Alzheimer's, Genetics, and Public Health: An Overview Term Paper by Peter Pen

Alzheimer's, Genetics, and Public Health: An Overview
A detailed account of the causes of Alzheimer's disease and a review of current research.
# 106725 | 1,203 words | 15 sources | MLA | 2008

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This paper discusses Alzheimer's disease (AD), a neurodegenerative disorder characterized by progressive memory loss and dementia that affects millions of people worldwide each year. Although no definitive cause has yet been discovered, this paper reviews current research into various possible causes and risk factors for AD, including pathological causes and lifestyle factors that have been shown to contribute to the development of Alzheimer's disease and the implications of these factors for health promotion, disease prevention, and treatment.

Pathological Causes of Alzheimer's Disease: Amyloid Plaques and Neurofibrillary Tangles
Genetic Factors in the Development of Alzheimer's Disease
Health Promotion, Disease Prevention, and Treatment

From the Paper:

"Briefly, the formation of amyloid plaques and neurofibrillary tangles are thought to contribute to the degradation of the neurons (nerve cells) in the brain and the subsequent symptoms of Alzheimer's disease. In AD, plaques develop in areas of the brain used for memory.8 Amyloid is a general term for protein fragments that the body produces normally. Beta-amyloid is a fragment of a protein that breaks off from another protein in the body. In a healthy brain, these protein fragments would be broken down. In Alzheimer's disease, the fragments accumulate to form hard, insoluble plaques.8
"Neurofibrillary tangles consist of a series of insoluble twisted fibers found inside the brain's cells. These tangles are made of a protein called tau, which forms part of a structure in the brain called a microtubule. The microtubule helps transport nutrients and other important material from one part of the nerve cell to another. In Alzheimer's disease, however, the tau protein is abnormal and these microtubule structures collapse."

Sample of Sources Used:

  • Tranjanowski J Q, Schmidt M L, Shin R-W, et al. PHFtau(A68): From pathological marker to potential mediator of neuronal dysfunction and degeneration in Alzheimer's disease. Neuron. 1993;1:184-191.
  • Morris, J C.; Heyman A. Mellits E D, Clark C. Clinical and neuropsychological assessment of Alzheimer's disease. Neurology 39(9):1159-1165, 1989.
  • Chui D H, Tabira T, Izumi S, Koya, G, Ogata J. Decreased beta-amyloid and increased abnormal tau deposition in the brain of aged patients. American Journal of Pathology 145(4):771-775, 1994.
  • Katzman R. Education and the prevalence of dementia and Alzheimer's disease. Neurology 43(1):13-20, 1993.
  • Whitson J S, Selkoe D J, Cotman C W. Amyloid beta protein enhances the survival of hippocampal neurons in vitro. Science 243(4897):1488-1490, 1996.

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