Author: Jean-Claude Muller, 穆卓Executive Editor at BtoBioInnovation email@example.com
SPECIAL REPORT #17
Abnormal Tau Protein Levels in Chronic Traumatic Encephalopathy (CTE)
In November 2016, we had reported the first case of a Mixed Martial Arts cage fighter, 25 years of age, to be publicly identified as having been diagnosed with the degenerative brain disease known as chronic traumatic encephalopathy (CTE). The diagnosis was disclosed by Dr. Bennet Omalu, a forensic pathologist who first discovered CTE in a professional football player (in 2003) and in a professional wrestler (in 2007). A few weeks later we had reported news from the Boston Globe that former Patriots running back Kevin Turner, who died in March 2016, at age 46, supposedly from amyotrophic lateral sclerosis, or ALS, commonly known as Lou Gehrig’s disease, in fact died from a severe case of football-related CTE. CTE is a neurodegenerative disease that has been associated with a history of repetitive head impacts in military veterans, in football players and in boxers. The post mortem neuropathological diagnosis is based on a specific pattern of tau deposition with minimal-beta amyloid deposition that differs from other neurodegenerative disorders, including Alzheimer’s disease.
Earlier this week, researchers led by Dr. Robert Stern, Director of Clinical Research at the Boston University CTE Center have published results in the latest edition of the New England Journal of Medicine opening the way to diagnose the brain disease in living people, advancing the knowledge and understanding of an illness that now can only be confirmed after death.
In the reported study, 26 National Football League (NFL) Players were compared to 31 controls while using flortaucipir positron-emission tomography (PET) and florbetapir PET to measure deposition of tau and amyloid-beta in their brains. The selected football players had already apparent cognitive and neuropsychiatric symptoms while the control group was composed of asymptomatic man with no history of traumatic brain injury. The living NFL players had higher tau levels measured by PET scans than controls in brain regions that are affected by CTE but did not have elevated amyloid-beta levels. There is still a misconception about the causes of the disease whereby some people believe a single concussion may trigger the disease. In an interview to WCVB Channel 5 Boston, Stern clearly stated that cumulative and repetitive subconcussive hits to the head are the root of the disease and that there is growing evidence that such hits before the age of 12 may be of utmost importance. But are still a lot of unanswered questions, why some people get the disease and others don’t and how CTE can be treated.
The experimental PET scan also showed differences in patterns between the NFL players group and the control group. “At the beginning of CTE, tau is found in patchy areas around small blood vessels located deep in the valleys of the cortex. From there it can spread throughout other areas of the brain, until the whole brain can become devastated” Stern said. “The PET scan measure cannot yet be used for individual diagnosis” Stern cautions. “We analyzed group data, not individual findings”. By the end of 2019 Stern and his group expect to complete tau and amyloid scans of up to 240 additional people. “In the next five years or so, we will be able to diagnose and detect CTE during life” Stern said. But whether or not the experimental PET scans detected signs of abnormality are linked to CTE or not will not be confirmed unless brains are examined after death. To make it possible Stern says “most of them have agreed to donate their brains”.
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