Alzheimers Disease Essay Research Paper Alzheimers DiseaseWe

Alzheimers Disease Essay, Research Paper

Alzheimer?s Disease

We are currently living in the age of technology. Our advancements in the past few decades overshadow everything learned in the last 2000 years. With the elimination of many diseases through effective cures and treatments, humans can expect to live a much longer life then that of their grandparents. The population of the United States continues to rise, and with the “baby boom” era coming of age, the number of elderly people is rising as well. This increase has brought with it a large increase in diseases associated with old age. Alzheimer’s dementia is one of the most common and feared diseases afflicting the elderly community. Alzheimer?s disease, once thought to be a natural part of aging, is a severely debilitating form of mental dementia. Although some other types of dementia are curable or effectively treatable, there is currently no cure for the Alzheimer variety.

A general overview of Alzheimer’s disease including the clinical description, diagnosis, and progression of symptoms, helps one to further understand the treatment and care of patients, the scope of the problem, and current research.

The clinical definition of dementia is “a deterioration in intellectual performance that involves, but is not limited to, a loss in at least 2 of the following areas: language, judgment, memory, visual or depth perception, or judgment interfering with daily activities.” (Institute, 1996, p.4). The initial cause of Alzheimer?s disease symptoms is a result of the progressive deterioration of brain cells (neurons) in the cerebral cortex of the brain. This area of the brain, which is the largest and uppermost portion, controls all our thought processes, movement, speech, and senses. This deterioration initially starts in the area of the cortex that is associated with memory and then progresses into other areas of the cortex, then into other areas of the brain that control bodily functions. The death of these cells causes an interruption of the electrochemical signals between neurons that are a key to cognitive as well as bodily functioning.

Currently Alzheimer?s disease can only be confirmed at autopsy. After death the examined brain of an Alzheimer victim shows two distinct characteristics. The first is the presence of neuritic plaques in the cerebral cortex and other areas of the brain including cerebral blood vessels. These plaques consist of groups of neurons surrounded by deposits of beta-amyloid protein. The presence of these plaques is also common to other types of dementia. The second characteristic, neurofibliary tangles, is what separates Alzheimer?s disease from all other forms of dementia. Neurofibliary tangles take place within the disconnected brain cells themselves. When examined under a microscope, diseased cells appear to contain spaghetti-like tangles of normally straight nerve fibers. The presence of these tangles was first discovered in 1906 by the German neurologist Alois Alzheimer, hence the name Alzheimer’s disease.

Although the characteristics listed above are crucial to the diagnosis of Alzheimer?s disease upon death, the clinical diagnosis involves a different process. The diagnosis of Alzheimer?s disease is only made after all other illnesses, which may have the same symptoms, are ruled out. The initial symptoms of Alzheimer?s disease are typical of other treatable diseases. Therefore doctors are hesitant to give the diagnosis of Alzheimer’s in order to save the patient from the worsening of a treatable disease through a misdiagnosis. Some of the initial symptoms include an increased memory loss, changes in mood, personality, and behavior, (symptoms that are common in depression) prescription drug conflict, brain tumors, syphilis, alcoholism, other types of dementia, and many other conditions.

The onset of these symptoms usually brings the patient to his family doctor. The general practitioner runs a typical battery of urinalysis and blood tests that he sends off to the lab. If the tests come back negative, and no other cause of the symptoms is established, the patient is then referred to a specialist. The specialist, usually a psychiatrist, will then continue to rule out other possible illnesses through testing. If the next battery of tests also comes back negative, then the specialist will call on a neurologist to run a series of neurological examinations including a PET and CAT scan to rule out the possibility of brain tumors. A spinal tap is also performed to determine the possibility of other types of dementias. The patient will also undergo a complete psychiatric evaluation. If the patient meets the preliminary criteria for Alzheimer?s disease, an examination of the patients? medical history is also necessary to check for possible genetic predispositions to the disease. The psychiatric team finally meets with the neurological team to discuss their findings. If every other possible disease is ruled out, and the results of the psychiatric evaluation are typical to that of a person with the disease, the diagnosis of Alzheimer’s disease is given.

The initial symptoms of Alzheimer?s disease are usually brushed off as a natural part of aging. The myth that a person’s memory worsens over time is just that – a myth (Myers, 1996, p.100-101). Alzheimer?s disease victims are mostly over the age of 65 and many delay treatment by attributing their problems to age. A victim might forget a well known phone number or miss an important appointment. These symptoms eventually escalate to the total disintegration of personality and all patients end up in total nursing care.

