Reasearch Paper
Reasearch Paper
Reasearch Paper
Kesterholt
Brady Kesterholt
Composition and Culture
SEL 106-04
4/12/18
As Humans, we take things for granted all of the time. One of the most important things
we take for granted is our ability to remember information, names, and the ability to perform a
certain task. Many of these tasks are so simple and easy for us but are also important in our
everyday lives. Losing our ability to remember is a serious and scary condition. This condition is
very real and present in our society today. Alzheimer's disease is a form of dementia that takes
this crucial, and often taken for granted, ability of our brains away from us. The question to
There is no agreeable research on how the disease is caused in humans. However, there is
research and studies to show clear symptoms of the disease and what age is the most at risk of
neurodegeneration of the brain. A study of 367 subjects, 300 of which had Alzheimer’s and 67
without (the control group), was conducted in 2016 by Dr. Ortiz and teammates. These subjects
also had different ethnicities to test the differences in their neurological behaviors and symptoms
of the disease between ethnic groups. These two ethnic groups were Hispanic and Caucasian.
The test was done at the University of California Los Angeles (UCLA) in their Alzheimer’s
Disease Research Center. The data collected from this study showed that there are 12 universal
signs of Alzheimer’s Disease (AD) in both ethnic groups. The universal signs were delusions,
motor behavior, nighttime behavioral disturbances, and appetite and eating abnormalities. (Ortiz,
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Freddy, et al. 265) These signs are also supported in Mary Ellen Connelly’s book (Jum& Muz: I
Forgot- a Caregivers View of Alzheimer’s p. 110). She points to ten early onset signs of the
disease that explain these finding in simpler terms. Her ten signs were memory loss, challenges
in planning and problem solving, difficulty completing a familiar task, time and place confusion,
trouble understanding visual images, new problems with spoken and written words, misplacing
objects, poor judgment, withdrawal from work or social activities, and changes in mood and
personality. Understanding the seriousness of this disease is crucial when trying to discover a
solution to prevent the disease. The statics for the United States are very alarming when it comes
to this disease and how it affects our country’s older population. The Alzheimer’s Association’s
data collected in 2017 showed that 5.5 million Americans has AD. Out of that 5.5 million
200,000 Americans have AD under the age of 65 (Baude). By 2050 16 million American will be
diagnosed with the disease (Baude). When it comes to the morbidity rate of AD it is the sixth
leading cause of death in the United States and kills more Americans than breast cancer and
prostate cancer combined. Furthermore, since 2000 14% of heart disease has deceased while
89% of deaths from AD has increased in only 17 years. (Baude). This disease is a serious threat
to our society and a prevention or cure should be researched to stop the destructiveness of AD.
The degeneration of the brain from Alzheimer’s disease is caused by a protein called Tau
protein. In my interview with Dr. Dale McNett, Internal Medicine, he described this change in
the Tau protein because of a beta-amyloid. "The brain is like a good summer growth tree and all
the neurons are leaves. Some of those leaves then begin to be blown away in the wind during the
fall (Dr. Dale McNett)" The wind in this metaphor is the folding of the Tau proteins. This folding
then causes a plaque to build on the brain. The buildup then causes a disconnection between the
neurons that tell the brain to perform certain functions. For example, if the neurons are blocked
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to the Hippocampus, which is the part of the brain that deals with memory. The disconnection to
those neurons does not allow the information to be retrieved from long-term memory to short-
term memory. This causes the lack of recalling information found in Alzheimer’s disease.
Proteins are made up of polymers called polypeptides which combine and separate to make and
erase proteins. When the proteins separate, the polymer breaks down and turns into a monomer
called amino acids. The plaque of the Tau protein is the tangling or knotting of the proteins. This
raised; is this biological phenomenon preventable? Dr. Pinder, in his article explains that the
percentage of the disease can be decreased, but not completely be eradicated in our country and
world. What he explains is that we have to be proactive in our own health to help us fight this
disease. Some lifestyle modifications that can lower the risk of AD are diet and exercise.
