The family of Aaron Hernandez learned only after his suicide that he had chronic traumatic encephalopathy, the degenerative brain disease that researchers believe might be caused by repeated hits to the head.
Why couldn’t they find out about it when the Patriots star was still alive?
Currently, only an examination of brain tissue after death can confirm the condition, commonly referred to as CTE, that causes impulsivity, mood swings, and impaired judgment. But researchers are working on developing diagnostic tools that may eventually be used to detect its presence during life.
Several research teams are fine-tuning brain scans that may eventually detect CTE in the living. And a nationwide study launched last year is looking for signs of CTE in blood, saliva, spinal fluid, and brain scans, by comparing men with and without symptoms over seven years.
Such work will advance the understanding of CTE, which is incurable — and perhaps eventually enable early detection and treatment that would prevent its worst effects.
Still, despite high-profile studies linking football to CTE, doctors caution that many questions remain about the relationship between the sport, or any contact sport, and developing the disease.
Boston University researchers have been studying the brains of football players that were donated by relatives concerned about the symptoms their loved ones experienced while alive. So inevitably, these brains are more likely to show signs of trouble. An unknown number of people suffer concussions and go on to live long, healthy lives. And researchers have not studied living people with CTE symptoms and later confirmed the condition after death.
“Does playing football cause CTE? We don’t know,” David A. Hovda, director of the UCLA Brain Injury Research Center, said Friday. “I’ve studied the phenomenon of brain injury for 34 years. I would love to give a specific answer. We just don’t know.”
But the evidence is building to implicate repeated hits to the head in the severe mental repercussions that some players have suffered. “It’s impossible to ignore this anymore,” Dr. Ann C. McKee, director of Boston University’s CTE Center, said in July after publishing a study of 202 deceased football players that found widespread signs of the disease.
Hernandez’s case was especially high profile. In 2015, he was convicted of the June 2013 murder of Odin L. Lloyd. Then in April, just five days after he was acquitted of two additional murders, he was found hanged inside his prison cell.
In three seasons with the Patriots, Hernandez sustained only one documented concussion, and none documented while playing at the University of Florida. On Thursday, BU researchers said that tests on Hernandez’s brain revealed he had Stage 3 CTE, an advanced form of the disease. The findings were released as part of a $20 million lawsuit against the Patriots and the NFL filed on behalf of Hernandez’s daughter.
Anthony G. Alessi, director of the University of Connecticut’s Neurosport Program, said he is troubled by the increasing number of patients who fatalistically believe they have CTE because they’re suffering from depression and also played football. “You need to go out and live life and get treated for depression like everyone else in the world,” he said. People need to be alert to signs of concussion and stop playing if they occur. But there is currently no way to know if any individual has CTE, Alessi said.
That may change soon, said Dr. Samuel E. Gandy, professor of neurology and psychiatry at the Icahn School of Medicine at Mount Sinai in New York, who is working on a method to diagnose CTE while patients are alive that focuses on the proteins known as tau.
CTE has been linked to the malfunction of tau, which enable nerve cells to hold their shape. In CTE, tau breaks down and nerve cells collapse into tangles and clumps, which trigger a cascade of neurological problems.
But tau tangles are involved with other conditions, including Alzheimer’s disease, and the challenge is distinguishing CTE tau from the other types.
Tau tangles can been seen through positron emission tomography, or PET, a method of scanning the brain in which radioactive tracers known as ligands light up to show activity. Researchers have developed about half-dozen ligands specific to CTE, Gandy said.
“We believe we have the tools to see CTE tau changes during life,” Gandy said.
To test the validity of his PET ligands, Gandy scanned the brains of two dozen retired NFL players. Of them, 10 met the criteria, based on symptoms, for probable CTE. Eight of those 10 were found to have tau tangles. None of the players without symptoms had tau problems showing in the scans.
As evidence like this accumulates, Gandy hopes that a consensus will build on the ligands that accurately detect CTE. He predicts that a scan for CTE in living people could be available in less than five years.
“We’re definitely on the path to doing that,” agreed Dr. Alexander Lin, whose team at Brigham and Women’s Hospital’s neuroimaging laboratory is also developing PET scans for CTE.
Lin and colleagues are also studying other imaging techniques. Magnetic resonance spectroscopy, which measures brain chemistry, may be able to detect changes in neurotransmitters that result from brain injury. MRIs show changes in the structure of the brain, such as differences in the thickness of the gray matter in the cortex, that can indicate CTE.
In the end, Lin thinks multiple tests will be needed to diagnose CTE. “I don’t think there’s going to be a silver bullet solution where one test defines everything,” Lin said. “It’s a very complex disease.”