The tragic death of college football player,
Zack Langston, has brought attention to brain injuries that are acquired during
longtime football careers. The death of Mrs. Langston’s son has led her to make
the statement, “I
absolutely do not feel kids should be playing football”. This mother’s fear is
one among many voices of opposition and those in legal battle against the NCAA
for their contribution to and perpetuation of the progressive neurodegenerative
brain disease Chronic Traumatic Encephalopathy (CTE). The cries of mothers are
outing the NFL and NCAA on their inadequate educational resources on CTE available
for current players and previous players who experience[d] successive brain
trauma from the consecutive hits and tackles associated with the game of
football. Their silence on CTE leaves players unaware of their risks associated
with playing football in their leagues. The character of CTE can be examined
through the case of Zack Langston and the neurodegenerative consequences that
led to Zack’s choice to commit suicide, a behavior so distinct from his personality
before his career in college football. Langston had a long history of football,
in fact one of his major accomplishments before he was recruited for his
college football team was receiving the “hammer” award for being his high
school football team’s hardest hitter. At the time of his death he was exiting
a career as a linebacker for Pittsburg State University in Kansas, whom he played
for all four years of his college career. During the time that he spent on his
college football team his mother remembers a specific instance in which he was
taken out of the game on a stretcher for dehydration. Although, it was at that
point, that as she looked into the eyes of her crying son, that she knew
something had changed. In fact, a few years after his college graduation, at
age 26, Zack shot himself. Before he took his own life (via a method in which
the brain was preserved) he told his girl friend that he wanted his brain to be
examined by scientists because he knew something was wrong. In fact, after the
conclusion of his college football career, he told his mother, “he believed
football had ‘messed up his brain’, but [he] could not explain how”. Even though
the coroner who examined his brain said that his brain was normal, his mother
still had her doubts. The character of her son had changed so drastically after
the termination of his football career. He began to develop depression, anxiety,
and bouts of aggression. It became evident that something else was going on
here that had to be further examined. Recently, more and more research is
successfully connecting brain degenerative diseases and concussive behavior
associated with football. Due to these new conclusions, and the connection that
Niki Langston made between those characteristics of CTE and those symptoms that
her son experienced, she sent her son’s brain to Boston University to be
further examined. It took eight months for researchers at Boston University to
conclude that her son did in fact have CTE.
Boston
University, the leading institution in CTE research, in a recent study “found
CTE in the brains of 48 of the 53 college football players, the largest such
study to date.” These brains were of people who experienced symptoms during
their lives that provoked the study of their brains after death. In order to
begin to identify symptoms of this disease, it is vital to examine the disease in its entirety. In
doing so, it is also helpful to compare it to another neurodegenerative disease
that already gets a lot of attention from the science community, Alzheimer’s
Disease (AD).
CTE is
characterized by similar signs as some other neurodegenerative diseases that
cause a substantial loss of neurons over a period of years, such as Alzheimer’s
Disease (AD). Like AD, CTE can only be identified after death via postmortem
neuropathological analysis, as those which were used by Boston University to
identify Zack Langston’s case of CTE. The symptoms that are identifiable after
the onset of CTE neurodegeneration include memory loss, confusion, impaired judgment,
depression, progressive dementia, symptoms of Parkinson’s disease, and an inability
to have impulse control which leads to increases in aggression. It is well
known that patients with AD experience memory loss, develop impairments in
decision making, suffer behavior and personality changes, as well as an
inability to recognize faces and process language. Similarly, both CTE and AD
are diseases resulting in dementia.
What
is troubling about CTE is that these repetitive hits sustained over a period of years, like
those experienced by a football career, whether classified as concussive or subconcussive
contribute to the development of the disease. In fact, the evidence of current
research points to hits to the head that do not cause full- concussions to be
the biggest factor contributing to this neural degeneration. Because of this
type of onset, CTE has also been identified in military veterans, other
athletes (even those who did not play sports past high school or college). The
subsequent degenerative alterations made to the brain as a result of concussive
or subconcussive behavior onset months, years, or even decades after the the
last brain trauma. These subconcussive hits are instances in which the brain
cells are shaken not violently enough to death (as seen with concussions) but
to the point in which the damage is severe enough to result in deficits and dysfunctions
of the cells that are seen as the neurons age. The successive amounts of subconcussive
hits continually damages the neuronal cells over and over again.
