Sports-related concussions and mild traumatic brain injuries
have grabbed headlines in recent months, as the long-term damage they can cause
becomes increasingly evident among both current and former athletes. The Centers
for Disease Control and Prevention estimates that millions of these injuries
occur each year.
Despite the devastating consequences of traumatic brain injury and the large number of
athletes playing contact sports who are at risk, no method has been developed
for early detection or tracking of the brain pathology associated with these
injuries.
Now, for the first time, UCLA researchers have used a
brain-imaging tool to identify the abnormal tau proteins associated with this
type of repetitive injury in five retired National Football League players who
are still living. Previously, confirmation of the presence of this protein,
which is also associated with Alzheimer's disease, could only be established
by an autopsy.
The preliminary findings of the small study are reported
in the online issue of the
American Journal of Geriatric Psychiatry, the
official journal of the American Association for Geriatric Psychiatry.
Previous reports and studies have shown that professional athletes in
contact sports who are exposed to repetitive mild traumatic brain injuries may
develop ongoing impairment such as chronic traumatic encephalopathy (CTE), a
degenerative condition caused by a build up of tau protein. CTE has been
associated with memory loss, confusion, progressive dementia, depression, suicidal behavior, personality
changes, abnormal gait and tremors.
"Early detection of tau proteins may
help us to understand what is happening sooner in the brains of these injured
athletes," said lead study author Dr. Gary Small, UCLA's Parlow-Solomon
Professor on Aging and a professor of psychiatry and biobehavioral sciences at
the
Semel Institute for Neuroscience and Human Behavior at UCLA. "Our
findings may also guide us in developing strategies and interventions to protect
those with early symptoms, rather than try to repair damage once it becomes
extensive."
Small notes that larger follow-up studies are needed to
determine the impact and usefulness of detecting these tau proteins early, but
given the large number of people at risk for mild traumatic brain injury - not
only athletes but military personnel, auto accident victims and others - a means
of testing what is happening in the brain during the early stages could
potentially have a considerable impact on public health.
For the study, the researchers recruited five retired NFL players who were 45
years of age or older. Each had a history of one or more concussions and some
were experiencing cognitive or mood symptoms. The players represented a range of
positions, including linebacker, quarterback, guard, center and defensive
lineman.
"I hope that my participation in these kinds of studies will
lead to a better understanding of the consequences of repeated head injury and
new standards to protect players from sports concussions," said Wayne Clark, a
player in the study who had normal cognitive function.
For the study,
the UCLA scientists used a brain-imaging tool they had developed previously for
assessing neurological changes associated with Alzheimer's disease. They
employed a chemical marker they created called FDDNP, which binds to deposits of
amyloid beta "plaques" and neurofibrillary tau "tangles" - the hallmarks of
Alzheimer's - which they then viewed using a positron emission tomography (PET)
scan, providing a "window into the brain." With this method, researchers are
able to pinpoint where in the brain these abnormal proteins accumulate.
After the players received intravenous injections of FDDNP, researchers
performed PET brain scans on them and compared the scans to those of healthy men
of comparable age, education, body mass index and family history of dementia.
The scientists found that compared to the healthy men, the NFL players
had elevated levels of FDDNP in the amygdala and subcortical regions of the
brain. These regions control learning, memory, behavior, emotions, and other
mental and physical functions. Those players who had experienced a greater
number of concussions were found to have higher FDDNP levels.
"The FDDNP
binding patterns in the players' scans were consistent with the tau deposit
patterns that have been observed at autopsy in CTE cases," said study author Dr.
Jorge R. Barrio, a professor of molecular and medical pharmacology at the David
Geffen School of Medicine at UCLA.
Each of the research volunteers also
received a standard clinical assessment to gauge their degree of depression
(Hamilton Rating Scale for Depression, or HAM-D) and cognitive ability
(Mini-Mental State Examination, or MMSE). The players had more depressive
symptoms than the healthy men and generally scored lower on the MMSE test,
demonstrating evidence of cognitive loss. Three players had mild cognitive
impairment, one had dementia and another had normal cognitive function.
Elevated levels of FDDNP have been shown in studies to be associated
with cognitive symptoms in normal aging, mild cognitive impairment and dementia,
according to Barrio. The FDDNP signals appear to reflect a range of mental
symptoms that have been observed in CTE cases, he noted.
Although the
FDDNP marker also binds to another abnormal brain protein called amyloid beta,
previous autopsy studies have shown the amyloid plaques are observed in less
than a third of CTE cases in retired football players, suggesting that the FDDNP
signal in the players represents mostly tau deposits in the brain.
"Providing a non-invasive method for early detection is a critical first
step in developing interventions to prevent symptom onset and progression in
CTE," said Small, director of the UCLA Longevity Center. "FDDNP is the only
imaging marker currently available that can provide a measure of tau in living
humans."
According to Small, a recent study of more than 3,400 retired
professional football players showed that they had a higher-than-average risk of
dying from Alzheimer's disease. Small's team also is studying lifestyle
interventions for delaying the onset of Alzheimer's symptoms. His new book "The
Alzheimer's Prevention Program," released in paperback this month, features the
latest research on this topic and offers the public practical strategies for
protecting brain health.
Research into CTE and the long-term effects of
mild traumatic brain injuries such as sports-related concussions has been
picking up momentum.
"It is the holy grail of CTE research to be able to
identify those who are suffering from the syndrome early, while they're still
alive. Discovering the effects of prior brain trauma earlier opens up
possibilities for symptom treatment and prevention," said study author Dr.
Julian Bailes, director of the Brain Injury Research Institute and the Bennett
Tarkington Chairman of the department of neurosurgery at NorthShore University
HealthSystem based in Evanston, IL.
The study was funded by the Brain Injury Research Institute; the Fran and Ray
Stark Foundation Fund for Alzheimer's Disease Research; the Ahmanson Foundation
and the Parlow-Solomon Professorship.
UCLA owns three U.S. patents on
the FDDNP chemical marker. Small and Barrio are among the inventors. Disclosures
are listed in the full study.
Additional study authors included Vladimir
Kepe, Ph.D.; Prabha Siddarth, Ph.D.; Linda M. Ercoli, Ph.D.; Dr. David A.
Merrill; Natacha Donghue, B.A.; Susan Y. Bookheimer, Ph.D.; Jacqueline Martinez,
M.S.; and Dr. Bennet Omalu.
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