Alzheimer's Disease is a Progressive Brain Disease

Alzheimer's patients typic solelyy live from five dollar bill to 10 years after diagnosis, though with recent improvements in health awe, they can live for 15 years or much. The disease is particularly stressful on those who have to c be for these patients, particularly as the disease progresses. Risk components for Alzheimer's include contribute trauma, epoch, Down's syndrome, and a genetic mutation.

Familial Alzheimer's disease accounts for approximately 10 percent of cases, and some of these patients develop symptoms before age 40 (Gale, 2001). The early onset genes be found on chromosomes 1, 14, and 21, and are termed presenilins. The gene on chromosome 14 appears to be primarily accountable for early onset Alzheimer's disease, which has a more rapid course. The presenilin on chromosome 1 seems to be responsible for Alzheimer's of later onset, with a more protracted course. Recently, genetic studies have shown that the gene for apolipoprotein E (ApoE), a protein which moves cholesterol in the bloodstream and can bind to gritty beta-protein, can affect the chances of getting Alzheimer's disease. There are lead forms of ApoE - ApoE2, ApoE3, and ApoE4. They are normally occurring variants, and it has been found that the inheritance of ApoE4 increases the risk and lowers the age of onset of the disease, and inheritance of ApoE2 decreases the risk and raises the age of onset. The gene is

Growdon, John L. (2002). Long-term residential care. A Guide to Alzheimer's Disease (Harvard Special health Reports). Stanford, CT: Harvard Health Publications.

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The use of stem cells to replace dying cells is in any case universe studied as a possible manipulation for Alzheimer's disease (Growdon, The Search, 2002). In theory, stem cells could be converted to cholinergic neurons which could restore acetylcholine to normal levels. However, this would not alter the other neurological deficits of Alzheimer's disease - synaptic loss and neuronal degeneration - which are responsible for the dementia seen in the disease. Gene therapy is also being explored as a means of restoring some or all of the nerve cell connections destroyed in Alzheimer's disease (Gilbert and Albert, 2000). genetically modified brain cells programmed to release nerve growth factor have been tested in monkeys, and these transplanted cells restored brain cell connections in the cortex that had deteriorated with age.

Company to market animal model for Alzheimer's disease. (2003, October 17). Genomics & genetics Weekly, 38.

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