The up-and-coming professional football player Chris Borland, of the San Francisco 49ers, is now leaving the sport out of concern that a career in football would increase his risk of brain disease. But what types of neurological problems have been linked with football, and how might these arise?
On Monday (March 16), Borland announced he was retiring from football after studying the link between football head injuries and degenerative brain disease, and discussing his decision with friends, family members, concussion researchers and teammates, according to ESPN.
"From what I've researched and what I've experienced, I don't think it's worth the risk," Borland told ESPN. "I just want to live a long, healthy life, and I don't want to have any neurological diseases or die younger than I would otherwise," Borland said. [ 6 Foods That Are Good for Your Brain ]
The types of brain damage that can occur as a result of being a professional football player have received increased attention in recent years. For example, there is growing awareness of a particularly severe degenerative brain disease called chronic traumatic encephalopathy (CTE). The disease has been linked to the deaths of Tom McHale, who played for the Tampa Bay Buccaneers, and Dave Duerson, who played for the Chicago Bears.
In fact, researchers at Boston University have now found signs of CTE in nearly 60 former professional football players when their brains were analyzed after their deaths, according to the university's CTE Center. (CTE can be diagnosed only after death.)
In most cases, CTE is thought to be caused by repeated blows to the head, which damage brain tissue and lead to a buildup of an abnormal protein called tau, according to the CTE Center.
In addition to football players, CTE has also been seen in boxers and hockey players. It causes symptoms such as impaired learning and memory loss, and has been linked with suicide. These symptoms often begin years or decades after players have ended their athletic careers, according to the Boston University center.
It's not known how many hits to the head or concussions a person needs to experience to develop CTE. A person's genetics also likely plays a role, because not everyone with a history of repeated brain trauma develops the disease, the CTE Center says.
Other studies have linked professional football with neurological problems that may or may not be related to CTE. In a 2013 study, researchers scanned the brains of retired football players while they performed certain tasks and found that the players were more likely to have abnormalities in their brain activity, compared with healthy people.
A 2012 study found that the risk of death from Alzheimer's and ALS (also called Lou Gehrig's disease) was 4 times higher among NFL players than the general population. It's possible that CTE may have been the true cause of death in some of these cases, but the study was not able to determine this because it examined death certificates, which didn't list CTE as a cause of death, the researchers said.
Another study of 34 retired NFL players who had suffered concussions found that those who had experienced more concussions had more symptoms of depression.
Concussions can damage the brain's white matter — the tissue that forms "cables" in the brain and allows different regions to communicate, according to the study. The researchers also found they could predict which players had depression by examining images of their brains' white matter, suggesting a link between white matter changes and depression.
Another theory as to why hits to the head increase the risk of brain disease points to the body's immune system as the culprit.
According to the hypothesis, from researchers at the University of Rochester Medical Center, hits to the head open up the blood brain barrier, and allow a brain protein called S100B to leak out into the blood and circulate around the body. Because the body is not used to seeing this protein in the blood, it may develop antibodies to it, as if it were a foreign compound. If these antibodies then find their way back into the brain, they could attack the brain itself, the researchers say. However, much more research is needed to evaluate this hypothesis.
Currently, CTE cannot be diagnosed in living people, but researchers are working on ways to identify the condition early. In a 2013 study of retired NFL players who had thinking and mood problems, researchers injected the players with a chemical marker, called FDDNP, which binds to the tau protein. The researchers found that FDDNP levels were higher in the brains of the former NFL players, compared with the brains of healthy people, suggesting that tau was in fact building up in their brains.
Identifying the disease early could potentially lead to ways to stop its progression, the researchers said.
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