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Andrew CoyleResearch PaperEnglish 12.

616 November 2007


Alzheimers Disease
Alzheimers disease is a growing concern among the worlds
retiredpopulation. At present, there are approximately 4,500,000 people in
theUnited States who have been diagnosed with Alzheimers disease, and
thatnumber is increasing every day. In fact, Alzheimers disease, not thought
tobe a normal part of aging, is now considered the most common form of
dementia among elderly people (Fact Sheet).First discovered in 1906, little
is still known about the debilitatingdisease. A German doctor named Alois
Alzheimer noticed that one of hispatients was experiencing memory and skill
loss. When the woman died of this unusual mental illness, Dr. Alzheimer
discovered strange proteinbuildups in her brain. These buildups, now known
as plaques andtangles, are considered to be the agents by which
Alzheimers diseaseslowly destroys the brain (Fact Sheet).Despite over a
century of research since Dr. Alzheimers initialdetection of the illness,
progress in the field of Alzheimers disease treatmenthas been extremely
limited. The cause of protein buildup in the brains of some where it is not
present in others is still unknown, and no reasonablysafe cure has been
discovered (Fact Sheet).
However, we do know significantly more about the process that Alzheimers
patients go through, aswell as the proper diagnosis of the disease. The
symptoms experienced by most patients are very similar, but theirreactions
to these symptoms often vary intensely (Dean 82). Thesesymptoms occur in
stages (Dean 83), and each can be classified as eithercognitive or psychiatric.
Aphasia is the loss of the ability to communicate.Expressive aphasia destroys
the patients ability to speak and write, whilereceptive aphasia destroys the
ability to understand speech and writing. Thepatient may still comprehend
nonverbal communication even after aphasiahas taken away his ability to
read, write, speak, and comprehend words.Apraxia is the loss of routine
motor skills like getting dressed or brushingones teeth. Agnosia is the loss of
ability to comprehend input from the fivesenses. Even internal feelings, such
as a full bladder or internal pain, cannotbe detected in the later stages of
Alzheimers disease (Symptoms).In the very first stage, the disease is
present but no symptoms can bedetected. Sufferer and family might notice
very minor slip-ups inremembering an appointment or an acquaintance from
the past, but chancesare good that these symptoms will be attributed to
normal aging (Wisniewski& Sadowski 44).In stage two, which is usually the
time when Alzheimers disease is firstperceived, a person may have concerns
about memory loss or have difficultyremembering words. Again, most
assume this is normal forgetfulness at
first, but after a time it becomes more obvious that something is
wrong(Wisniewski & Sadowski 45).Stage two progresses into stage three,

during which the suffererexperiences difficulty learning, impaired short-term


memory, and an inabilityto gain new technical skills. This stage lasts about
seven years, and officialdiagnosis typically takes place near the end of this
stage or the beginning of the next (Wisniewski & Sadowki 45).In stage four,
memory loss becomes significantly more obvious, andthe patient has trouble
recalling dates and specific details. The ability toperform complex tasks and
complicated math problems is affected. Stagefour lasts for approximately two
years (Wisniewski & Sadowski 46).When patients can no longer remember
major events that haveoccurred in their lives, they have reached stage five
(Wisniewski & Sadowski46). At this stage, which lasts between one year and
eighteen months, thepatient is likely to remember the names of immediate
relatives but can nolonger live alone (Wisniewski & Sadowski 47).In stage six,
the patient can no longer perform basic tasks such asgetting dressed,
bathing, or brushing his or her teeth without assistance(Wisniewski &
Sadowski 47). In the later parts of this stage, the names of close relatives are
forgotten, loss of bladder and bowel control isexperienced, very basic math
skills are impaired, and speech is simple andlimited (Wisniewski & Sadowski
48).
Psychological symptoms such as hallucination, delusions, and paranoiaare
another part of stage six. The patient may see or hear things from thepast
(Wisniewski & Sadowski 135), feel, smell, or taste things that are notpresent
(Wisniewski & Sadowski 136), or believe that there are strangerspretending
to be their loved ones (Wisniewski & Sadowski 139). The fearcreated by
paranoia and hallucination often contributes to insomnia(Wisniewski &
Sadowski 133). This advanced stage continues for two to twoand a half years
(Wisniewski & Sadowski 48). The final and most severe stage of Alzheimers
disease is stage seven. This stage lasts from the end of stage six until death.
The patient needsconstant assistance and cannot be left alone for extended
periods of time.Speech is extremely limited at first and eventually disappears
altogether.Basic functions like walking, sitting up, and even smiling are lost
over time(Wisniewski & Sadowski 48). Just before death, the patient will begin
to havespasms and lose even the ability to hold his head up without aid. This
stagemay last several years with strenuous medical attention, but in the end
thepatient will die (Wisniewski & Sadowski 49).In order to diagnose
Alzheimers disease, a doctor looks at severalfactors. He must be certain that
the symptoms that the patient isexperiencing are not caused by another
disorder. Problems with similarsymptoms can include thyroid disorders, drug
side effects or reactions,depression, brain tumors, and blood vessel problems
in the brain (FactSheet). The first step in diagnosis is a set of questions and
tests. The
doctor will make sure the patient has a sense of time and is able to tellwhere
he is. He will then test verbal and memory skills. Finally, he willcheck the
patients ability to perform regular, everyday tasks (Petersen 60).After using
all the tools at his disposal, the doctor will make one of threepossible
diagnoses. If the symptoms are not those of Alzheimers disease, adifferent
form of dementia will be diagnosed (Petersen 61). If Alzheimersmay be
causing the symptoms experienced but is being masked by otherproblems,

