Chronic traumatic encephalopathy (CTE) is a progressive degenerative disease that develops in the brains of people with a history of head injuries or multiple concussions. Common examples of those most at risk for developing the condition include former football players, boxers, hockey players, mixed martial arts fighters, and military combat veterans. To date, a definitive diagnosis can only be made through an autopsy and partial dissection of the brain, though a few pilot programs aimed at diagnosing CTE in the living are under development.
Researchers have discovered that repetitive head trauma is the only known primary cause of CTE. Not all people who suffer repetitive head injuries will develop CTE later in life, but patients (such as professional athletes) who do experience more than one serious concussion face an exponentially higher probability of developing the degenerative disease in their 50s, 60s, or 70s.
CTE’s Effect on the Brain – What does it do?
CTE is a progressive degeneration of the brain tissue, involving the build-up of an abnormal and potentially toxic protein called tau. Research has shown that a human brain riddled with CTE actually loses weight, associated with atrophy of the frontal and temporal cortices as well as the medial temporal lobe. On a cellular level, neurons are subject to atrophy and eventually die off as a result of a series of chemical changes and the formation of tau protein.
Physical changes in the brain can begin months, years, or even decades after someone experiences their last known concussion. As tau formation sets in, early brain degeneration has been known to cause many of the following emotional and psychological impairments:
- Aggression, short temper
- Confusion
- Impulse control problems
- Memory loss
- Progressive dementia (gradual)
- Sleep disruptions
- Depression
- Emotional imbalance, mood disorders
- Headaches, migraines
- Impaired judgment
What has Science Learned about Chronic Traumatic Encephalopathy?
In 2013, a research team completed a CTE pilot study at UCLA. This team claims to have established the first effective model geared toward diagnosing CTE in living patients. The new approach used to confirm the presence of CTE in living brains is based on positron emission tomography, or PET scans. UCLA scientists developed an intravenous radioactive compound that binds to tau proteins in the brain. The amount of compound that becomes “stuck” to tau in the brain can then be viewed more closely using the PET scan.
Former Dallas Cowboys’ running back, Tony Dorsett was among the first volunteers to participate in a pilot-phase test. Tony received preliminary positive results, indicating that he does show early signs of tau formation in his brain tissue. However, the UCLA test is still in its pilot phase and has not yet received government approval. A brain autopsy is still the only way to officially diagnose CTE.
Notably, scanning for the presence of tau protein could also lead to advances in spinal cord injury research. In the UCLA study, pathologists use special dyes to identify tau proteins, including astrocytes and glia. The formation of astrocytes and glia is a major part of the same reaction that causes secondary damage after a spinal cord injury (SCI). When nerves are severed in the spinal cord, astrocytes and glia form glial scars across damaged neurons. Glial scars cover broken axons, blocking them from reconnecting and preventing neurons from transmitting signals. This appears to be a shared trait common to injured nerve cells. Eventually discovering a way to block or break apart glia formations could unlock a potentially effective treatment for spinal cord injuries in addition to providing a way of deterring or even preventing the development of CTE in those with a history of multiple concussions.
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