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.
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.