The Centers for Disease Control and Prevention estimates that millions of sports-related concussions and mild traumatic brain injuries occur each year. Despite the consequences of traumatic brain injury and the large number of athletes playing contact sports who are at risk, no method has been developed for early detection or tracking of the brain pathology associated with these injuries.

Now, UCLA researchers have used a brain-imaging tool to identify the abnormal tau proteins associated with this type of repetitive injury in five retired National Football League players who are still living. Previously, confirmation of the presence of this protein, which is also associated with Alzheimer’s disease, could only be established by an autopsy.

The preliminary findings of the small study were reported January 22 in the online issue of the American Journal of Geriatric Psychiatry, the official journal of the American Association for Geriatric Psychiatry.

Previous reports and studies have shown that professional athletes in contact sports who are exposed to repetitive mild traumatic brain injuries may develop ongoing impairment such as chronic traumatic encephalopathy (CTE), a degenerative condition caused by a build up of tau protein. CTE has been associated with memory loss, confusion, progressive dementia, depression, suicidal behavior, personality changes, abnormal gait and tremors.

Larger follow-up studies are needed to determine the impact and usefulness of detecting these tau proteins early, but given the large number of people at risk for mild traumatic brain injury — not only athletes but military personnel, auto accident victims and others — a means of testing what is happening in the brain during the early stages could potentially have a considerable impact on public health.

For the study, the UCLA scientists used a brain-imaging tool they had developed previously for assessing neurological changes associated with Alzheimer’s disease. They employed a chemical marker they created called FDDNP, which binds to deposits of amyloid beta “plaques” and neurofibrillary tau “tangles” — the hallmarks of Alzheimer’s — which they then viewed using a positron emission tomography (PET) scan, providing a “window into the brain.” With this method, researchers are able to pinpoint where in the brain these abnormal proteins accumulate.

After the players received intravenous injections of FDDNP, researchers performed PET brain scans on them and compared the scans to those of healthy men of comparable age, education, body mass index and family history of dementia.

The scientists found that compared to the healthy men, the NFL players had elevated levels of FDDNP in the amygdala and subcortical regions of the brain. These regions control learning, memory, behavior, emotions, and other mental and physical functions. Those players who had experienced a greater number of concussions were found to have higher FDDNP levels.