the diagnosis will be possible Alzheimers (Petersen 60). If thedoctor is


nearly certain that Alzheimers disease, not another disorder, iscausing the
symptoms, the diagnosis will be probable Alzheimers.For a patient to be
diagnosed with probable Alzheimers, he must haveat least two cognition
issues that change his way of life. The symptomsexperienced must be ever
present and become worse with time.Additionally, they must not be ascribed
to any other medical or emotionaldisorder (Petersen 56). This diagnosis
process is accurate in about 90% of cases. The only way to make a 100%
accurate diagnosis is to find plaquesand tangles in the patients brain during
an autopsy, which obviously cannotbe performed while the patient is living
(Fact Sheet).Scientists know that it is a diminishing of brain cells over time
thatcreates the symptoms associated with Alzheimers disease. Nerves
cannotcommunicate properly, and individual neurons become isolated
andeventually die (Dean 1). This isolation is thought to be caused by
plaquesand tangles in the brain (Dean 2).
Plaques are a buildup of a protein called beta amyloid around cells in the

brain that prevents signals from beingsent between neurons (Dean 34). The amount of beta amyloid allowed toenter the brain is normally
limited by the blood-brain barrier, but if largeamounts of the protein
are being produced, this barrier cannot keep up(Wisniewski & Sadowski
23). Tangles are a buildup of tau, another protein,inside nerve cells.
Tangles prevent the cell from transmitting signals andeventually cause
it to die. Plaques and tangles both occur in healthy brains,but they are
far less frequent (Dean 4). The most prevalent cause of the
development of plaques and tanglesis aging. However, many factors
contribute to the production of excess betaamyloid and tau proteins
(Dean 10). Some of the other major contributorsare head injury,
strokes, a fatty diet (Dean 11), high blood pressure, anddiabetes
(Wisniewski & Sadowski 38). Even stress can be a
contributor,especially when combined with other health problems
(Dean 12). Anyonewho has Down syndrome will eventually develop
Alzheimers disease if helives long enough (Wisniewski & Sadowski
33).Although the disorder is not considered to be genetic, a single
genethat creates a protein called apolipoprotein E (or ApoE) has been
isolated asa factor that increases the risk of Alzheimers disease. ApoE
normally aidesin delivering cholesterol throughout the body, but a
mutated form of thisgene exists in about 15% of the worlds
population. It is, however, assumedthat there are other genes which
increase the risk of developing Alzheimersdisease that have not yet
been isolated (Fact Sheet).
Coyle 7 There are many ways to reduce the risk of Alzheimers
disease. Anyuse of the mind has some effect in decreasing the
chances, but certainactivities are more effective than others. Reading,
studying a foreignlanguage, and traveling are activities that are
considered to be highlyeffective. Activities such as watching television,