In descending order, the patient goes from (1) decreased ability to handle a complex job to (2) decreased ability to handle such complex activities of daily life as (3) managing finances, (4) complex meal preparation and (5) complex marketing skills. Next comes (6) loss of ability to pick out clothing properly, (7) or to put on clothing properly, followed by (8) loss of ability to handle the mechanics of bathing properly. Then (9) progressive difficulties with continence and (10) toileting occur, followed by (11) very limited speech ability and (12) inability to speak more than a single word. Next comes (13) loss of ambulatory capability. Last to go are such basic functions as (14) sitting up, (15) smiling and (16) holding up one’s head (Brassard, 1993, p.10).

The average time from diagnosis to inevitable death is 8 years. The family of the victim is usually able to care for the victim for an average period of about 4 years (Alzheimer’s, 1996, p.44). During the progression of the disease between 10% and 15% of patients hallucinate and suffer delusions, 10% will become violent and 10% suffer from seizures (Alzheimer’s, 1996, p.46).

Once a person is diagnosed as having Alzheimer?s disease, an assessment is made of the disease’s stage of progression and of the strengths and weaknesses of the victim and the victim’s family. There are different types of assessments available to evaluate the level of dysfunction of the patient. Based on one of these assessments a care plan is put together by a team consisting of a family member, a paid or unpaid care provider, and the victim’s physician. Throughout the progression of the disease, and depending on the needs of the patient, a wide range of expensive medication, such as psychoactive drugs to lift depression and sedatives to control violence may be required.

Unfortunately, although a wide range of treatments have been tested, most prove to be ineffective. At the beginning of the disease the family is usually able to look after the patient without much effort. Frequently families will hire a care giver in order to alleviate some of the work.

Simple changes in the home can make life much easier for the sufferer, help them keep their self esteem, and prolong their stay at home. Examples of low-cost modifications to the environment include reducing the noise levels in the home (telephones, radios, voices, etc.); avoiding vividly patterned rugs and drapes; placing locks up high or down low on doors leading outside (Alzheimer?s disease sufferers are known to wander off); clearing floors of clutter; and reducing the contents of closets in order to simplify choices (Alzheimer, 1992, p.17). Costs are typically paid for by the victim’s family. Many of these, and other more expensive modifications are introduced in long-term care settings. They help in maintaining the safety and security of the victim as well as reducing their confusion.

The patient’s and the family’s condition should be assessed every six months (Alzheimer, 1992, p.21). In response to constantly changing needs, the aspects of care must be constantly modified. Other issues that usually arise during the care of the patient are assessment of the competence of the victim, power of attorney, and response to and prevention of abuse (Aronson, 1988, p.124). Eventually the victim’s condition deteriorates to the point where home care is no longer possible and they must be moved to a long-term care facility.

Any care giver must obtain information and education about the disease in order to effectively care for the victim. During the course of the disease victims might wander, hallucinate, or become suspicious. This behavior can place a large strain on the care giver as well as causing depression and deterioration of their own health (Aronson, 1988, p.132). An Alzheimer?s disease support group is crucial to alleviating some of the stress on the care giver. Through a support group the care giver is given the emotional and practical help needed to accomplish the large task of looking after the victim for as long as possible.

An estimated four million Americans currently have Alzheimer’s disease, and about one in every 10 Americans 65 and older has the disease (Evans, 1989, p.131). But that overall figure is misleading. According to a large survey of retired individuals, risk of Alzheimer’s disease changes considerably during the older years: From age 65 to 74, about 3% of people are affected. From age 75 to 84, the figure rises to 19%, and for those 85 and older, Alzheimer’s afflicts 47% (Evans, 1990, p. 4). Currently the U.S. population is aging, with people over 85 becoming the nation’s fastest-growing age group. Because this is also the group most affected by Alzheimer’s disease, experts warn that unless researchers discover how to prevent the disease, by the year 2050, as many as 15% of those over 65 might have Alzheimer’s.

These large and increasing figures translate into a large burden on the health care system. Even when using the most conservative estimates of the average number of years spent in an institution and the number of afflicted Americans, the costs to health care are immense. At $33,000 per patient per year in an institution and with an average stay of three years until death, the cost of Alzheimer?s disease will amount to $3 billion over the next few years; and if the entry into the disease state remains constant, it will cost the American taxpayer [an added] $1 billion per year thereafter (Brassard, 1993, p.11).

Alzheimer?s disease is a democratic disease. It affects persons of both sexes and all races and ethnic backgrounds. The major risk factors for Alzheimer?s disease are age and heredity. Persons with a high incidence of the disease in their family history are most susceptible. A specific subtype of Alzheimer?s disease exists that is solely connected to heredity. This subtype is known as Familial Alzheimer’s disease (FAD). FAD is also known as Early Onset Alzheimer’s disease, named so because its symptoms start to develop much earlier than in the regular sporadic type. Only 5%-10% of all cases are of this type. FAD is suspected when Alzheimer?s disease can be traced over several generations and there is a history of (among previously affected family members) a similar age of onset and duration of the disease (usually 4 years). Approximately 50% of the children of an affected parent go on to develop the disease (Pollen, 1993, p.89).

