Gary Mihoces, USA TODAY Sports

Doctors create test that detects CTE signs in patient before potentially fatal side effects

Five former NFL players participate in the study%2C and each shows signs of CTE

%22This%2C I hope%2C will advance everybody%27s understanding%2C%22 says participant Wayne Clark

The new research comes too late for Junior Seau, but in decades to come it may help ex-football players and others cope with and prevent brain disease related to head impacts.

A study released Tuesday reported signs of chronic traumatic encephalopathy (CTE), a brain disease linked to concussions, had been found in five living former NFL players via scanning that uses low-dose radioactivity. The investigators admit the study was small and more research is needed, but it is potential breakthrough in fighting a disease that has been only diagnosed after death.

"One of the problems with CTE cases is that some of them end in suicide. The suicides are often precipitous, without warning," said neurosurgeon Julian Bailes, a co-author of the report and co-director of the NorthShore Neurological Institute in Evanston, Ill.

Seau, a former NFL linebacker and a member of the Pro Football Hall of Fame, shot himself to death last May. The National Institutes of Health recently said tests of Seau's brain showed CTE, which has been linked to depression and dementia.

"The hope would be if you could identify them while they are in the early states that they could be treated,'' said Bailes, who describes the search for a way to identify the disease in living people as the "Holy Grail" of CTE research.

The study is based on research at UCLA headed by Gary Small, professor of psychiatry and biobehavioral sciences at the Semel Institute for Neuroscience and Human Behavior. Bailes and Small collaborated in launching the study about two years ago.

"Even though the results are extremely encouraging, we've got to do more studies," said Small. "What we're hoping is that we'll be able to test new treatments and have better ways of diagnosing problems earlier. We're looking toward preventive treatments to protect them rather than repair the damage."

One of the five former players was identified, former 1970s backup quarterback Wayne Clark, 65, of Tustin, Calif. He said he sustained three concussions, one in college and two in the NFL. Though his scan found signs of CTE, Clark said he is doing "fine." But one question in CTE research is why some players with a history of concussions show ill effects and others don't.

"This, I hope, will advance everybody's understanding of what's going on," said Clark, who played with the San Diego Chargers, Cincinnati Bengals and Kansas City Chiefs. "If this turns out to be as groundbreaking as it promises to be, it would be an opportunity for me, and I really feel privileged to be a part of it.''

Clark said he is among more than 4,000 former NFL players currently suing the league in federal court, alleging the NFL knowingly failed to protect players for decades from the long-term effects of concussions.

"I don't know what will happen with that. I don't know how this research will play in any of that," said Clark. "I just wanted to join my voice with a lot of other ex-players … in expressing that I don't think that the NFL has treated a lot of my peers particularly well in their after football lives."

Other former NFL players who have been diagnosed with CTE after committing suicide include former defensive backs Ray Easterling of the Atlanta Falcons and Dave Duerson of the Chicago Bears.

Until now, CTE (chronic traumatic encephalopathy) has been diagnosed by using a microscope to analyze the cells contained in cross sections of the brain. The cells are stained to reveal buildup of what is called tau protein, which forms clusters (called neurofibrillary tangles). They are the signature signs of CTE.

In the new research, published in online issue of the American Journal of Geriatric Psychiatry, the living former players were injected with a compound developed by Small and other at UCLA for research of Alzheimer's disease. The compound, known as FDDNP, attaches itself to tau protein.

Under a PET (positron emission tomography) scan, the low dose radioactivity in the tau protein can be seen. Smalls says it works like a Geiger counter.

"What was really striking in this study was that the areas of the brain that showed the deposits were identical to that seen in that seen with the autopsy studies of patients with CTE," said Small.

The scans showed what researchers have been seeing under microscopes.

"Nobody had tried it for CTE," said Bailes. "You inject the (compound) in a vein. It circulates through the body. It binds with any tau in the brain, and then you put them inside the scan and you see the picture of it."

All of the five players who participated in the study showed the tau protein markers for CTE. The players were between the ages of 45 and 73 and each had a history of at least one concussion.

Four of the players were unnamed. They were identified in the report as a linebacker, two offensive linemen and a defensive lineman. They had various conditions including mild cognitive impairment, depression and dementia.

A UCLA press release said Clark has "normal cognitive function," but he showed the signs of CTE.

"We need to understand why some of these athletes have concussions and have a lot of tau deposit in their brain, but they don't get symptoms," said Small. "I suspect that there are going to be genetic factors, other brain abnormalities and other things that come into play."

Bailes also acknowledged the limitations of the study.

"Five people don't prove anything," said Bailes, director of the Brain Injury Research Institute, which helped fund the study. "It just proves that we have preliminary data which is strongly suggestive that we need to take a bigger study … that has enough subjects to really answer the question statistically. To do that is a several million dollar study, probably."

Bailes said that pending further research widespread screening of active and retired players could be worthwhile for players with early stages of CTE.

"There are some medication approaches, including anti-depressants," said Bailes.

Are there any treatments to eliminate tau protein in the brain cells? "There is some research on anti-tau medications, but they're not on the market. We don't know what role that may play."

Here is another complex area. What if an active player was diagnosed with CTE?

"You could see someone is accumulating tau in their brain to the extent that you think maybe they ought to end their career," said Bailes.

"I think this would be kind of a paradigm shift for us and the athlete. It's going to conjure up a lot of questions. And certainly I don't have the answer for all those. It may be taking this into a new area. If proven, we have to see how this is approached."