Originating from the Latin word demens, meaning "without a mind," the term dementia historically designated social and intellectual deterioration associated with old age. However, beginning in the late 19th century, the medical characterization of dementia increased in specificity with the rise of biological sciences and the advent of new technologies to study the brain. As a diagnostic category, the term now encompasses about 70 different conditions associated with abnormal cognitive decline. Seminal in this evolution was the 1906 description by German neuropathologist Alois Alzheimer of a presenile form of dementia in a younger woman in her early 50s. In 1910, famous psychiatrist Emil Kraepelin reviewed Alzheimer's findings and claimed them to be suggestive of a new condition he called "Alzheimer's disease" to distinguish it from senile dementia, a disease experts then believed to occur only at a later stage in life. Later research revealed that Alzheimer's disease and senile dementia shared similar clinical and histological features, and by the 1970s, the medical community reached a consensus to use the term Alzheimer's disease to designate both conditions, irrespective of age of onset.

The 1980s marked the development of standardized diagnostic criteria under the impetus of the Alzheimer Disease and Related Disorders Association and the National Institute of Neurological and Communicative Diseases. This development allowed more precise clinical identifications of distinct forms of dementia, including Alzheimer's disease, vascular dementia, and Pick's disease, among others. It also permitted more accurate estimates of the number of dementia cases within the general population.

Current findings put the prevalence of dementia in Western countries at between 2 and 9 percent of people over the age of 65, with rates for those age 85 years and over as high as 50 percent. Alzheimer's disease is by far the most common form of dementia and accounts for approximately three quarters of all cases. In the United States alone, the Alzheimer Society reports that Alzheimer's disease currently affects an estimated 4.5 million Americans, and projections for 2050 put this number at between 11.3 and 16 million. Worldwide, dementia affects an estimated 28 million individuals, a figure projected to increase to 80 million by 2040. These estimates make dementia one of the most common causes of morbidity in elderly people.

Asignificant recent development in dementia research has been the discovery of several genes associated with familial and sporadic types of Alzheimer's disease. Familial Alzheimer's disease implicates the action of a number of mutated genes that follow an autosomal dominant pattern of inheritance whereby each child has a 50 percent chance of inheriting the disease if one of the parents is a carrier. Individuals with familial Alzheimer's disease account for about 10 percent of all cases and typically develop the disease before the age of 60. By contrast, sporadic Alzheimer's disease involves a combination of genetic factors not necessarily mutational that likely interact with a host of poorly understood environmental factors. Sporadic Alzheimer's disease accounts for the majority of cases of the disease, and onset typically occurs after the age of 60. So far, only a variant of the apolipoprotein E gene, called apoE4, has been determined to increase susceptibility for sporadic Alzheimer's disease.

A number of caveats have prevented the widespread use of genetic testing for Alzheimer's disease in clinical settings. First, testing to identify asymptomatic individuals who will develop the disease later in life is only useful for a small subset of familial cases. Predictive testing in sporadic cases remains problematic because apoE4 is an unreliable marker for Alzheimer's disease. Also found in individuals who do not develop the disease later in life, this variant likely needs to interact with other factors to cause the disease. A key concern with genetic discoveries is their potential for redefining Alzheimer's disease as an inherited condition that clinicians can accurately detect early in life. This mischaracterization of the predictive power of genetic testing raises concerns about the misguided use of test results by employers and health care insurers for eliminating high-risk cases from their rosters.

The neuropathological consequences of dementia have been well documented in the medical literature as a gradual decline in intellectual function that affects memory, thinking, and behavior. Through the artifacts of computer tomography scans, autopsied brain matter, and psychometric scores, biomedicine has legitimized dementia as a disease that unfolds independently from social circumstances, gradually erasing the identity of those afflicted by its pathology. In the popular imagination, dementia exists as rhetoric of irrevocable decline that robs afflicted individuals of self and dignity. Yet, this inevitability is increasingly being challenged by research that seeks to understand the influences of culture, social location, organizational practices, and health policies on how dementia is interpreted, and responded to, by both diagnosed persons and their social partners. Adhering to the tenets of social constructionism, this perspective critically interrogates the different discourses that construct dementia in relation to social, historical, and political contexts. The suggestion is that a nihilistic understanding of dementia sets expectations and responses that undermine the moral status of those afflicted and creates the conditions under which expressions of the self are subsumed to pathology. This alternate conceptualization acknowledges the impact of pathology but also recognizes people with dementia as having the ability to maintain a sense of valued self when supported by person-centered care practices.

Bibliography:

1) Ballenger, Jesse F. 2006. Self, Senility, and Alzheimer's Disease in Modern America: A History. Baltimore: Johns Hopkins University Press.

2) Gubrium, Jaber F. 1986. Old Timers and Alzheimer's: The Descriptive Organization of Senility. Greenwich, CT: JAI.

3) Kitwood, Tom. 1997. Dementia Reconsidered: The Person Comes First. Buckingham, England: Open University Press.

4) Leibing, Annette and Lawrence Cohen, eds. 2006. Thinking about Dementia: Culture, Loss, and the Anthropology of Senility. New Brunswick, NJ: Rutgers University Press.

5) Sabat, Steven R. 2001. The Experience of Alzheimer's Disease: Life through a Tangled Veil. New York: Blackwell.

6) Traphagan, John W. 2000. Taming Oblivion: Aging Bodies and the Fear of Senility in Japan. Albany, NY: State University of New York Press.

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