Cultures that consume the Mediterranean diet, which substitutes red meat and saturated fats for
more seafood, poultry, and olive oil, have lower incidences of AD. Another part of the diet is the
consumption of a moderate amount of wine. “The properties of wine of antioxidant and anti-
inflammatory properties of the polyphenols present in the wine provide chemicals to fight off
disease and to run the homeostasis processes of our body” (Pinder, Roger 1). Another benefit to
our health is exercising which allows oxygen to flow through our body and in our brain. The
oxygen that is absorbed by our body during and after exercising allows for cellular respiration to
happen which provides energy to our body. This energy is used in the protein formation and
serration. This energy is important to regulate the separation of proteins because without the
separation of proteins it allows for the plaque to form in the white matter of the brain. Both of
genetics. The disease is classified as a gene mutation of the Tau protein. This mutation causes the
tangling of the protein. All though this is a valid point because genetic mutations are practically
apolipoprotein. This chromosome comes in many forms “APOE ε2 is relatively rare and may
provide some protection against the disease. If Alzheimer's disease occurs in a person with this
allele, it usually develops later in life more than it would in someone with the APOE ε4 gene.
APOE ε3, the most common allele, is believed to play a neutral role in the disease—neither
decreasing nor increasing risk. APOE ε4 increases the risk for Alzheimer's disease and is also
associated with an earlier age of disease onset. A person has zero, one, or two APOE ε4 alleles.
Having more APOE ε4 alleles increases the risk of developing Alzheimer's.” (Anon)
Even though these gene mutations increase the chance of AD, the same study found no
genetic link that specifically causes the AD in either the early or late stage of Alzheimer’s
disease. Genetics of an individual plays a major role in the chance of Alzheimer’s disease, it does
not mean that just because you are susceptible to the disease that it cannot be prevented through
multiple treatments being researched and tested. Dr. Pinder explains some possible treatments
like "therapeutic targets include the enzymes involved in the formation or degradation of the
amyloid or Tau proteins responsible for the classical Alzheimer pathology of plaques and
tangles. Therapeutic vaccines are also being developed to target aberrant proteins as soon as they
appear in the aging brain."(Pinder, Roger1). These treatments can be used to prevent the disease
in many ways. For example, using the therapeutic vaccine can give our immune system an
advantage in recognizing an abnormality in our Tau proteins and can stop them from knotting
and become plaque. This vaccination can be very important especially if a genetic trait causes the
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disease, this vaccination can help aid patients with this genetic trait fight this disease using their
own immune system. Using the enzymes involved in the formation and separation to prevent the
protein from forming in the first place or very early on in the disease.
designed to assess reasons to prevent Alzheimer’s disease their study found these results: “Two
hundred and five patients were selected according to the four initial criteria. Reasons for
subsequently not including some of patients in clinical trials were abnormalities on MRI (56.9%,
88.9% of which were WML), unauthorized medication (37.3%), the lack of a study
MRI (9%), a change in diagnosis over time (3.9%), visual/auditory impairments (2.9%), alcohol
abuse (2%) and an insufficient educational level (1%).” (British Journal of Clinical
Pharmacology 2013 Apr; 75(4): 1089-97). These results state that almost 88.9% of AD patients
have white matter lesions or (WML). If we prevent these lesions from occurring in the white
matter of our brain, we can reduce and prevent Alzheimer’s Disease in the United States and
In conclusion, when looking for preventable treatment, it is clear that the white matter
and the Tau protein are the centers of therapeutic treatment to diminish AD in a medical setting
and more useful in a genetics-based issue. At the same time, the best way to prevent this disease
is to take an active approach to our own health. Though many years of research, the two-main
proven preventative methods are exercise and a healthier diet with less saturated fat and more
white meat and fish. Alzheimer's disease can be preventable through many kinds of treatments
and healthy lifestyles. We still have more research to do to find a firm method of treatment that
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can halt this mutation of the Tau protein. AD is preventable, and this notion can change hundreds
Connelly, Mary Ellen. Jum & Muz: I Forget - a Caregivers View of Alzheimers. Xlibris Corp, 2016.
Baude, Bruce, et al, directors. Latest Alzheimer's Facts and Figures. Alzheimer's Association, 29
Pinder, Roger. “Is Alzheimer's a Preventable Disease?” Annals of General Psychiatry, vol. 7, 2008, pp.
1–1. doi:10.1186/1744-859X-7-S1-S59.
Ortiz, Freddy, et al. “Neuropsychiatric and Behavioral Symptoms in a Community Sample of Hispanics
with Alzheimer's Disease.” American Journal of Alzheimer's Disease & Other Dementiasr, vol.
Rollin-Sillaire A, et al. “Reasons That Prevent the Inclusion of Alzheimer's Disease Patients in Clinical
Trials.” British Journal of Clinical Pharmacology, vol. 75, no. 4, 2013, pp. 1089–97.,
doi:10.1111/j.1365-2125.2012.04423. x.
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