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Alzheimer's Disease, The Facts

Alzheimer's, the disease of the degeneration of the brain, was identified in 1907 by German physician Alois Alzheimer. Four million Americans suffer from the disease which deprives the victimof the ability to remember, think, reason, and eventually coordinate movement. This most common form of dementia is caused physically by the gradual change in nerve cells, which leads to the destruction of brain cells. Studies find that this fourth leading cause of death affects more women than men, and more Hispanics and African-Americans than Caucasians. The disease can be present in two forms; early onset Alzheimer's affects those younger than age 65, whereas late onset Alzheimer's affects those older. "Late onset Alzheimer's affects more than 90 % of sufferers."(Internet 1) This more common form has been recently discovered to affect those who possess a certain allele of the APOE, apolipoprotein E, gene located on Chromosome 19. APOE, which encodes a protein that helps transport cholesterol in the body and also is involved in nerve cell repair, comes in three alleles, e2, e3, and e4. Those with one or two e4 alleles are deemed at higher risk of Alzheimer's disease, although those who possess APOE-e4 are not guaranteed to develop the diseas


e. APOE-e4 may simply be unable to efficiently repair nerve cells. The presence of e4 does not signify if person will develop Alzheimer's; instead, it signifies when he or she will get it. Recent studies suggest that Alzheimer's may be affected by an interaction between APOE and the newly discovered risk factor alpha-2-macrogobulin, A2M, a gene mutation on chromosome 12. A2M is a protein that deactivates proteases, enzymes that carve up other proteins. Alpha-2-macrogobulin's involvement in Alzheimer's development is especially likely because it attaches to the same cell surface protein as APOE and amyloid precursor-protein (APP). The unmutated form of A2M helps to get rid of the APP fragment beta-amyloid, which is present in excess amounts in the brains of Alzheimer's patients. The mutant A2M, which does not properly remove protein, but only makes the aging brain vulnerable; it does not guarantee affliction. Another possible genetic risk factor for Alzheimer's disease is the presence of the bleomycin hydrolase gene, which comes in the two alleles A and G. People who have two G alleles and no APOE-e4 are also susceptible to the disease.

becomes impossible; immobility prevails, to be followed by death. Autopsies on many Alzheimer's Disease sufferers show that a large number of differences were present when comparing a normal brain to their's. There was a loss of nerve cells from the cerebral cortex in the Alzheimer's victim: approximately 10% of the neurons in this region were lost. Although a 10% loss is relatively minor, and cannot account for the severe impairment suffered by Alzheimer's victims. Neurofibrillary tangles are found in the brain within the cell bodies of nerve cells in the cerebral cortex, and take on the structure of a double helix.Neuritic plaques are patches of clumped material lying outside the bodies of nerve cells in the brain. They are mainly found in the cerebral cortex, but have also been seen in other areas of the brain. At the core of each of these plaques is a substance called amyloid, an abnormal protein not usually found in the brain. This amyloid core is surrounded by cast off fragments of dead or dying nerve cells. The cel

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Approximate Word count = 1462
Approximate Pages = 6 (250 words per page double spaced)


  

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