Chronic traumatic encephalopathy (CTE) is a brain disease that has been observed in army veterans and hockey and football players. This brain disease originated in the 1900’s, when a study reported about boxers who appeared to act “punch drunk” by displaying motor deficits as well as speech and memory problems. Today, CTE is widely thought to be caused by repetitive head traumas, such as sustaining a concussion during a sporting event. These head traumas cause a protein called Tau to abnormally clump together in different brain regions and kill brain cells. As a result, symptoms of CTE include impulse control problems, motor deficits and memory loss. Research has shown that even mild head trauma can have long term effects on the brain and can result in the development of CTE. In perhaps the most famous finding to date, a postmortem analysis of brain tissue from 111 ex-NFL football players found that 99% of the brains examined displayed the hallmark pathology of CTE. While these findings were the first of their kind, there was some pushback. The biggest caveat of the findings is that many of the donated brains were studied because families suspected a CTE diagnosis. In addition, like Alzheimer’s disease, an official diagnosis of CTE cannot be made until after an individual dies. If researchers were able to diagnose CTE in living individuals, this would be a major step towards identifying CTE susceptible populations or possible risk factors for developing the disease.
A study published in Neurosurgery claims to be the first to diagnose CTE in a living ex-NFL football player. Scientists used a PET scan to study the brain of a 59-year old man who had played football for 22 years (12 years in the NFL). The study used a radioactive tracer called FDDNP which binds to Tau, and identifies the Tau clusters that are indicative of CTE. At the time of the scan, the man exhibited memory problems, a short temper, and behaved inappropriately as if “his filter was gone”. At the age of 61, 18 months after the PET scan, his wife noticed that he showed declining motor skills, which continued to deteriorate until his death at the age of 63. After his death, his brain was stained for tau deposits, and the deposit levels were compared to the FDDP tracer findings. Researchers found that the PET scan detected a high level of tau deposits in several brain regions like the frontal and temporal cortex. The PET-detected Tau deposit values were very similar to the levels observed postmortem, suggesting that the PET scan using the FDDNP tracer may accurately identify the distinctive CTE pathology in living individuals.
Some scientists claim that the FDDNP tracer may not be specific enough to be used as a diagnostic for CTE. For example, FDDNP also binds to a protein called amyloid, whose plaques can be seen individuals with Alzheimer’s disease. However, the authors argue that the distribution pattern of FDDNP in a CTE brain is distinct from patients with Alzheimer’s disease. Perhaps one of the biggest unanswered questions about CTE is the understanding the incidence of the disease. In the Neurosurgery study, the ex-NFL player had only one reported concussion in his life, and researchers acknowledge that there is no magic number on how many concussions it takes to develop CTE. Furthermore, not everyone with numerous concussions or head trauma goes on to develop CTE. Addressing these problems will be difficult, as CTE symptoms can take months or even years to develop. However, the development and utilization of the FDDNP tracer may put researchers one step closer to identifying and diagnosing CTE before it’s too late.
Article: Postmortem Autopsy-Confirmation of Antemortem [F-18]FDDNP-PET Scans in a Football Player With Chronic Traumatic Encephalopathy
Published November 10, 2017 in Neurosurgery