Andrew Coyle

Research Paper

English 12.6

16 November 2007

Alzheimer’s Disease

Alzheimer’s disease is a growing concern among the world’s retired

population. At present, there are approximately 4,500,000 people in the

United States who have been diagnosed with Alzheimer’s disease, and that

number is increasing every day. In fact, Alzheimer’s disease, not thought to

be 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 debilitating

disease. A German doctor named Alois Alzheimer noticed that one of his

patients was experiencing memory and skill loss. When the woman died of

this unusual mental illness, Dr. Alzheimer discovered strange protein

buildups in her brain. These buildups, now known as “plaques” and

“tangles,” are considered to be the agents by which Alzheimer’s disease

slowly destroys the brain (“Fact Sheet”).

Despite over a century of research since Dr. Alzheimer’s initial

detection of the illness, progress in the field of Alzheimer’s disease treatment

has 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 reasonably

safe cure has been discovered (“Fact Sheet”). However, we do know

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significantly more about the process that Alzheimer’s patients go through, as

well as the proper diagnosis of the disease.

The symptoms experienced by most patients are very similar, but their

reactions to these symptoms often vary intensely (Dean 82). These

symptoms occur in stages (Dean 83), and each can be classified as either

cognitive or psychiatric. Aphasia is the loss of the ability to communicate.

Expressive aphasia destroys the patient’s ability to speak and write, while

receptive aphasia destroys the ability to understand speech and writing. The

patient may still comprehend nonverbal communication even after aphasia

has taken away his ability to read, write, speak, and comprehend words.

Apraxia is the loss of routine motor skills like getting dressed or brushing

one’s teeth. Agnosia is the loss of ability to comprehend input from the five

senses. Even internal feelings, such as a full bladder or internal pain, cannot

be detected in the later stages of Alzheimer’s disease (“Symptoms”).

In the very first stage, the disease is present but no symptoms can be

detected. Sufferer and family might notice very minor slip-ups in

remembering an appointment or an acquaintance from the past, but chances

are good that these symptoms will be attributed to normal aging (Wisniewski

& Sadowski 44).

In stage two, which is usually the time when Alzheimer’s disease is first

perceived, a person may have concerns about memory loss or have difficulty

remembering words. Again, most assume this is normal forgetfulness at

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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 sufferer

experiences difficulty learning, impaired short-term memory, and an inability

to gain new technical skills. This stage lasts about seven years, and official

diagnosis 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, and

the patient has trouble recalling dates and specific details. The ability to

perform complex tasks and complicated math problems is affected. Stage

four lasts for approximately two years (Wisniewski & Sadowski 46).

When patients can no longer remember major events that have

occurred in their lives, they have reached stage five (Wisniewski & Sadowski

46). At this stage, which lasts between one year and eighteen months, the

patient is likely to remember the names of immediate relatives but can no

longer live alone (Wisniewski & Sadowski 47).

In stage six, the patient can no longer perform basic tasks such as

getting 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 is

experienced, very basic math skills are impaired, and speech is simple and

limited (Wisniewski & Sadowski 48).

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Psychological symptoms such as hallucination, delusions, and paranoia

are another part of stage six. The patient may see or hear things from the

past (Wisniewski & Sadowski 135), feel, smell, or taste things that are not

present (Wisniewski & Sadowski 136), or believe that there are strangers

pretending to be their loved ones (Wisniewski & Sadowski 139). The fear

created by paranoia and hallucination often contributes to insomnia

(Wisniewski & Sadowski 133). This advanced stage continues for two to two

and a half years (Wisniewski & Sadowski 48).

The final and most severe stage of Alzheimer’s disease is stage seven.

This stage lasts from the end of stage six until death. The patient needs

constant 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 have

spasms and lose even the ability to hold his head up without aid. This stage

may last several years with strenuous medical attention, but in the end the

patient will die (Wisniewski & Sadowski 49).

In order to diagnose Alzheimer’s disease, a doctor looks at several

factors. He must be certain that the symptoms that the patient is

experiencing are not caused by another disorder. Problems with similar

symptoms can include thyroid disorders, drug side effects or reactions,

depression, brain tumors, and blood vessel problems in the brain (“Fact

Sheet”). The first step in diagnosis is a set of questions and tests. The
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doctor will make sure the patient has a sense of time and is able to tell

where he is. He will then test verbal and memory skills. Finally, he will

check the patient’s ability to perform regular, everyday tasks (Petersen 60).