Much research has been conducted in an attempt to locate the gene that is responsible for FAD. Currently, researchers have isolated genes 1, 14, and 21 (Alzheimer’s, 1996, p.36). However, the evidence still remains inconclusive (Statement, 1996, p.2). There is also a possibility that a specific genetic mutation merely puts a person at risk to the disease and Alzheimer?s disease is triggered by an external force, like a head injury (Statement, 1996, p.4). Finding the specific location of the gene will pave the way for a diagnostic or even predictive test for FAD.

Similar genetic tests already exist for cystic fibrosis and muscular dystrophy. Locating the Alzheimer?s disease gene will also allow scientists to study why the particular gene is not functioning properly and may give clues for treatment and possible cures. The long term goal of this research is the same as that of any other genetic research and that is gene therapy – which is the possibility that science could one day alter our genetic make-up.

The other much more common type of the disease is Sporadic Alzheimer’s Disease (SAD). This includes all other types of the disease which are not linked to heredity. Genetic research is also playing a major role in the progress towards a diagnostic or predictive test for SAD. Recently, a gene involved in the transport of cholesterol has been identified to be associated with Alzheimer?s disease. Apolipoprotein E is located on chromosome 19 and seems to contribute to the susceptibility of a person with Alzheimer?s disease (Statement, 1996, p.6). The gene exists in three different forms or alleles (Apo E 2,3,4) and each person has a combination of two of the three. Thus an individual can have any one of the following combinations: Apo E 2/2, 3/3, 4/4, 2/3, 3/4 or 2/4.

Researchers have found a relationship between the number of copies of the 4 allele and the person’s probability of developing the disease. For example a 75 year old individual with the Apo E 4 genotype has approximately a 20% chance of remaining normal; Apo E 3/4 or 2/4, 40%; 2/2, 3/3 or 2/3, a 75% chance (Institute, 1996, p. 6).

For many years, scientists believed that aluminum was at the root of Alzheimer?s disease. High levels of aluminum were detected in the areas surrounding the beta-amyloid plaques associated with neural atrophy (Pollen, 1990, p.77). Recently however, this theory has been abandoned. Scientists concluded that the build-up of aluminum was a direct result of the wrongful use of a particular test agent employed in the studies (Brown, 1992, p.6).

Some of the current pursuits of research are in the areas of viral infection, malfunction of the immune system, and chemical imbalances. One of the hardest theories to disprove is that Alzheimer?s disease is the result of a slow acting virus present at birth (Carlton, 1996, p.13). Others believe that Alzheimer?s disease is an immune system disorder. Support for this theory comes from the presence of beta-amyloid plaques identical to those found in Alzheimer-diseased brains in the post-mortem examinations of immuno-deficiency disease victims (Alzheimer’s, 1996, p.22).

The detection of lower neurotransmitter substances such as acetylcholine, serotonin, norepinephrine and somatostatin in Alzheimer?s sufferers forms the basis of another theory that says Alzheimer?s disease is brought on by a chemical imbalance in the brain. Treatment of patients with drugs that block the breakdown of neurotransmitter substances in the brain have been met with limited success (Brassard, 1993, p.16).

Alzheimer?s disease is an enormous social and economic problem. As the population ages, the number of victims will steadily increase, imposing a massive burden on the health care system. Until a cure and effective treatment are found, Alzheimer?s will remain a terrible disease that slowly eats away at that which is the very essence of a person: their mind, leaving in its wake a mere empty shell of that person. It takes away from all of us the insightful wisdom of one of society’s most prized possessions – the elderly.

Bibliography

References

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Alzheimer’s Disease Education and Referral Center.(1996). Internet. http://www.alzheimers.org/adear.drct.txt, 22, 36, 44-46.

Aronson, Miriam.(1988). Understanding Alzheimer’s Disease. New York: Scribner’s, 124,132.

Brassard, Daniel.(1993). Alzheimer’s Disease. Library of Parliament, Science and Technology, 10-11, 16.

Brown, Phyllida.(1992, November 7). Alzheimer’s May Not be Linked to Aluminum. New Scientist Supplement, 6.

Carlton University Department of Health Sciences. (1996). Internet. http:\\www.nct.carltonca/fp/social.services/alzheimer/disease.dir, 13.

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Myers, David.(1996). Exploring Psychology. New York: Worth. 100-101.

Pollen, Daniel.(1990). Hannah’s Heirs: The Quest For the Genetic Origins of Alzheimer’s Disease. London: Oxford University Press, 77, 89.

Statement on Use of Apolipoprotein E Testing for Alzheimer’s Disease. (1996). American College of Medical Genetics/American Society of Human Genetics, 2-6.