The news that former NHL player Derek Boogaard, only 28 when he died last May, had a degenerative brain disease linked to repeated head trauma has invigorated the debate over violence in hockey, and highlighted how little we know about chronic traumatic encephalopathy (CTE).
It has been linked to repeated concussions and has been found in former boxers, professional football players and four NHL players examined by a team of researchers at Boston University. It can only be diagnosed after death, by performing an autopsy.
But the fact Boogaard had already developed the Alzheimer’s-like disease shows the urgency of learning how to detect the condition while athletes are still alive.
This is a key step towards answering crucial questions about CTE: Why do some athletes who experience multiple concussions get it, while others don’t? How does CTE start? How early does permanent brain damage begin?
WHAT IS CTE?
Like Alzheimer’s, the disease results in a progressive decline in memory and brain power and eventually leads to dementia. Symptoms also include depression, suicidal behaviour, personality changes and poor impulse control. It is now diagnosed, after death, by a highly unusual buildup of a protein, called tau, that clogs and kills the brains of Alzheimer’s patients. But in Alzheimer’s there is also a buildup of clumps of aberrant protein called amyloid plaques. This isn’t the case with CTE, so while the symptoms of the two diseases are similar, the patterns of damage are distinctive.
HOW IS DAMAGE DETECTED?
Researchers cut part of the brain into thin slices, then apply a brown stain that will indicate the presence of the tau protein. In healthy brains, scientists need a microscope to detect it; but there is so much of it in the brains of people with CTE, they don’t need one. That buildup – so obvious in the slices – can’t currently be detected with brain imaging, which is why it is not possible to diagnose CTE before death. Until recently, this was also the case with Alzheimer’s disease. But scientists have developed a way to detect a buildup of amyloid plaques using positron emission tomography (PET) scan.
One approach is to find a substance that would bind to tau and show up in a PET scan, building on the success with detecting Alzheimer’s. Tau can also be detected in cerebrospinal fluid, which may be another option. At McGill University in Montreal, Alain Ptito is hoping a more sensitive brain scanner now being developed may allow researchers to spot the telltale damage. He wants to look at changes in white matter, which connects different parts of the brain. In the United States, researchers plan to study 100 retired NFL players to learn how to diagnose the condition.
Long-term studies that follow athletes for years and see which ones develop CTE are essential for answering key questions – as well as the critics who note there is, as yet, no proof concussions cause CTE. In Canada, scientists who are part of the Canadian Sports Concussion Project have begun tracking former CFL players, comparing kickers and non-kickers. “We are trying to understand who gets it and what are the risk factors,” said Robin Green, a Canada research chair in traumatic brain injury at Toronto Rehabilitation Institute.