VB News Desk: Advances in Diagnosing Chronic Traumatic Encephalopathy (CTE)

CTE — or chronic traumatic encephalopathy — is a neurodegenerative disease that occurs as a result of repeated head trauma. Concussions can play a role, but even more insidious are the sub-concussive impacts that happen when the brain moves around within the skull. Tackles and collisions in football are frequent causes of this type of trauma.

These repetitive head injuries eventually lead to the buildup of a protein called tau in the brain, causing symptoms such as memory loss, trouble concentrating, and mood swings. Over time, dementia, paranoia, and suicidal thoughts may occur. In addition, CTE presents with aggression and a loss of impulse control. Though many CTE symptoms are similar to those of Alzheimer’s Disease (AD), CTE typically shows up earlier, when patients are in their 40s (as opposed to their 60s).

As it stands right now, CTE diagnoses are made post-mortem. That is, CTE can be confirmed only when medical professionals analyze brain tissue from a deceased person, looking for elevated levels of tau proteins in specific regions.

Here’s the good news: a study published in April in the New England Journal of Medicine provides a potential path to diagnosing CTE in living patients. The study’s authors used flortaucipir and florbetapir positron-emission tomography (PET) to look for tau and amyloid-beta protein deposition in former NFL players with symptoms of CTE. This group was compared to an asymptomatic control group.

PET scans are frequently used in the diagnosis of cancer, heart disease, and brain disorders. First, patients take a radioactive drug called a tracer (in this case, flortaucipir or florbetapir). Then, they undergo a scan similar to a CT scan. Areas where the tracer concentrates are typically areas of increased chemical activity, and they show up as bright spots on the scan.

These imaging techniques showed that, when compared to a control group without a history of traumatic brain injury, the NFL player group had higher tau levels in several regions of the brain where tau had been found in people posthumously diagnosed with CTE. Elevated amyloid-beta levels (that is, elevated levels of the protein associated with Alzheimer’s) were not found, meaning that the former football players’ cognitive and neuropsychological symptoms weren’t caused by AD.

Ultimately, the results of this study are exciting because finding and refining an imaging technique that can detect elevated tau levels in living brains is a great first step towards being able to diagnose this disease on an individual level.

To learn more about head injuries, the brain, and the skull, check out these articles:  

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