Chronic Traumatic Encephalopathy
Karyna Lipai
Touro College



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The purpose of this paper
is discussing (CTE) cause, diagnosis, treatment, advancements and ways of
prevention. Existing and current methods of treating of CTE have been
investigated with the purpose of bringing some more light in diagnose and
treatment of CTE. Deficits of the existing methods have been identified as well
as the probable future ways of mitigating the situation of CTE treatment and
prevention. There still identification that researchers of CTE should have a
clear understanding of the pathology of CTE. The conclusion is that no current
method is available to diagnose CTE in premortem approach; only postmortem is


Chronic Traumatic Encephalopathy

The disorder is believed
to be linked with contact to recurrence of skull trauma. It was realized in the
1900’s and it was reported in clinical cases that were defined in boxers. The
term Chronic Traumatic Encephalopathy is the replacement of the term ‘punch drunk’
that was in use by then and was introduced by a Dr. Harrison Martland, about 86
years ago (Martland, 1928). Later, the disorder became popularly known as
pugilistic dementia and then the name moved to chronic progressive traumatic
encephalopathy of boxers, before changing to the current term, Chronic
Traumatic Encephalopathy (Critchley, 1957; Millspaugh, 1937). Furthermore, the
disorder consists of a number of an array of clinical manifestations, which
range from behavior and motor dysfunction, complete dementia, to mild

On the other hand, it has
been identified that CTE takes place in patients who have a history of
closed-head trauma. The condition is highly found in individuals that are prone
to repetitive symptomatic concussions. The individuals include military
old-timers, athletes, and domestic violence sufferers. What trauma does is that
it precipitates the neurodegeneration of the flesh found in the brain and this
lead to forming of tau protein (Blumbergs et al, 2010). Basically, the point is
that CTE the accumulation of p-tau.

More specifically, the
tau proteins are neuro-specific initiators of the formation of the microtubule.
The result of this is the issue that the cerebral transportation of wastes and
nutrients is affected (Castillo-Carranz, 2014). In addition to this, it is
worth noting that cells communicate to enable metabolic processes, and in
reference to the buildup of the defective tau, the communication in between the
cells is interfered with. On the other hand, McKee et al (2009) identified
that lack of healthy tau causes what is death termed as neuronal death.

Diagnose of CTE

For the purposes of
developing treatment and diagnostic methodologies, researchers required a clear
understanding of the CTE pathology. They are needed to identify differences
that exist in between neurodegenerative diseases and Chronic Traumatic
Encephalopathy. A study conducted in 2009 identified a pervasive cerebral fluid
buildup of mutated tau protein in all the athletes that were used in the study.
On the side of the 24 control subjects, there was no accumulation of tau. The
conclusion of the research was that head the athletes; the head injury was a
result of motor neuron degeneration, and in turn, led to a disease and not
advanced life support. The findings of this research helped in defining the
variations that exist in between Chronic Traumatic Encephalopathy and other
neurological degenerative disorders whose basis are tau.


The research experienced
a development later, and at this time, McKee and Gavett (2011), explained the
buildup of tau protein and the role it has in the degenerative process of
Chronic Traumatic Encephalopathy. The report includes that information that the
brain temporary deformation is due to the motion of the initial trauma as well
as the aggravation by traumatic injuries following each other, which were
identified to cause stretching of the axons (Critchley, 1957). This then would
lead to damage that in turn changes the degree of the axon membrane
permeability, which causes a larger amount of calcium inflow.  Also, the
permeability enhances the release of apoptotic aggregation of tau proteins. In
this regard, this means that the neurodegeneration was identified to originate
from the cortical sulci, and before then from the blood vessels surrounding on
a small area, which then extends to bigger slices of the brain. On the other
hand, McKee et al (2011) argued that neuropsychological and physical sequelae
of Chronic Traumatic Encephalopathy are caused by the tau-toxic factor that is
associated with systematic degeneration in parts of the brain that have the
task of regulating emotions, memory, and other cognitive functions.

McKee et al (2011)
research suggested genetic susceptibility to the post-trauma buildup of the tau
proteins for the individual who have inherited cholesterol transport gene known
as Apolipoprotein E4 ( McKee et al, 2011). The Apolipoprotein E4 gene has been
noted as the risk factor for a number of Alzheimer’s and Sclerosis
disorders.  The gene can also increase the risk of developing Chronic
Traumatic Encephalopathy for about ten times. The gene comprises of one type of
amino acid, where the string of this amino acid has 299 amino acids units that
lead to misfolding. The brain responds to the abnormality recognizing it, and
then releases enzymes that cut the tail of the protein. The clumping together
of the brain tau is caused by free-floating pieces of neurotoxic through
mutations (Mahley & Huang, 2012). With this back in mind, can help in
explaining the reason behind the development of Chronic Traumatic
Encephalopathy due to repetitive closed-head trauma in some victims while
others fail to.


