Like anyone else who is getting a little older, former NFL player Wayne Clark sometimes forgets someone’s name. But unlike most people, Clark has an extra reason to worry -- as a retired  football player, he’s had more than his fair share of knocks and is now nervously watching report after report linking concussions with a brain condition known as chronic traumatic encephalopathy (CTE).

“Recalling names, which I recall used to be pretty easy for me, and now I go through stages where I think ‘Why can’t I remember that’?  I always wondered are these age-related or are they concussion-related?” Clark, 65, says.

A new study using brain scans might be able to answer that question. The technique may allow scientists to peer into the brains of the living and spot signs of the abnormally tangled clumps of a protein called "tau" that can cause such symptoms as memory loss, impulse control, mood volatility and, eventually, dementia in people with CTE.

Researchers from the University of California, Los Angeles, used the new technique to scan the brains of five former NFL players 45 and older, along with five healthy men of the same age, according to a preliminary report published Tuesday in the American Journal of Geriatric Psychiatry.

The hope is that studies like this will enable scientists to better understand CTE, says Dr. Gary Small, director of the UCLA Longevity Center, who led the study.

“Then maybe we will be able to detect it sooner and possibly come up with a preventive treatment rather than trying to repair what is damaged,” Small says.

A study of five people doesn’t say much about what might be found in a larger population. But Small and his colleagues are encouraged by what they've seen.

Each of the football players in the study had a history of one or more diagnosed concussions and several had cognitive and/or mood symptoms. The players represented a wide range of positions: linebacker, quarterback, guard, center, and defensive lineman.

At the outset, the players were asked to fill out questionnaires designed to detect signs of cognitive decline and mood symptoms.

To look for signs of CTE, Small and his colleagues injected each study volunteer with a newly developed radio tracer that locks on to the tau protein and shows up in bright colors ranging from red to yellow on PET scans.

The scans from the healthy non-players showed no signs of tau build-up, but the images from the players showed a range that correlated with the number of hits they’d sustained during their football careers.

UCLA

Brain scans of living former NFL players show evidence of the damage linked to a brain-destroying condition called CTE, researchers said on Tuesday.

Though the researchers had asked 19 players initially to participate in the study, only five were willing, Small says. And only one was willing to have his name released to the public. That was Clark, a former quarterback for the San Diego Chargers.

Clark, who had sustained only one concussion while playing football, didn’t have much evidence of tau build-up. But he did have some.

“And when I first saw the scan I thought, whoa, that looks pretty extensive,” Clark says in an video interview on UCLA's website.

“Wayne’s scans show the abnormal protein deposits, just like the other football players in the study,” Small says. “Now he's in his mid-60s and he has very minor memory complaints, which could be part of normal aging, but they also could be related to his concussion. When we do further studies, we’ll be able to find out if there’s a solid connection between the two.”

Clark hopes the research will help doctors eventually identify which players might be at risk of developing permanent brain damage. “My hope is that this study will help diagnose the condition before a player dies and is autopsied,” Clark says. "If we can diagnose it when a player is alive, then we can learn how best to intervene and how to improve equipment and rules and practice habits to we can make the game safer.”

It’s not just NFL players. Brain injuries are common among war veterans, victims of accidents and younger athletes.

The researchers don’t completely understand the relationship between tau deposits and jolts to the head. Clark’s scan suggests that one hit might possibly lead to some accumulation of the abnormal protein -- just not enough to lead to symptoms.

“We don’t know how many hits it takes,” says Dr. Joseph Maroon, a professor of neurosurgery at the University of Pittsburgh Medical Center, and team neurosurgeon for the Pittsburgh Steelers. He was not involved in this study. “We don’t know if one severe hit can lead to this progression. Some players can get thousands of hits and never develop CTE. There are millions of football players in high school, college, and pro level who have taken multiple blows to the head and not developed CTE.”

Another unresolved question is whether multiple “sub-concussive” hits, such as those sustained by linemen on every play, can lead to CTE.

Perhaps the biggest question scientists hope to solve with this type of research is what percentage of concussed players end up with CTE.

Many believe that there is a genetic component that can make a person more susceptible and that those with resilient genetics can take a number of jolts to the brain without developing the disease.

Though most of the former NFL players’ brains autopsied up to this point have shown signs of CTE, those brains have come from players who tended to have pronounced symptoms of the disease before their deaths.

Two years ago when former football star Dave Duerson committed suicide, he left a note explaining that he’d decided to shoot himself in the chest, rather than the head, so scientists might examine his brain to see if the concussions he’d suffered in his 11-year NFL career as a hard-hitting safety for the Chicago Bears, the New York Giants and the Phoenix Cardinals could explain the symptoms that were making his life a misery.

Thus far, Boston University’s Center for the Study of Traumatic Encephalopathy has found evidence of CTE in the autopsied brains of 33 former NFL players, including that of Duerson, according to a report published in December in an early online version of the journal Brain.

Some hope that the new research is just the beginning.

“This is a step forward and it emphasizes the importance of what PET scanning might hold as we go forward in trying to diagnose the condition [in living players],” says Maroon.

Maroon and others say they believe that CTE is the result of a normal inflammatory response to brain injury that runs amok. The theory is that the inflammation switch gets turned on and stays on in people with a certain genetic predisposition, Maroon says.

“One might conjecture that it’s like starting a small brush fire in a dry forest,” Maroon said. “If the predisposition is there and the fire is lit, then it may continue inexorably.”

