BU-Led Research Maps the Route to Dementia
Largest-ever study of chronic traumatic encephalopathy
The youngest weren’t even old enough to drink legally—six high school football players who developed the degenerative brain disease chronic traumatic encephalopathy (CTE) before dying. Their brains were among 68 cases in a new, largest-of-its kind study that describes for the first time four progressive stages of CTE.
Published today in the journal Brain, the study “extends our knowledge concerning the spectrum of the clinical and pathological abnormalities associated with CTE,” says Ann McKee, a School of Medicine professor and a codirector of the Center for the Study of Traumatic Encephalopathy (CSTE). McKee led the study, which included 10 BU researchers and was done by the CSTE, the Veterans Affairs Boston Healthcare System, and the Sports Legacy Institute, a nonprofit founded in 2007 by former Harvard football player and professional wrestler Christopher Nowinski and Robert Cantu, a MED clinical professor of neurosurgery and a CSTE codirector. The institute partnered with MED in 2008 to form the CSTE.
CTE is associated with repeated brain trauma and has been found in professional athletes, military veterans, and even some people who injure themselves with repetitive head-banging, the researchers write.
The 68 brains came from men ages 17 to 98; 64 had been athletes (more than a third were also veterans), 3 were vets with no sports background, and one had repeatedly injured himself with head-banging. Almost half (33) of the men had played in the National Football League, one in the Canadian Football League, and 4 in the National Hockey League, and 7 had been professional boxers. Among the athletes whose identities the researchers were permitted to release were several NFL players who died last year: Hall of Fame tight end John Mackey, Hall of Fame running back Ollie Matson, and running back Cookie Gilchrist.
The researchers also interviewed survivors of the brain donors to learn about behaviors exhibited as the disease progressed. In stage I of the illness, CTE victims suffered headaches and had trouble concentrating and remaining attentive; stage II victims showed depression, explosive tempers, and short-term memory problems; in stage III, cognitive impairment and difficulty with planning, organization, handling multiple tasks, and judgment appeared. The researchers report that by the final stage IV, the patients suffered full dementia.
McKee says that despite the study’s advances, information vital to effective treatment of CTE remains elusive, including the disease’s prevalence, distinctions between CTE’s symptoms and those of similar conditions, the influence of genetics, “and whether other environmental exposures also play an additive role” in the illness.
In particular, the paper says, “Inclusion of more rigorous control subjects, such as individuals who experienced repetitive mild traumatic brain injury and did not develop behavioral or cognitive abnormalities, will be extremely useful in future studies.”
Cantu, a coauthor of the paper, says the researchers don’t know how much exposure to brain trauma might trigger CTE, though there’s no evidence that “occasional, isolated, or well-managed concussions” cause it.
The CSTE is a leader in researching the disease, and it maintains a bank of more than 135 donated brains, 80 percent of them showing signs of CTE. More than 600 athletes have pledged their brains to the bank for research after their deaths. The center has spurred the National Football League to make rule changes to better protect players from head trauma.
As a former mid level athlete and proud owner of countless concussions, this issue is pretty terrifying. Are we at a point where we are just learning about the complications or are we close to identifying a way to slow or even stop the degeneration?
Does your research include tauopathies? I was told my first husband who passed away in 1979 at age 45, was the first ever diagnosed with an inherited disorder called Chromosome 17 Disinhibition, Dementia, Parkinsonian, Amyotrophy Complex. The inheritance rate is 50% and it is caused by tau inclusions in the brain. You can find it all over the internet. I now have a terrible dilemma with my son who is 54 years old. In his mid 30’s he seemed to become disinhibited and depressed. I took him to the doctor who had discovered the disorder in his father’s family for an opinion. There was very little knowledge at that time but my son was thought to involved and we continued along that line as he became more disabled. However in December of 2008, one researh doctor had a test done in England showing my son did not as that time display tau inclusions so he was put out of the research. We have no contact with the rest of this large family since my son’s father and I had been divorced although we both went back when he became sick. An American doctor told me that while he could tell of some has Chromosome 17 DDPAC, he could not say that given a negative test for tau, the patient did not have this disorder. I wonder if we could be included in the research as my son is getting worse and I have no answers. Also I think it would be very helpful to the present studies that they know about all the work that has been done on tauopathies. God Bless your endeavors.
In submitting the above information I forgot to mention that son also played high school football and took some terrible hits to the head. When he was fifteen he was knocked unconscious in a game for about five minutes while a doctor tended to him. I had to work that day and since he didn’t tell me I didn’t find out until a week later during which time he continued football practice. I know realize there are two possibilities for his present dilemma.