After using all the tools at his disposal, the doctor will make one of three

possible diagnoses. If the symptoms are not those of Alzheimer’s disease, a

different form of dementia will be diagnosed (Petersen 61). If Alzheimer’s

may be causing the symptoms experienced but is being masked by other

problems, the diagnosis will be “possible Alzheimer’s” (Petersen 60). If the

doctor is nearly certain that Alzheimer’s disease, not another disorder, is

causing the symptoms, the diagnosis will be “probable Alzheimer’s.”

For a patient to be diagnosed with probable Alzheimer’s, he must have

at least two cognition issues that change his way of life. The symptoms

experienced must be ever present and become worse with time.

Additionally, they must not be ascribed to any other medical or emotional

disorder (Petersen 56). This diagnosis process is accurate in about 90% of

cases. The only way to make a 100% accurate diagnosis is to find plaques

and tangles in the patient’s brain during an autopsy, which obviously cannot

be performed while the patient is living (“Fact Sheet”).

Scientists know that it is a diminishing of brain cells over time that

creates the symptoms associated with Alzheimer’s disease. Nerves cannot

communicate properly, and individual neurons become isolated and

eventually die (Dean 1). This isolation is thought to be caused by plaques

and tangles in the brain (Dean 2). Plaques are a buildup of a protein called
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“beta amyloid” around cells in the brain that prevents signals from being

sent between neurons (Dean 3-4). The amount of beta amyloid allowed to

enter the brain is normally limited by the blood-brain barrier, but if large

amounts 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 and

eventually 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 tangles

is aging. However, many factors contribute to the production of excess beta

amyloid and tau proteins (Dean 10). Some of the other major contributors

are head injury, strokes, a fatty diet (Dean 11), high blood pressure, and

diabetes (Wisniewski & Sadowski 38). Even stress can be a contributor,

especially when combined with other health problems (Dean 12). Anyone

who has Down syndrome will eventually develop Alzheimer’s disease if he

lives long enough (Wisniewski & Sadowski 33).

Although the disorder is not considered to be genetic, a single gene

that creates a protein called apolipoprotein E (or ApoE) has been isolated as

a factor that increases the risk of Alzheimer’s disease. ApoE normally aides

in delivering cholesterol throughout the body, but a mutated form of this

gene exists in about 15% of the world’s population. It is, however, assumed

that there are other genes which increase the risk of developing Alzheimer’s

disease that have not yet been isolated (“Fact Sheet”).

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There are many ways to reduce the risk of Alzheimer’s disease. Any

use of the mind has some effect in decreasing the chances, but certain

activities are more effective than others. Reading, studying a foreign

language, and traveling are activities that are considered to be highly

effective. Activities such as watching television, listening to music, and

speaking with friends are stimulating, but somewhat less effective (Dean

130). Specialized memory exercises can also be used (Wisniewski &

Sadowski 92). Physical activity reduces cholesterol, blood pressure, and

other health risks that contribute to Alzheimer’s disease over time (Dean

130). It has been shown that omega-3 fatty acids, which can be found in

sardines, salmon, cod, mackerel, herring, tuna, flaxseed, flax oil, soybeans,

spinach, walnuts, and various other foods, help stimulate the brain and

decrease risk (Dean 122). Hormone replacement therapy in women causes a

decrease in the rate of Alzheimer’s disease, but it has been shown to

increase the rates of breast cancer, heart disease, and stroke. No hormone

replacement treatment has been developed for men (Wisniewski & Sadowski

94). Long-term use of anti-inflammatory drugs and the reduction of free

radicals prevent damage to the brain (Wisniewski & Sadowski 95-96). These

preventative measures only slow the course of Alzheimer’s disease once it

has begun. In advanced stages, other treatments must be used.

Cholinesterase inhibitors, which perform best in the early and middle

stages of Alzheimer’s disease, work by slowing the progression of symptoms.

They do not, however, slow the biological process of the disease (Wisniewski
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& Sadowski 97). The dosage used must be increased over time (Wisniewski

& Sadowski 99), and they do not even work in about half the patients who

use them (Dean 103). Luckily, these drugs have very few significant side

effects (Wisniewski & Sadowski 100).

