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Biology 202
2004 First Web Paper
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Alzheimer's Disease: The Loss of One's Self

Sarah Caldwell

Our class discussions of late have related behavioral characteristics to the anatomy of the brain. We have questioned what it is that defines a persons "self?" What is it that processes various sensory inputs in an individual and formulates that individual's personal outputs, feelings and attitudes in response to these inputs? For the time being, we have given the responsibility of input processing to the I-box. There are several mental illnesses that may accompany dementia. A person suffering from one or more of these illnesses can be characterized as having "lost one's self" (1). In this paper, I hope to understand how Alzheimer's disease causes loss of memory and, eventually, the loss of one's "self." What factors of the disease determine how much of one's original "self" is lost from day to day?

Four and one - half million Americans are estimated to have Alzheimer's Disease (AD) in greater or lesser degree (2). Alzheimer's disease is a complex condition that affects the brain and is one which is considered to be a major public health problem for the United States. AD has a huge impact on individuals, families, the health care system and society. While scientific research has enabled scientists to develop a better understanding of Alzheimer's, and consequently develop more effective diagnosis, effective treatments have been elusive. Overall, the disease remains enigmatic.

Alzheimer's disease was first observed and described in 1906 by German physician Dr. Alois Alzheimer during the autopsy of a woman with dementia (2). Alzheimer's is an irreversible, progressive brain disease that slowly destroys memory and thinking skills. As the disease progresses it eventually prevents those suffering from the disease from performing simple tasks (4). Although once viewed as rare, research has shown that AD is the leading cause of dementia. Dementia is an umbrella term for several symptoms all of which result in a decline in thinking and cognitive capabilities. Such symptoms include: gradual memory loss, reasoning problems, judgment problems, learning difficulties, loss of language skills, and a decline in the ability to perform normal, routine tasks. People with dementia also experience personality and behavioral changes such as agitation, anxiety, delusions and hallucinations (4). It is important to note that dementia is not a disease itself, but a group of symptoms that usually accompanies a disease. Accordingly, dementia is not solely a result of Alzheimer's it is also experienced in many related disorders of the brain.

The progression of AD varies widely and can last anywhere from 3 to 20 years. Alzheimer's first affects the areas of the brain that control memory and thinking skills, as the disease progresses cells in other regions of the brain die as well (2). Researchers aren't certain of the causes of AD and theories of its cause have ranged from intake of excessive aluminum from modern cookware to exposure to pesticides. At present, the causes remain open to scientific debate. What is known is that people with the disease have an abundance of two abnormal structures in the brain: plaques and tangles. Plaques are dense accumulations of a protein called beta-amyloid. Tangles are twisted fibers caused by changes in a protein called tau. The beta-amyloid plaques reside in the spaces between neurons, in the brain, and the neurofibrillary tangles clump together inside the neurons. Plaques and tangles block the normal transport of electrical messages between the neurons that enable us to think, talk, remember and move. As AD progresses, nerve cells die, the brain shrinks, and the ability to function deteriorates (5). The destruction and death of nerve cells causes the memory failure, personality changes and other features of AD (5). To be sure, plaques and tangles develop in the brains of many older people, however the brains of AD patients have them to a much greater extent. While there is strong evidence that suggests these protein accumulation are involved in AD, their exact role in the disease continues to elude scientists.

The two biggest risk factors for getting AD seem to be genetic predisposition; about 30 percent of people who have AD have a family history of dementia, and age (6). As many as 10 percent of people 65 years of age and older have AD and nearly 50 percent of people 85 years and older have the disease (6). Sporadic AD refers to cases of AD where no other blood relatives are affected by the disease, this type of AD occurs in about 75 percent of cases (4). In these cases, the risk of developing AD increases as a person gets older. The remaining 25 percent of AD cases are hereditary, which means they are caused by mutated genes and tend to cluster within families. These cases can be divided into early-onset disease (symptoms begin before 65 years of age) and late-onset disease (symptoms begin after age 65) (4). Scientists have identified several genes that play a role in early-onset AD, the more rare form of the disease that strikes people as young as in their 30s (7). Research has also identified a gene that produces a protein which may play a role in late-onset AD, although this is far from certain.

There is no cure for AD. While there are a number of treatment regimes, none are capable of reversing the effects of the disease and overall effectiveness is far from clear. Several drugs have been FDA approved to treat some of the symptoms of AD in an attempt to improve the quality of life of those afflicted with the disease (7). Interestingly, some studies have shown that participating in mentally stimulating activities such as reading books, doing crossword puzzles, or going to museums, may be associated with a reduced risk of AD (7). In addition, this "use-it-or-lose-it" theory postulates that repetitive actions may improve certain cognitive skills and make them less susceptible to brain damage (7).

While scientific research has furthered the understanding of AD, it has yet to address the possibility of the I-function in Alzheimer's patients being impaired. The protein build-up of plaques and tangles as well as genetic mutations play a role in the etiology of AD. However, no investigations have questioned how factors affect the I-box. Alzheimer's is viewed as a disease which causes patients to lose their "self." If this is the case, and the I-function is the part of the human brain responsible for defining one's "self," then it would seem logical that AD directly affects the I-function. The possible connection between AD and the I-function is one worth investigating further. Perhaps insight into the I-box is the missing link in understanding, completely, the mechanism of Alzheimer's.


1)Alzheimer's Disease: A Family Affair and a Growing Social Problem,

2)What is Alzheimer's,

3)Alzheimer's Association: About Alzheimer's,

4)The National Women's Health Information Center: Alzheimer's Disease,

5)Alzheimer's Disease: Unraveling the Mystery,

6)National Institute of Neurological Disorders and Strokes: Alzheimer's Disease Information Page,

7)FDA: Alzheimer's Searching for a Cure,

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