A new brain-imaging technique has been developed to identify chronic traumatic encephalopathy (CTE) in living patients.
Sports-related head injuries and mild traumatic brain injuries have been plastered among headlines during the previous few months, informing the public of long-term damage that has become more apparent among former and current athletes – most notably, professional football players.
No method for early detection or tracking of brain changes caused by these types of injuries has been created before, despite the catastrophic outcomes associated with them and the vast number of athletes engaging in contact sports who put themselves at risk.
For the first time, a group of researchers from UCLA have developed a brain-imaging tool to recognize the unusual tau proteins linked with this type of recurring head injury in five former NFL players who are still living. Before this, identification of the presence of this protein, which is also linked to Alzheimer’s disease, could only be confirmed via autopsy.
These initial findings came from a small study that was published in the American Journal of Geriatric Psychiatry.
Previous studies have shown that professional athletes in contact sports who receive recurring concussions or mild traumatic brain injuries could develop CTE, a degenerative condition characterized by an excess of tau protein.
CTE is linked to the following:
- progressive dementia
- abnormal gait
- memory loss
- suicidal behavior
- personality changes
Lead study author Dr. Gary Small, UCLA’s Parlow Solomon, Professor on Aging and a professor of psychiatry and biobehavioral sciences at the Semel Institute for Neuroscience and Human Behavior at UCLA, says:
“Early detection of tau proteins may help us to understand what is happening sooner in the brains of these injured athletes. Our findings may also guide us in developing strategies and interventions to protect those with early symptoms, rather than try to repair damage once it becomes extensive.”
The researchers recruited five former NFL players who were 45 years of age or older. Each participant had a history of at least one concussion and a few were suffering from mood or cognitive symptoms. The players were from all different positions: guard, center, defensive lineman, linebacker, and quarterback.
Wayne Clark, a player in the study who had normal cognitive function, commented: “I hope that my participation in these kinds of studies will lead to a better understanding of the consequences of repeated head injury and new standards to protect players from sports concussions.”
Scientists from UCLA used a brain-imaging tool that was originally developed for examining neurological changes linked to Alzheimer’s disease.
They put to work a chemical marker they made named FDDNP, which binds to deposits of amyloid beta “plaques” and neurofibrillary tau “tangles” (telltale signs of Alzheimer’s) – then they viewed it using a PET (positron emission tomography) scan. The researchers were able to identify where in the brain these irregular proteins built up.
Participants received intravenous injections of FDDNP, while the researchers then performed PET brain scans and compared them to those of healthy men with comparable BMI, education, age, and family history of dementia.
The scientists discovered that in comparison to healthy men, the NFL players had increased levels of FDDNP in the amygdala and subcortical regions of the brain – the areas that control emotions, behavior, memory, and learning. Participants who had a greater number of concussions had higher levels of FDDNP.
Study author Dr. Jorge R. Barrio, a professor of molecular and medical pharmacology at the David Geffen School of Medicine at UCLA, said, “The FDDNP binding patterns in the players’ scans were consistent with the tau deposit patterns that have been observed at autopsy in CTE cases.”
The participants also received a standard clinical assessment to measure their degree of depression and cognitive ability. The NFL players had more depressive symptoms than the healthy men and scored lower on cognitive ability tests, exhibiting evidence of cognitive loss. The signs of FDDNP appear to show a range of mental symptoms that have been previously seen in CTE cases, the authors point out.
Small points out that larger follow-up studies are required to measure the impact and usefulness of identifying these tau proteins early, but with the large number of people at risk for concussions, a testing method showing what happens in the brain during the early stages may have a significant influence on public health.
Study author Dr. Julian Bailes, director of the Brain Injury Research Institute and the Bennett Tarkington Chairman of the department of neurosurgery at NorthShore University HealthSystem based in Evanston, IL, concluded on the topic of CTE research:
“It is the holy grail of CTE research to be able to identify those who are suffering from the syndrome early, while they’re still alive. Discovering the effects of prior brain trauma earlier opens up possibilities for symptom treatment and prevention.”
Written by Kelly Fitzgerald