Maroon hopes that new radio tracers will be found that highlight the early signs of inflammation before tau has even begun to accumulate. Then there might be a chance to find therapies that stop CTE from developing, he says. 

See more NBC Health news: 

• Contact sports leave pattern of brain injuries, study finds
• US launches study into youth sports concussions

Each morning, 48-year-old Troy Prater starts his day by getting breakfast for his teenage triplets. On weekdays he checks homework and then hurries them off to school. Then it’s back home to take care of his mom, Ella, who suffers from Alzheimer’s disease. Life, Prater says, “is organized chaos.” 

Prater is among the millions of Americans who have stepped up to do the right thing and take care of family members who can’t take care of themselves. Unfortunately, most caregivers are spread so thin that they don’t have time to take care of their own needs, NBC's Dr. Nancy Snyderman reports.

“Caregivers don’t go to the dentist; they don’t get mammograms or annual checkups,” says Melissa Gartenberg Livney, a clinical
psychologist with the PENN Memory Center at the Perelman School of Medicine at the University of Pennsylvania. “So they get sick.”

Even worse, Livney says, “there’s some evidence that this kind of stress can contribute to the onset of dementia" which is why she and others are trying to encourage caregivers to get help, to find ways to take breaks, and to make and keep their own doctors’ appointments.

How many people have stepped up to take care of a family member?  

One survey found that nearly one third of American households had someone serving as an unpaid family caregiver. That adds up to almost 40 million households with a caregiver present, according to the 2009 survey conducted by the National Alliance for Caregiving in conjunction with the AARP.

Many of those caregivers are dealing with Alzheimer’s, which Livney says can be incredibly stressful.

"Alzheimer's disease is 10 or 15 years of slow and steady loss of the person you once knew," she says. "Caregivers often suffer in silence and feel guilty when they don't feel up to the work."

Currently, there are 5 million Americans who have been diagnosed with the disease, says Beth Kallmyer, vice president of constituent services at the Alzheimer’s Association. “And we estimate that there are 15 million people caring for them.”

Unfortunately, the number of Alzheimer's patients is growing. The Alzheimer’s Association estimates that there will be 16 million Americans with the disease by mid-century if nothing changes. And that means there will be even more of us taking care of spouses and parents suffering from dementia.

Prater, who juggles caregiving along with his normal responsibilities as a dad, acknowledges the dual roles can be very taxing.

“I’m running on adrenaline,” he says. “I’ve lost quite a few pounds.”

What's the answer to getting caregivers to care for themselves?

People like Prater need to ask for help, Kallmyer says. But most seem to feel that caregiving is something they need to do on their own. And that's a setup for disaster, she says.

“When you’re taking care of someone over a period of time, you can’t just soldier on,” Kallmyer says. “At some point your health will be impacted and that will keep you from being the best caregiver you can be. We often ask people, ‘If you get sick and land in the hospital then what is going to happen?’”

Kallmyer suspects that the urge to go it alone is part of the American character. She’d like to see that change.

So would Livney.

"[Caregivers] need to allow themselves to not be perfect," she says.  

They also need to learn to look after their own needs.

“People need to give themselves permission to take care of themselves,” says Livney. “That’s what we focus on. We don’t spend much time talking about the disease and functional aspects of caring for someone with dementia. We try to help people understand how to take care of themselves."

Should high school kids get a genetic test for the risk for Alzheimer’s disease before they’re allowed to play football? Two prominent scientists who study both Alzheimer’s and the traumatic brain injury suffered by some football players raise that ethically charged question in an editorial out Wednesday in the journal Science Translational Medicine.

We all carry a gene called APOE which comes in three forms. If we carry one copy of the form called E4, it triples our lifetime risk for Alzheimer’s. About 10 percent of the U.S. population falls in that category. If we have two copies of E4, the lifetime Alzheimer’s risk is 15 times greater. About 2 percent of us have that genetic makeup.

Although the connection between APOE E4 and Alzheimer’s risk has been known for years, few have suggested it as a screening tool because there’s no known way to prevent the mind-robbing disease. But, now as scientists want to test drugs as early as possible as potential methods of preventing Alzheimer’s, APOE is getting more attention, as are brain scans and other techniques that might determine who is at risk.

At the same time, scientists have been finding that football players, boxers and soldiers suffering blast injuries are more likely to develop chronic traumatic encephalopathy (CTE), the form of dementia that can follow a brain injury -- if they have one or two copies of the E4 version of APOE.

Neurologist Dr. Sam Gandy of Mt. Sinai Medical Center in New York and Alzheimer’s researcher Dr. Steven DeKosky of the University of Virginia School of Medicine, Charlottesville, conducted a poll of 49 colleagues. By a 2 to 1 decision their fellow scientists said it is not yet appropriate to test high school students, and by a 3 to 1 ratio they opposed testing military recruits. But few of the scientists dismissed the ideas out of hand.

As the evidence of a connection mounts, testing may become more of an imperative.

There are obvious, enormous ethical difficulties. Telling a 14-year-old that he or she faces an increased lifetime risk of Alzheimer’s could lead to unknowable future strains on individuals and families, as well as a lifetime of difficulty in getting health and life insurance. But if scientists learn how to intervene to prevent the Alzheimer’s, or if the evidence of increased risk from sports or on the battlefield becomes overwhelming, the question may be asked more often.

Robert Bazell is NBC's chief science and medical correspondent. Follow him on Facebook and on Twitter: @RobertBazellNBC.

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