Although the
symptoms of CTE resemble those of Alzheimer’s Disease, there are evident differences
between the two neurodegenerative diseases. For one, symptoms of CTE present
themselves earlier on than those of AD. CTE symptoms become apparent in people
in their late 20’s or 30’s verses those with AD that become identifiable in
their late 60’s. A way that people can think of CTE is that “ ‘[i]mpulsive,
explosive and sometimes violent behavior; depression; and a tendency toward
suicidality” becoming associated with “younger age and an earlier stage of CTE
pathology’, as identified by the most recent study published in the Journal of the American Medical Association.” CTE symptoms appear in younger generations,
and are becoming increasingly identifiable in previous athletes/ football
players as more and more research is executed to classify CTE. Moreover, there are differences in the
severity and timing of specific symptoms between the type of neurodegeneration seen
in CTE verses AD. The central symptoms of AD involve those of memory, and
oftentimes begins with short- term memory impairment. While the major areas
that suffer and are the most symptomatically identifiable for CTE patients
involve deficits in judgment, reasoning, problem solving, impulse control, and
aggression. Those with CTE and AD can be characteristically identifiable and
separated by the onset of symptoms, and by which types of symptoms appear from
the onset of degeneration. Currently there is not a cure for either CTE or AD,
for one, because both can not be classified until an examination of the brain
after death, and two, according to Dr. Stutzmann of the Neuroscience department
at Rosalind Franklin University of Medicine and Science, neurodegenerative
diseases are not being approached correctly.
Specifically in the work of Dr.
Grace Stutzmann, the problem with current methods of tackling AD is that researchers are targeting
late stage features of the disease instead of problems associated with early
memory formation. AD is examined by complications associated with amyloid
plaques, the degradation of tau proteins, degeneration of synapses, and
cholinergic deficits. Her research is targeting the prevention of early
synaptic loss and degeneration. Dr. Stutzmann was able to identify that
presynaptically something is going wrong in the brains of AD patients. The AD
animals used in her studies both have less presynaptic vesicles on hand to
support high levels of activity and have a more spontaneous release of vesicles
at the synaptic cleft. These factors have led to the identification of early
onsets in the disease, in which increased levels of calcium is present in order
to counteract the losses in synaptic strength in these areas of degeneration.
The impact in the increase of calcium is a higher and more spontaneous release
of vesicles from the synapses as well as a significant contribution to the maintenance
of neural plasticity. However, in the end, Dr. Stuzmann concluded that the
identification of an increase in calcium levels in AD mice blunted neuronal
activity and that this increase is what starts the pathway of degeneration.
As the scientific and
medical community continue to look for a cure for both CTE and AD, there are
evident factors that seem to make CTE preventable while AD remains under
investigation. Avoiding contact sports
in which tackling is involved would seem to prevent the onset of degeneration
of neurons in CTE patients. This concern of developing CTE has moved to younger
generations of children who have increasing begun to play contact sports at a
younger age. There are thousands of middle school, high school, and college
football players who are unaware of the consequences/ risks of developing CTE.
Nicki Langston and many others whose sons suffer[ed] from CTE suggest that kids
younger than 14 years of age should not be playing tackle football at the least
as a preventative measure.
The identification and
continued research of CTE has posed a problem for the
lucrative business of football in the United States. As the research in CTE
advances, the number of lawsuits against the NCAA and NFL rise. As new
attention is given to the connection between CTE and football, there is an
increase in tactics of large corporations such as the NCAA and the NFL to keep
the new findings silent among the football community and the general public who
fund the football league. Those in opposition, like Niki Langston, have already
successfully won a lawsuit against the NCAA, which forced them to establish a
$70 million monitoring fund for their former college players. Others are
currently fighting for compensation for former players and their families who
have developed CTE.
Overall, steps to prevent AD remain unknown,
but the direct cause of CTE can be prevented by simply avoiding head injuries
while playing football. How the United States’ football leagues will address
the new established risks of CTE when it comes to educating their players and
how they will react to the potential of its continued research to diminish
monetary funding to the lucrative sport is unknown. The fact is that CTE is a
neurodegenerative disease that should no longer be kept silent because it has
such a large impact on the participants in the one game that American society revolves
around, football. When held on a comparative level to AD, maybe people will
start to pay attention to the impact of CTE on society.
Works Cited
Chakroborty,
S., Kim, J., Schneider, C., West, A., Stutzmann, G.(2015). Nitric Oxide Signaling Is Recruited As a
Compensatory Mechanism for Sustaining Synaptic Plasticity in Alzheimer’s
Disease Mice. The Journal Of
Neuroscience. 35(17):6893– 6902. Retrieved November 22, 2017.
CTE
Resources. (n.d.). Retrieved from
Concussion Legacy Foundation:
https://concussionfoundation.org/CTE-resources/subconcussive-impacts
Frequently Asked Questions About CTE. (n.d.). (B.
University, Producer) Retrieved from Boston University Research: CTE Center:
https://www.bu.edu/cte/about/frequently-asked-questions/
Glenza, J. (2017, November 25th). A tragic death and college football's
reckoning over brain injuries amid a new class-action lawsuit. Retrieved
from The Guardian:
https://www.theguardian.com/sport/2017/nov/25/college-football-cte-ncaa-lawsuit-zack-langston
