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 Elevated tau levels found in some concussed former athletes were
associated with signs of damage to brain-cell connection bundles on
brain scans and with poorer performance on cognitive tests, the
study team reports in Neurology.
Past research suggests that elevated levels of certain versions of
the tau protein are a marker of brain cell damage and degeneration,
the authors note.
"We're moving closer to being able to tell at a single-person level,
what they might be in danger of developing," said study coauthor,
Dr. Carmela Tartaglia, the Marion and Gerald Soloway Chair in Brain
Injury and Concussion Research at the University of Toronto.
The elevated levels of tau found in some of the athletes in the
study "make us concerned that there is neurodegeneration going on,"
Tartaglia said. "But we don't know if they have CTE. That can be
determined only after death."
CTE, chronic traumatic encephalopathy, is a neurodegenerative
disease that other studies have linked to repeated jolts to the
brain. Currently it can only be diagnosed on autopsy.
One important finding from the new study, Tartaglia said, is that
not all people who experience multiple concussions end up with
long-lasting brain damage. And that falls in line with what has been
observed in the past.
"Lots of people are exposed to repetitive head injury," Tartaglia
said. "But it definitely looks like not everybody gets this. We're
going to have to start looking very hard at what the difference is
between the two groups."
For the new study, Tartaglia and her colleagues recruited 22 male
former pro athletes - most of them former Canadian Football League
players or pro hockey players, and one snowboarder. For comparison,
they also recruited five healthy volunteers and 12 volunteers who
had been diagnosed with Alzheimer's disease, both groups a mixture
of men and women.
All 39 participants agreed to undergo lumbar punctures so that the
researchers could examine their cerebrospinal fluid for levels of
tau. They also agreed to take cognitive tests and to undergo a type
of brain scan, diffusion tensor imaging, that can provide
information on the integrity of the white matter that sheathes long
brain-cell connections known as axons.
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Tau levels were highest among the volunteers with Alzheimer's and
lowest in the healthy control group. Among the former athletes, 12
out of 22 had higher levels of tau compared to the healthy controls,
but lower than the volunteers with Alzheimer's. The other athletes
had tau levels comparable to those of the healthy controls.
When the researchers analyzed just these two groups of athletes,
they found that the number of concussions an individual experienced
or the number of years he played were not related to his levels of
tau.
They also noted that higher tau levels did correlate well with poor
performance on the cognitive tests and with brain scan findings. In
the brain scans of athletes with higher levels of tau, there were
signs of white matter damage.
The small study does show that axonal degeneration related to brain
injuries can persist for months and years, said Dr. Douglas Smith,
director of the Center for Brain Injury and Repair at the Perelman
School of Medicine in Philadelphia, who wasn't involved in the
research.
Smith's group has found that "in severe traumatic brain injury there
is ongoing axonal degeneration and white matter loss," he said.
"This study tends to support the idea that this may also be the case
in some individuals with repeat concussion exposure."
While the findings show that elevated tau levels appear to indicate
some type of injury process is going on in the brain, they can't
tell you whether this is going to develop into CTE, said Michael
Alosco, associate director of the Alzheimer's Disease Center
Clinical Core at Boston University, who wasn't involved in the
study.
Nevertheless, Alosco said, "it does suggest a pathway through which
repeated head trauma leads to white matter injury and also that
elevations in total tau could be used to detect that injury."
SOURCE: https://bit.ly/2DX0zpc Neurology, online May 8, 2019.
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