Aaron Hernandez died by suicide in a prison cell at age 27 in April 2017. The former New England Patriots tight end had just begun serving a life sentence for a 2015 murder conviction. Shortly after the young man’s death, a coroner removed his brain and sent it to neuropathologists at Boston University. The doctors who examined the deceased football player’s brain say his case of chronic traumatic encephalopathy, a neurodegenerative condition caused by severe and repetitive traumatic brain injury, is the worst they’ve ever seen in someone his age.

Dr. Ann McKee, a neuropathologist who directs CTE research at Boston University, presented her team’s findings this week at BU’s second annual CTE conference on Thursday. The New York Times reported that Hernandez’s brain appeared normal when it was delivered to the lab, but when neuropathologists began dissecting it by separating it into half-inch slices, it was clear there was something wrong.

This slide from Ann McKee's presentation shows Aaron Hernandez's brain alongside an average 27-year-old's brain. While it appears normal from the outside, the inside exhibits signs of severe chronic traumatic encephalopathy.

Where there should have been small ventricles in Hernandez’s brain, there were large, fluid-filled ventricles that had expanded as brain tissue shrank. Where there should have been an intact septum pellucidum membrane at the center of his brain, there was a degraded membrane. The doctors who examined his brain reported that it had atrophied in multiple regions, including the hippocampus and the formix, and that these symptoms presented way more obviously, even to the naked eye, than those in CTE patients much older than Hernandez.

Other signs of CTE pathology presented themselves readily to the doctors, too, including tau protein clumps in the frontal cortex.

His unique case could help doctors study CTE in the future, since he was so young and didn’t present with any other complicating factors like age-related cognitive decline.

Dr. Ann McKee, shown examining brains in her lab for the July 2017 study that showed CTE in 110 out of 111 deceased football players studied.

Tau pathology, which scientists have connected to CTE, is also an area that researchers are hoping to target with therapies to prevent the damage these toxic proteins cause after traumatic brain injury. This is a sensitive area of study, though, especially in light of the controversy the NFL has caused through its efforts to downplay and question the connection between traumatic brain injury and CTE.

But scientists’ efforts to study CTE have progressively moved this conversation forward, making the role of football in CTE clearer than ever, and Boston University has been right in the middle of this effort. McKee led the study that reported finding CTE in 110 of 111 football players’ brains in July 2017.

Aaron Hernandez of the New England Patriots on December 10, 2012 in Foxboro, Massachusetts.

In the case of Aaron Hernandez, McKee says she has never seen such a severe case of CTE in someone younger than 46. The fact that his brain injury was overlooked is now the subject of additional controversy, as his estate has filed a lawsuit against his former employer, the Patriots, for failing to protect him against the damaging injuries he sustained.

And while McKee and her colleagues don’t want to speculate whether Hernandez’s brain pathology is to blame for his violent behavior, it is well documented that CTE often presents itself in living people as aggression and depression, among other signs.

“I didn’t want to contribute to the sensationalism,” she said.

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