Senile Dementia of the Alzheimer Type

The Role of Acetylcholinesterase Inhibitors

As the United States' population grows older, the chronic degenerative diseases of the elderly have become increasingly important. One condition that has received considerable attention is Alzheimer's disease, otherwise known as Senile Dementia of the Alzheimer Type (AD/SDAT). In recent years, researchers have begun to begun to elucidate the biochemical and physiological mechanisms which characterize this disorder. Moreover, despite the brain's inherent complexity and inaccessibility, several promising therapeutic modalities have emerged. Of these different agents, perhaps the acetylcholinesterase inhibitors exhibit the most potential. At the turn of the century, the average life expectancy in the United States was only 47 years (19:3). By 1989, however, the life expectancy for newborns had reached 75 years. By the year 2030, it is estimated that over 50 million Americans will live to be 65 (29:1). This demographic trend--both in the U.S. and abroad--has focused international attention on the mental disorder known as dementia. With each decade beyond 60 years, the relative number of persons at risk for a dementing illness increases. For example, while dementia afflicts only 5% of people over the age of 65 years, about 15% of those over 80 suffer from the condition (4:1169). In the U.S. alone, over 3 million people have the most common dementing illness, Alz

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d Ishii and Haga (1976), both observed IgG in senile plaques. Moreover, all of the major components of the classical complement pathway occur in Alzheimer's disease brain tissue (30:82). Lastly, the disease has also been associated with the activation of various immune system cellular components. Reactive microglial cells are known to vigorously express the MHC class II surface glycoprotein, HLA-DR. The primary function of this glycoprotein is to present antigen to lymphocytes to stimulate an immune response. HLA-DR may, therefore, be partially responsible for the presence of large numbers of macrophages and infiltration by T-cells (both T-helper inducer and T-cytotoxic suppressor cells) in Alzheimer's affected tissue. Such phenomena could certainly represent a cell-mediated immune response. It is not known though, whether or not the response is pathogenic. For example, rather than causing Alzheimer's, observed immune responses could also result from some invading pathogen. During both normal and pathological aging, such protective structures as the blood-brain barrier appear to undergo alteration. This may make the nervous system more vulnerable to transmissible infective agents. Despite the apparent plausibility of su
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Approximate Word count = 5621
Approximate Pages = 22 (250 words per page)

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