Corbis

San Diego Chargers Junior Seau during a game in 2002. Seau killed himself last May. A new imaging technique may help identify damage to the brain – while a player is still alive -- after hard hits.Corbis

When Junior Seau killed himself last May, the former National Football League (NFL) star linebacker had degenerative brain disease, likely due to all the hard hits he took and inflicted throughout his career. Here's the rub, though: Seau didn't know he had it and neither did his family, friends or doctors.

Researchers from the National Institutes of Health analyzed Seau's brain (at his family's request) and announced earlier this month that his abnormalities were consistent with chronic traumatic encephalopathy, or CTE, a degenerative condition caused by a build up of tau protein. CTE has been linked with memory loss, confusion, progressive dementia, depression, suicidal behavior, personality changes, abnormal gait and tremors.

Previous studies and reports have shown that professional athletes who play contact sports and are exposed to repetitive mild traumatic brain injuries, like concussions, are at high risk of developing the devastating consequences of CTE. Despite this, no method has been developed for early detection of the brain pathologies associated with these injuries. In fact, the only way to confirm the presence of tau proteins -- also associated with Alzheimer's disease -- was to preform an autopsy. Well, not any more.

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Now, for the first time, researchers at UCLA have used a brain-imaging tool to identify these abnormal tau proteins in five former NFL players who are still alive. Preliminary findings of the study were recently published in the online edition of the American Journal of Geriatric Psychiatry and could mount to what some researchers call the "holy grail" of CTE research and prevention: early detection.

“Recent studies have shown that the tau protein deposits actually spread from cell to cell," Dr. Gary Small, lead study author and UCLA's Parlow–Solomon Professor on Aging, told Discovery News. "The basic idea is that it’s probably going to be easier to protect a healthy brain rather than try to repair damage once it sets in.”

Small and his colleagues used a brain-imaging tool they previously developed for evaluating the neurological mutations associated with Alzheimer's disease. The researchers used a chemical marker known as FDDNP that, when injected intravenously, binds to deposits of amyloid beta "plaques" and neurofibrillary tau "tangles" in the brain, also known as the calling cards of Alzheimer's.

When viewed using a positron emission tomography (PET) scan, the chemical marker provided a "window into the brain," in that it highlighted where these abnormal tau proteins accumulated. Once the five former players were given FDDNP injections, researchers administered PET scans and compared the scans to those of healthy men of comparable age, education, body mass index and family history or dementia.

All five players showed high FDDP binding of tau proteins in the amygdala and the subcortical regions of the brain, the parts that control learning, memory, behavior, emotions and other mental and physical functions.

"The areas of the brain that showed the high signal" of FDDNP "were exactly those areas that showed a high tau deposition in autopsy of these other cases," said Small, also a professor of psychiatry and biobehavioral sciences at the Semel Institute for Neuroscience and Human Behavior at UCLA.

Furthermore, researchers found a direct correlation between the number of concussions a player had experienced and the amount of FDDNP binding.

The left image shows a normal brain scan and middle and right images show scans of pro football players from the study. The green and red colors demonstrate the higher level of tau protein found in the brain. UCLA

Of the five retired NFL players who were recruited for the study, all were 45 years or older and each had a history of one of more concussions. Three players had mild cognitive impairment, one had dementia and one had normal cognitive function. Each research volunteer was clinically screened to gauge their level of depression and cognitive ability. The players exhibited more depressive symptoms than the healthy men and generally scored lower on cognitive tests, indicating diminished cognitive function.

"I'm very, very hopeful that this will be groundbreaking and that we're on the cutting edge of ways to diagnose these conditions without having to wait for autopsies," said Wayne Clark, a former back-up quarterback for the San Diego Chargers in the early 1970s and the study participant with normal cognitive function.

"Ultimately, I hope this leads to rules and equipment that'll make the game safer so more people can enjoy it," he added.

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Although the results of the study were strongly positive, researchers stress the results are preliminary and that more research needs to be done on a larger group of people. Still, researchers are optimistic and already say this technology isn't limited to former NFL players.

"This has applications not just for professional and amateur athletes, but for college or high school students, military personnel, and people who have suffered from motor vehicle accidents," said Small.

Dr. Julian Bailes, director of the Brain Injury Research Institute and the Bennett Tarkington Chairman of the department of neurosurgery at NorthShore University HealthSystem, says he envisions two potential applications for technology. The first would be to administer the chemical marker to anyone exposed to head trauma and suspected of having pre-CTE symptoms.

The other way, he added, would be using it "to make a decision about whether an athlete or soldier needs to retire and get out of harms way, if there’s a certain amount of tau protein burden in their brain."

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Bailes, who was also an author on the study, said some researchers are investigating anti-tau pharmaceuticals, but since they haven't been developed yet, intervention and treatment of CTE -- either with pharmaceuticals, natural dietary supplements, psychotherapy, treatment for depression, and watchfulness by the family -- are still the best chances for suicide prevention.

"A lot of these cases that end in suicide are precipitous -- they're not prolonged with the dragging out of symptoms," said Bailes.

He says that the majority of people who commit suicide are depressed, talk about it, exhibit warning signs, seek treatment and council, or go on antidepressants.

"But in CTE and suicides, as we saw with people like Dave Duerson" -- another former NFL player with neurodegenerative disease who committed suicide -- "and Junior Seau, those cases were without warning,” said Bailes.

Duerson, a two-time Super Bowl champion, chose to shoot himself in the chest so that, as he requested in text messages to his family before he died, his brain could be studied for signs of CTE. Three months after his death neurologists at Boston University confirmed Duerson's brain showed "moderately advanced" evidence of CTE.

"While it's great to make the diagnosis at autopsy, the frustration was all the people were dead by that point," Bailes said. "In the very least, if we could find out who has a lot of this tau protein in their brain, you would think we'd have a chance to intervene."