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Researchers studying the brains of former professional football players say they may have found a way to identify a damaging brain condition while people are still alive.

The condition, called chronic traumatic encephalopathy, or CTE, is linked with repeated brain damage, such as concussions from playing contact sports or traumatic brain injuries sustained in combat.

Currently, the only way to definitively diagnose the disease is by looking at the brain tissue after a person has died.

But a team at Boston University has found a possible way to diagnose the disease while someone is alive by testing their spinal fluid. They found that a specific compound known as a cytokine was elevated in people who died with CTE, but not in healthy people, healthy older people or patients with Alzheimer’s, another degenerative brain disease.

“It was a striking abnormality,” said Dr. Ann McKee, director of Boston University’s CTE Center and Chief of Neuropathology at the VA Boston Healthcare System.

“It gives us clues as to how this disease develops. We are hoping that it also gives us hints as to how to treat it.”

CTE has most recently been in the headlines because McKee’s team found that former NFL Patriot star Aaron Hernandez had serious CTE when he died by suicide at age 27 last April.

The elevated cytokine that they found is called CCL11. Like other cytokines, it can do both good and bad in the body. These inflammatory compounds are released to help heal damage or fight off infections. But if there are too many, they can cause damage.

It’s not clear what is happening to raise CCL11 levels in the people with CTE. It may be a response to the injury. But McKee said it could be that there’s an over-reaction that worsens the damage.

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“We know that the pathology advances even after a person stops being hit in the head,” McKee told NBC News.

“Even though the person retired from the sport, is no longer being exposed to the head impact, we know the pathology and the clinical injury progresses. There seems to be a cascade, a vicious cycle …that once it’s started we can’t stop,” McKee added.

Related: Reports Finds Evidence of CTE in Most Former NFL Players

“It’s possible that this protein is part of that progressive cascade and that by interrupting this, we could tone down or slow down the progression or maybe even stop the progression. But that’s all fanciful.” It would take years of research to show this.

For now, what the team found was that the bodies of people diagnosed with CTE had higher levels of CCL11.

“It gives us clues as to how this disease develops. We are hoping that it also gives us hints as to how to treat it.”

They studied the brains and spinal fluid of 23 former college and professional football players diagnosed with CTE. They compared them to the brains and spinal fluid of 50 non-athletes who had Alzheimer's disease and 18 healthy people who had not played contact sports.

Levels were notably higher in the football players with CTE, and the longer they’d played football, the higher the levels of CCL11 in their brains and spinal fluid, the team reported in the Public Library of Science journal PLoS ONE.

Not only could the research perhaps one day lead to treatment, but it could help people now, said McKee.

“You certainly would want to limit their future head impact exposure,” she said.

"Not only did this research show the potential for CTE diagnosis during life, but it also offers a possible mechanism for distinguishing between CTE and other diseases,” added Jonathan Cherry, a researcher who worked on the study.

Related: Head Injuries Clearly Linked to Brain Damage

CTE is linked with behavioral issues.

“If you look at our research, collectively certainly, we see symptoms of depression and hopelessness and we see impulsivity and poor judgment, violence and suicidality,” said McKee.

But, she noted, it’s not possible to ascribe any individual’s behavior to CTE. There haven’t been enough cases studied to do that.

McKee, who has been studying this brain damage for years, said she is glad to have something positive to offer patients.

“For the first time for me I am not reporting depressing news,” she said.

“I’m just not sitting here cataloging people that have died and what their brains look like. We are trying to learn as much as possible from them so that we can apply it to living people.”