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Certain age related diseases are known to be caused by shortened telomeres. Outside of the general treatment of human aging,
age-related diseases represent a promising use for telomere therapy. Some of the specific diseases of aging encompass:
atherosclerosis, osteoporosis, macular degeneration, skin atrophy, emphysema, cirrhosis, certain aspects of AIDS,
Progeria, Werner’s Syndrome, forms of hearing and sight loss, types of organ failure, reduced immune system
functionality, age-related metabolic dysfunction, and non-healing ulcers among other diseases. The specific
treatment of age related disease represents a significant economic opportunity in some of the following areas.
http://www.iovs.org/cgi/content/full/43/5/1622
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As we age, our arteries lose their elasticity. Those arteries called upon to deliver blood to our most critical organs are
subject to the most wear and tear. Because of this stress, these arteries have the most cell turnover. Therefore, their
telomeres shorten faster. Some research has shown that those arteries with the shortest telomeres are the ones with the
most age-related deterioration. Research published in the February 1, 2003, issue of the Lancet showed that among a
group of 143 persons over age 60, those with the shortest telomeres in their blood cells were three times more likely
to die of heart disease than those with the longest telomeres.
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Our livers have the reputation of being the organs with the greatest capacity for self-repair after injury or illness.
(Perhaps this explains why some people seem to be able to abuse alcohol for years with apparent impunity.) But this
capacity for self-repair is not infinite. Chronic hepatitis, cirrhosis and advanced age are all known to produce a
reduction in liver function. Japanese researchers have shown that telomere length in those with chronic hepatitis,
cirrhosis or even in healthy octogenarians is substantially shorter than in healthy young adults. This suggests,
though doesn't prove, that the telomere shortening that occurs with each liver cell division is what eventually
leads to the aging and death of these cells, and thus the aging and loss of function of the liver itself.
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Unlike our livers, our kidneys possess less capacity for self-repair. Age-related diseases like high blood pressure and heart
failure reduce kidney function, but so does aging itself. A healthy 80-year-old does not generally have the kidney function
of a healthy 30-year-old. A study of the cells retrieved in a series of kidney biopsies revealed that shorter telomeres
correlated positively with advancing age, providing more evidence that telomere shortening is a factor in age-related conditions.
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Although the shortening of telomeres is associated with the decline in cell function in a variety of conditions, other
factors also play a part. Some scientists have theorized that shortening of telomeres in the immune system contributes
to the decline in our ability to fight infectious disease as we age. However, other studies have shown that mice and
rats, whose telomeres are much longer than ours, also experience age-related immune decline. This has led some to
speculate that factors other than telomere shortening are responsible for immune decline with age.
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Researchers are exploring the role telomeres may play in inherited diseases that can take time to express themselves.
Some people inherit a gene for a disease from one parent and a healthy gene from the other. As they grow and develop,
their healthy gene predominates. Over time, however, the shortening of their telomeres with successive cell divisions
leads to all sorts of cellular chaos, and defective genes then have the opportunity to manifest themselves.
This has been proposed as a possible factor in the development of such diseases as type II diabetes and high blood pressure.
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