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Alzheimer's disease is a neurodegenerative disorder

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Alzheimer=s disease is a neurodegenerative disorder which causes the destruction of certain brain cells resulting in a decline in mental functions. The damage occurs in the association area of the cerebral cortex, the hippocampus and the middle and temporal lobes, and result in a decreased concentration of the neurotransmitter acetylcholine (Sadovsky, 2000, p. 877). Alzheimer=s disease affects the memory, thinking, language, and behavior. It usually occurs in people over the age of 65, but can occur in those as young as 40 years of age. Symptoms can range from mild to severe, and when dementia occurs, patients are often placed in full-time residential care. It is estimated that about 10 percent of the population over the age of 65 suffer from Alzheimer=s disease (Alzheimer=s, 1999). Of these, between five percent and 10 percent have the familial form of the disease. That is, they have a family history of Alzheimer=s and show signs of the disease before age 65.

Chemical and structural changes in patients with Alzheimer=s interfere with a person=s ability to process, store and retrieve information. Symptoms of Alzheimer=s vary, and change with progression of the disease. The first symptoms are usually forgetfulness, memory loss and difficulty understanding written material (Alzheimer=s, 1999). Recent memory is affected more severely than longterm memory. As Alzheimer=s progresses, the person becomes disoriented and confused and can no longer remember major facts a

. . .
ized the data presented at the 6th International Conference on Alzheimer=s disease that year on the genetic basis for Alzheimer=s (Edwardson and Morris, 1998). Evidence was presented at the conference that missense mutations in three genes causes autosomal dominant forms of early onset Alzheimer=s, as described above, and one genetic factor indisputably linked with the late onset forms of Alzheimer=s that is the ApoE, also described above. It has now been found that three common allelic variants of ApoE exist - e2, e3, and e4 - encoded as a single gene locus on chromosome 19. ApoE can be used to predict risk of Alzheimer=s, but is not necessary or sufficient to cause the disease. At most, only half of late onset Alzheimer=s patients carry an ApoE allele. A whole string of genetic associations have been reported with late onset Alzheimer=s, including polymorphisms in angiotensin converting enzyme, antichymotrypsin, bleomycin hydrolase, butyrylcholinesterase, HLA, low density lipoprotein receptor related protein, various mitochondrial enzymes, and the presenilin 1 intronic mutation. So far none of these has been systematically replicated in experiments, so their significance in relation to Alzheimer=s is unknown at present (Ed
. . .

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Approximate Word count = 2505
Approximate Pages = 10 (250 words per page)

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