Awareness of CTE and the long-term consequences of repeated head trauma has been steadily rising as the NFL’s concussion crisis – and the accompanying Hollywood blockbuster about the crisis – has brought the conversation into households across America. Despite this, CTE has only been informally recognized as a unique disease until very recently.
The decision came from a consensus panel of expert neuropathologists who concluded that CTE has a unique signature in the brain, a decision that will help solidify the disease in the medical world and lay the foundation for future studies to better define the clinical symptoms, genetic risk factors, and therapeutic strategies for CTE.
The current neuropathological criteria defining CTE, or the NINDS CTE criteria was published earlier this year in the journal Acta Neuropathologica and announced at the Foundation of the National Institutes of Health (NIH) board meeting.
CTE is a degenerative brain disease associated with repeated brain trauma. The condition has been directly tied to clinical concussions, but there is evidence that it may also be associated with repetitive sub-concussive hits which do not immediately cause clinical symptoms. This trauma causes the build-up of an abnormal protein in the brain called tau, which eventually causes memory loss, confusion, impaired judgment, impulse control problems, aggression, depression, and other cognitive issues.
The panel of seven highly respected neuropathologists independently reviewed slides from 25 cases of different diseases associated with tau deposits in the brain without access to any clinical information such as age, sex, clinical symptoms, or athletic exposure, using provisional diagnostic criteria developed by Ann McKee, MD, director of the CTE program at Boston University and Chief of Neuropathology, VA Boston Healthcare System.
The panel found that the criteria distinguished CTE from other similar conditions such as Alzheimer’s disease or age-related memory loss.
“The specific feature considered unique to CTE was the abnormal perivascular accumulation of tau in neurons, astrocytes and cell processes in an irregular pattern at the depths of the cortical sulci,” explained McKee who is corresponding author of the study. “This lesion was not characteristic of any of the other disorders, including Alzheimer’s disease, age-related tauopathy or progressive supranuclear palsy, and has only been found in individuals who were exposed to brain trauma, typically multiple episodes,” she added.