedly during a routine operation. He starred at the University of Florida even as off-field trouble, in the form of drugs and violence, dogged him. The problems caused some teams to remove him from consideration in the NFL draft, and he lasted until the Patriots plucked him in the fourth round.

Hernandez formed a dominating tandem with fellow 2010 draftee Rob Gronkowski and convinced the Patriots he had straightened out his life. The Patriots signed him to a seven-year, $40 million contract after the 2012 season. Months later, in the summer of 2013, Lloyd was murdered, his body found in a gravelly field a mile away from Hernandez’s mansion in North Attleboro.

Hernandez’s estate filed a federal lawsuit against the Patriots in September, alleging the Patriots knew hits to the head could lead to brain damage and failed to protect him.

A jury convicted Hernandez of the killing in 2015. Hernandez hanged himself in his cell just four days after a jury had acquitted him of the murders of Daniel de Abreu and Safiro Furtado, two strangers whom the state argued Hernandez killed in 2012 after an altercation at a Boston club.

Thursday’s news conference coincided with the release of an NFL study consisting of video reviews of the 459 known concussions that occurred over the 2015 and 2016 seasons, from preseason games through the playoffs.

The NFL has attempted to make the sport safer for its players through rule changes, policies designed to remove concussed players and technological advances. But brain trauma occurs when a football player’s brain accelerates or decelerates after it hits another player or the turf, bashing the sides of the head, an action no helmet can prevent.

“It happens inside the skull,” McKee said. “It’s an intrinsic component of football.”