Other medications which have been shown to slow the process of the

disease include tacrine (Cognex), donepezil (Aricept), rivastigmine (Exelon),

and galantamine (Razadyne). As with cholinesterase inhibitors, these drugs

are effective only in the early and middle stages of Alzheimer’s. Memantine

(Namenda) is the only drug shown to work into the late stages of the

disease, but its effects are extremely limited at that point (“Fact Sheet”). It

is also relatively free of harmful side effects and interactions with other drugs

(Wisniewski & Sadowski 103).

Antioxidants cannot improve a patient’s health, but they can slow its

decline. Vitamin E and selegiline are the most common antioxidants. They

work by reducing the number of free radicals, particles that have harmful

effects on neurons, found within the brain (Wisniewski & Sadowski 104).

These treatments cannot be used if the patient is on blood thinners because

they have an additional blood thinning effect that could cause the patient to

bleed excessively (Wisniewski & Sadowski 105).

Different treatments exist for the psychotic symptoms of Alzheimer’s

disease. In the very earliest stages, agitation can be controlled with

antidepressant medications. As the disease progresses, more powerful drugs

called antipsychotics must be used. Not all Alzheimer’s patients become

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violent, 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 Alzheimer’s

disease (Dean 107).

Medications can be combined for a stronger overall effect on the

disease. Certain combinations work better than others, and medications do

not have the exact same effects in all patients. Care must be taken to avoid

harmful drug interactions and side effects, however (Wisniewski 106). A

physician will recommend a trial period of any drug prescribed to make sure

they are not detrimental to the patient’s health (Dean 103).

While options seem fairly grim at present, there is always some hope

for the future with constant advances in the medical field. Scientists,

supported by the federal government and the National Institute on Aging as

well as private organizations, are hard at work researching new Alzheimer’s

tools and treatments that may soon become available (Petersen 89).

MRI scans of the brain have shown that the brains of people who will

eventually develop Alzheimer’s disease lose volume (or “shrink”) more

quickly than those of people who will remain healthy (Petersen 88). PET

scans can show the activity of different parts of the brain during stimulating

activity. SPECT is another scan similar to PET which measures blood flow in

select regions of the brain (Petersen 89). In the future, these scans may

become useful in predicting the eventual onset of Alzheimer’s disease and

beginning preventative measures as early as possible.

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Neurotrophic agents and nerve growth factor, chemicals that help

neurons grow and remain healthy, could repair or prevent damage to

neurons (Petersen 85). Research is currently being conducted to find out the

best way to deliver these chemicals to the correct parts of the brain for the

highest success rates. Leteprinim potassium, a chemical that appears to

improve memory, is being tested as a treatment or preventative for

Alzheimer’s disease (Petersen 86).

A vaccine for Alzheimer’s disease called AN-1792 was created in labs

which caused the body’s immune system to actively find and remove beta

amyloid in the brain (Petersen 86-87). At first this vaccine seemed to be a

miracle in the field of Alzheimer’s disease research, but then problems began

to 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. This

began to cause dangerous inflammation of the brain, and one patient died.

Testing was immediately stopped, and so far the vaccine has not been tested

again in humans (Wisniewski & Sadowski 113).

As with most modern diseases, our methods of treatment become

more and more diverse by the day. With the aid of funding, awareness, and

scientific research, a true cure for the mysterious Alzheimer’s disease may

soon be discovered.
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Works Cited

“Alzheimer’s Disease Fact Sheet.” Alzheimer’s Disease Education & Referral

Center. 26 October 2007. National Institute on Aging. 7 November

2007. <http://www.nia.nih.gov/Alzheimers/Publications/adfact.htm>.

Dean, Carolyn. The Everything Alzheimer’s Book. Avon, MA: Adams Media,

2004.

Petersen, Robert. Mayo Clinic on Alzheimer’s Disease. New York: Kensington,

2002.

“Symptoms.” About Alzheimer’s. 2007. Alzheimer’s Foundation of America. 7

November 2007. <http://www.alzfdn.org/alzheimers/symptoms.html>.

Wisniewski, Thomas, and Marcin Sadowski. 100 Questions & Answers About

Alzheimer’s Disease. Sudbury, MA: Jones and Bartlett, 2004.