Researchers investigating chronic traumatic encephalopathy, or CTE, may be able to use a test originally developed to detect Alzheimer’s disease to identify the condition in living people, early findings suggest.
The approach centers on a protein that is a well-known hallmark of Alzheimer’s disease. The same protein, the findings suggest, may also serve as a biological marker for CTE, a degenerative brain condition associated with repeated head trauma in contact sports. If the link holds up in larger studies, the finding could eventually give doctors a way to diagnose CTE during life rather than only after death.
CTE has become a major concern in sports medicine and public health because of its connection to concussions and repeated blows to the head. The disease has been found in the brains of former athletes in a range of contact sports and has been linked to symptoms that can appear years after someone stops playing. Those symptoms can include memory problems, confusion, impaired judgment, impulse-control difficulties and changes in mood.
At present, however, no established clinical test can confirm CTE in a living person. The diagnosis is typically made by examining brain tissue after death, when the characteristic protein deposits of the disease can be identified. This reality has left athletes, families and physicians with limited tools for assessing the long-term effects of head injuries while a person is still alive.
The new research, described as preliminary, builds on a strategy already familiar in Alzheimer’s research. Tests that measure proteins linked to Alzheimer’s disease are increasingly used to help diagnose the condition and track its progression. The findings suggest that one of those proteins could also help identify the telltale changes of CTE in the brain. If that proves true, an Alzheimer’s-related protein test could be adapted or extended to answer a question that has long troubled people affected by repetitive head impacts: whether the biological changes of CTE have begun.
Because the findings are early, much more work is needed before the approach could be used in clinical practice. Future studies will need to determine how accurately the protein signal distinguishes CTE from Alzheimer’s disease and other forms of dementia, whether it can detect the condition at an early stage and whether test results match tissue changes observed after death. Future efforts will also need to examine people from different sports and with different levels of head-trauma exposure, along with people who have no history of head injury, to understand the test’s strengths and limitations.
The potential payoff is significant. A test that could identify CTE in a living person would change how the condition is managed, allowing earlier counseling, closer monitoring and more targeted research on possible treatments. It could also help in the design of clinical trials by making it easier to enroll participants known to have the biological changes associated with CTE, rather than waiting for symptoms to become obvious. Such a tool might eventually give doctors and patients a clearer picture of neurological risk after years of involvement in contact sports.
For now, the study stands as an early step. The possibility that an Alzheimer’s-related protein marker could also point to CTE highlights the fact that brain diseases often share underlying biological features, and that tools developed for one condition can sometimes prove useful for another. The new findings offer a starting point for larger efforts aimed at answering whether CTE can be reliably detected during life.