Chronic Traumatic
Encephalopathy disorder has been on the high profile in the media for its
relationship with professional athletes. Chronic Traumatic Encephalopathy is
marked depression, aggression, and behavior that appears of more of suicidal
(Omalu, 2010).  Currently, there is no consistent way to identify Chronic
Traumatic Encephalopathy. Diagnosis of a disorder needs degeneration evidence
of the tissue of the brain, tau deposits as well as other proteins in the
brain. The drawback associated with evidence is only possible upon inspection
after death (autopsy) (Fainaru & Fainaru-Wada, 2013). To mitigate the current
situation, research is continuing with the purpose of finding a test for
Chronic Traumatic Encephalopathy that can be applied while individuals are
still living (Wetjen, Pichelmann, & Atkinson, 2010).  Another
continuing research is on the study brain of people that may be having the
disorder, for example, the footballers.

In attempts to diagnose
CTE, a number of neuropsychological tests are carried out and include
biomarkers and brain imaging (Scrimgeour, 2014).


Due to the fact that
there has been a deficit of premortem diagnostic methodology for CTE, the
approach that has been in use is its treatment. However, due to premortem
advances in the process of identifying the tau biomarkers, there has been a
clinical progress aimed at treating and preventing CTE has been completed
(Small et al, 2013).

On the other hand,
despite the phenomenon of no clinically proven treatment of CTE, a number of
experiments have elevated the state of the situation. A recent study has
indicated that an intervention of the treatment by use of a fish that is rich
in omega-3 oil might need neuroprotective features that can reduce the brain
injury of the trauma.  What really happens is that the metabolized fatty
acids of the omega-3 resolve and metabolize and fights the inflammation by
suppressing the proinflammatory cytokines (Mills et al, 2011). The use of the
fish oil immediately after traumatic brain injury has taken place can be
rewarding in the sense that this act would bring down the inflammation,
repairing of the damaged cells; and at the same time reduces the incidence of
the second impact syndrome (Scrimgeour & Condlin, 2014).

Towards the success of
treating of CTE, early trials have been made and they are promising, Dr.
Trojanowski, from the University of Pennsylvania, has shown that use of an
experimental drug stops tau degeneration progression as well as reversing the
tau tangle pathology, hence improving the functionality of
cognitive.(Bachstetter et al, 2012)

An additional probable
action that is being researched on by Dr. William and Margret. The method being
used in this research comprise of LED light being passed through the skull of
the children’s and veterans with post-concussive symptoms for the purposes of
stimulating the healing after injuries have taken place in the brain. The
motivating thing on this study is on the belief that light is important when
stimulating ATP production, an energy molecule that identified to facilitate
the restoration of the chemical balance of cells of the brain after the injury
has occurred (Sportingjim, 2013).

There is a complication
of the context of the strategic treatment by the intricacies of aiming at the
defective protein by avoiding injuring the protein functionality.

Despite advancement in
the area of treatment and prevention of CTE, the available ways of inhibition
signify dodging of the overall damage of brain by the disturbance (Stoller,
2011). The improvements in the area of care apparatus for interaction
sporting.. Alteration of the lifestyles, for example, regular practices, having
a diet that is healthy, and at the same time avoiding alcohol and drugs are
preferred. This should be done together with a therapist in order to cope with
the emotional difficulties.



CTE is a late impact of
closed-head trauma that lacks a treatment that is clinically proven. Although
this is the case, it is worth noting that CTE diagnosis is done through
post-mortem examination of the tissues of the cerebral tissues. The research
that is going on is providing promising advances with the aim of premortem
identification of biomarkers by cutting the edge of the image method (Goldstein
et al, 2012). There exists a belief by clinical investigators that the finding
of the researchers that are being carried on, could lead to possible treatments
and detection in stopping of neurodegeneration. We are having the current
strategies being focused on the clinical management of symptoms and signs
only.  All in all, prevention of the head trauma is the only option
available for preventing Chronic Traumatic Encephalopathy. Individuals prone to
CTE should be aware of developmental determinants in for the purposes of
protecting themselves appropriately.





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