listening to music, andspeaking with friends are stimulating, but


somewhat less effective (Dean130). Specialized memory exercises can
also be used (Wisniewski &Sadowski 92). Physical activity reduces
cholesterol, blood pressure, andother health risks that contribute to
Alzheimers disease over time (Dean130). It has been shown that
omega-3 fatty acids, which can be found insardines, salmon, cod,
mackerel, herring, tuna, flaxseed, flax oil, soybeans,spinach, walnuts,
and various other foods, help stimulate the brain anddecrease risk
(Dean 122). Hormone replacement therapy in women causes
adecrease in the rate of Alzheimers disease, but it has been shown
toincrease the rates of breast cancer, heart disease, and stroke. No
hormonereplacement treatment has been developed for men
(Wisniewski & Sadowski94). Long-term use of anti-inflammatory drugs
and the reduction of freeradicals prevent damage to the brain
(Wisniewski & Sadowski 95-96). Thesepreventative measures only slow
the course of Alzheimers disease once ithas begun. In advanced
stages, other treatments must be used.Cholinesterase inhibitors, which
perform best in the early and middlestages of Alzheimers disease,
work by slowing the progression of symptoms. They do not, however,
slow the biological process of the disease (Wisniewski
Coyle 8& Sadowski 97). The dosage used must be increased over time
(Wisniewski& Sadowski 99), and they do not even work in about half
the patients whouse them (Dean 103). Luckily, these drugs have very
few significant sideeffects (Wisniewski & Sadowski 100).Other
medications which have been shown to slow the process of thedisease
include tacrine (Cognex), donepezil (Aricept), rivastigmine (Exelon),and
galantamine (Razadyne). As with cholinesterase inhibitors, these
drugsare effective only in the early and middle stages of Alzheimers.
Memantine(Namenda) is the only drug shown to work into the late
stages of thedisease, but its effects are extremely limited at that point
(Fact Sheet). Itis also relatively free of harmful side effects and
interactions with other drugs(Wisniewski & Sadowski 103).Antioxidants
cannot improve a patients health, but they can slow itsdecline.
Vitamin E and selegiline are the most common antioxidants. Theywork
by reducing the number of free radicals, particles that have
harmfuleffects on neurons, found within the brain (Wisniewski &
Sadowski 104). These treatments cannot be used if the patient is on
blood thinners becausethey have an additional blood thinning effect
that could cause the patient tobleed excessively (Wisniewski &
Sadowski 105).Different treatments exist for the psychotic symptoms
of Alzheimersdisease. In the very earliest stages, agitation can be
controlled withantidepressant medications. As the disease progresses,
more powerful drugscalled antipsychotics must be used. Not all
Alzheimers patients become

Coyle 9violent, but for those who do, there exist preventative
medications.Sedatives can help the patient overcome insomnia, but the side
effects of sedatives are often confused with worsening symptoms of
Alzheimersdisease (Dean 107).Medications can be combined for a stronger
overall effect on thedisease. Certain combinations work better than others,
and medications donot have the exact same effects in all patients. Care must
be taken to avoidharmful drug interactions and side effects, however
(Wisniewski 106). Aphysician will recommend a trial period of any drug
prescribed to make surethey are not detrimental to the patients health (Dean
103).While options seem fairly grim at present, there is always some hopefor
the future with constant advances in the medical field. Scientists,supported
by the federal government and the National Institute on Aging aswell as
private organizations, are hard at work researching new Alzheimerstools and
treatments that may soon become available (Petersen 89).MRI scans of the
brain have shown that the brains of people who willeventually develop
Alzheimers disease lose volume (or shrink) morequickly than those of
people who will remain healthy (Petersen 88). PETscans can show the activity
of different parts of the brain during stimulatingactivity. SPECT is another
scan similar to PET which measures blood flow inselect regions of the brain
(Petersen 89). In the future, these scans maybecome useful in predicting the
eventual onset of Alzheimers disease andbeginning preventative measures
as early as possible.
Coyle 10Neurotrophic agents and nerve growth factor, chemicals that
helpneurons grow and remain healthy, could repair or prevent damage
toneurons (Petersen 85). Research is currently being conducted to find out
thebest way to deliver these chemicals to the correct parts of the brain for
thehighest success rates. Leteprinim potassium, a chemical that appears
toimprove memory, is being tested as a treatment or preventative
forAlzheimers disease (Petersen 86).A vaccine for Alzheimers disease called
AN-1792 was created in labswhich caused the bodys immune system to
actively find and remove betaamyloid in the brain (Petersen 86-87). At first
this vaccine seemed to be amiracle in the field of Alzheimers disease
research, but then problems beganto occur in trial patients. After about a
year of using the vaccine, the over-stimulated immune system began to
attack healthy brain tissue as well. Thisbegan to cause dangerous
inflammation of the brain, and one patient died. Testing was immediately
stopped, and so far the vaccine has not been testedagain in humans
(Wisniewski & Sadowski 113).As with most modern diseases, our methods of
treatment becomemore and more diverse by the day. With the aid of funding,

awareness, andscientific research, a true cure for the mysterious Alzheimers


disease maysoon be discovered.
Works Cited
Alzheimers Disease Fact Sheet. Alzheimers Disease Education &
ReferralCenter . 26 October 2007. National Institute on Aging. 7
November2007.
<http://www.nia.nih.gov/Alzheimers/Publications/adfact.htm>.
Dean, Carolyn.The Everything Alzheimers Book. Avon, MA: Adams
Media,2004.
Petersen, Robert. Mayo Clinic on Alzheimers Disease. New York:
Kensington,2002.
Symptoms. About Alzheimers. 2007. Alzheimers Foundation of America. 7
November 2007. <http://www.alzfdn.org/alzheimers/symptoms.html>.
Wisniewski, Thomas, and Marcin Sadowski. 100 Questions & Answers About
Alzheimers Disease. Sudbury, MA: Jones and Bartlett, 2004

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