In 2002, Dr. Bennet Omalu wrote in the journal Neurosurgery about a patient with a history of repeated head trauma and severe psychiatric problems, personality changes, and cognitive decline. The patient, Mike Webster, had been a football player for the Pittsburgh Steelers who had died of a heart attack at age 50.
Dr. Omalu’s report revealed extensive accumulation in Webster’s brain of an abnormal protein deposit known as tau, which is one of the hallmark abnormalities observed in Alzheimer’s disease. He termed the condition chronic traumatic encephalopathy, or CTE.
However, no one knew whether the tau deposits found in autopsies were a cause or an effect of the symptoms observed. Also unknown was whether something else was going on in the brains of CTE victims to cause their depression, personality changes, and cognitive impairment.
In addition to the abnormal tau accumulation, disruption of the brain’s white matter was observed. This white matter, or myelin, serves as the insulation for the wire-like axons that connect one brain cell to another, allowing neurons to communicate effectively.
Another theory is that dysfunctional brain wiring from multiple brain injuries result in the tau deposits that cause additional damage. Pathologists have also seen evidence of brain inflammation, which many experts believe contributes to the degeneration in Alzheimer’s disease.
Other pathological findings include brain atrophy (shrinkage) and abnormal amyloid protein deposits that are associated with Alzheimer’s disease. However, amyloid is much less extensive than tau in people who have experienced head trauma.
Despite the devastating consequences of CTE and the large number of people at risk, the syndrome has only recently received widespread attention. Specific treatments have not been developed, and no method for early detection has yet been established.
As an Alzheimer’s and brain aging researcher, I understood that early recognition and identification of those at high risk would allow doctors to develop strategies and interventions to protect a healthy brain, rather than attempt to repair damage once it becomes extensive.
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