autopsy on a deceased person who has it. When the patient is living, health care workers must rely on a series of questions and external symptoms to make a diagnosis of Alzheimer’s. Previous studies have demonstrated that “between 50 and 75 percent of a person’s risk of getting the disease is genetic” (Goldberg Goff D1).
Many argue that Alzheimer’s is a natural outcome of growth and aging. During the 1980s, researchers discovered that a class of sticky proteins known as beta amyloids formed plaque and tangles in the brains of deceased Alzheimer’s patients. A few years later, researchers discovered the gene responsible for producing the protein responsible for the plaque that is a hallmark sign of Alzheimer’s. The plaque builds up on the empty spaces between the nerve cells of the brain, while the neurofibrillary tangles erupt from within the cells. Scientists have now discovered that the APP gene, Presenilin-1 and Presnilin-2 appear to be the most likely genetic culprits in hereditary cases of Alzheimer’s, while the APOE4 gene is considered to be the culprit of late onset non-hereditary cases of Alzheimer’s (Nash 3).
Scientists have already developed some types of methods to help ameliorate the effects of Alzheimer’s. Since the disease kills cells it affects, most of the efforts have focused on preventing the formation of lesions and plaque. Gamma-secretase blockers, which are necessary in the formation of beta amyloid plaque, have proven to be somewhat effective in slowing the progression of Alzheimer’s. However, many people who do not acquire Alzheimer’s hereditarily contract the illness at a much older age than
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