CTE Brain








Until now, Chronic Traumatic Encephalopathy (CTE), a progressive brain disease linked to repetitive head trauma from rough sports, military service and abuse has only been diagnosed after death. Scientists at Boston University’s CTE Center have recently identified a protein in brain tissue and cerebrospinal fluid that is higher in brain samples and spinal fluid of people with diagnosed CTE, which may enable doctors to diagnose CTE in living patients.

“The whole playing field changes because once there’s a way to diagnose CTE before death, we can start to evaluate different treatments to see if they’re efficacious,” said Dr. Ann McKee of Boston University’s CTE Center. “If it enables us to diagnose CTE in the very earliest stages, we would be able to advise an individual on whether or not to continue in the activity that’s causing the exposure to head impacts.”

In July 2017, Dr. McKee with researchers at VA Boston Healthcare System (VABHS) and Boston University School of Medicine examined the brains of 202 deceased American football players, and found 87 percent of them had CTE, as measured by the amount of damage. The brain of someone with CTE is marked with abnormal clumps of tau protein in a pattern unique to the disorder. Among NFL players, that percentage increased to 99 percent.

Two months later, Dr. McKee and her team of researchers discovered a protein in postmortem brain tissue and cerebrospinal fluid called CLL11, which is also present in Alzheimer’s disease, Amyotrophic Lateral Sclerosis and Huntington’s disease, but at higher levels in the brains of those with CTE. Elevated levels of CLL11 were found among people with CTE who had played sixteen or more years of football, with levels increased with the number of repetitive head impacts those people had sustained during their lifetime. CTE causes memory loss, mood swings and impulsive behavior, depression, and suicidal thoughts. A number of NFL players who committed suicide in recent years were found to have had CTE.

When CTE is suspected, doctors may be able to use spinal taps to analyze spinal fluid in living patients for levels of CLL11. Dr. McKee predicts that examination of CLL11 in cerebrospinal fluid could serve as one of several biomarker tests, along with brain scans and body fluid tests, to measure the tau protein used to diagnose CTE. A fluid biomarker test to measure levels of CLL11 would be less expensive than imaging tests and brain scans that require patients to be exposed to low levels of radiation. Football players also can be too large for conventional scanners or they may have metal implants.

Once CTE is diagnosed at the earliest stages, a patient can be advised on whether or not to continue in the activity that causes the exposure to head impacts and given a treatment plan incorporating the most appropriate therapies for CTE. Currently, there is no cure for CTE, but a diagnosis during a patient’s lifetime could help offer clues about what the patient can expect down the road, to make activity changes and guide treatment.

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