Werner Syndrome
Nowadays those involved in aging research view aging in terms of a genetic disease rather than as a natural, evolution-driven process by which the old make way for the young. A condition of aged friends and relatives seems terrible to conceive; they are afflicted with a ghastly wasting disease, a plague whose effects are inescapable because of our own genes. People plagued with Werner syndrome do not even have the opportunity to experience this natural progression we call aging, instead this disease causes its victims to die of old age by their mid 40's or 50's.Just about everyone dreads the physical decline often associated with aging, but people with the rare inherited disease known as Werner syndrome have to face the aging process far sooner than most. Unexpectedly, while they are still in their early twenties, their hair grays, their skin loses its suppleness, and their vision clouds from cataracts. Even worse, they get cancer, heart disease, and a host of other diseases that usually don't strike until later in life. Most people afflicted with Werner syndrome die before age 50. Aging experts have long wondered just what kind of molecular defect could cause such a striking acceleration of the
The function of the Werner syndrome helicase is currently unknown. What is clear is that subjects with the syndrome probably do not produce a functional form of this protein. It is known that DNA in affected subjects appears to contain a large number of damaged sites. This accumulation of DNA damage is probably the cause of the symptoms we call Werner syndrome. Cells from Werner syndrome subjects do not appear to be defective for any known DNA repair process, so the primary defect probably involves a defect in a process that causes DNA damage, rather than one that repairs damage caused by other agents. Whatever the specific mechanisms involved in the Werner syndrome phenotype, identification of the Werner syndrome gene now provides evidence that at least some components of normal aging and disease susceptibility in late life may be related to disfunctions in DNA metabolism. Fortunately, we have the responsible gene in hand, giving a tool to begin answering all of these puzzling questions.
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Approximate Word count = 3055
Approximate Pages = 12 (250 words per page double spaced)
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