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Biology 11 Online
OpenStudy (anonymous):

Scientists are researching on aging is there any Idea about that how it happens why it happens.

OpenStudy (anonymous):

I know there is a link between telemerase in the chromosomes and aging, I learned about it in genetics. This is straight from wikipedia under "telomerase" The enzyme telomerase allows for replacement of short bits of DNA known as telomeres, which are otherwise shortened when a cell divides via mitosis. In normal circumstances, without the presence of telomerase, if a cell divides recursively, at some point all the progeny will reach their Hayflick limit.[13] With the presence of telomerase, each dividing cell can replace the lost bit of DNA, and any single cell can then divide unbounded. While this unbounded growth property has excited many researchers, caution is warranted in exploiting this property, as exactly this same unbounded growth is a crucial step in enabling cancerous growth. Embryonic stem cells express telomerase, which allows them to divide repeatedly and form the individual. In adults, telomerase is highly expressed in cells that need to divide regularly (e.g., in the immune system), whereas most somatic cells express it only at very low levels in a cell-cycle-dependent manner.[citation needed] A variety of premature aging syndromes are associated with short telomeres.[14] These include Werner syndrome, Ataxia telangiectasia, Ataxia-telangiectasia like disorder, Bloom syndrome, Fanconi anemia, and Nijmegen breakage syndrome. The genes that have been mutated in these diseases all have roles in the repair of DNA damage, and their precise roles in maintaining telomere length are an active area of investigation. While it is currently unknown to what extent telomere erosion contributes to the normal aging process, maintenance of DNA in general and telomeric DNA, to be specific, have emerged as major players. Dr. Michael Fossel has suggested in an interview that telomerase therapies may be used not only to combat cancer but also to actually get around human aging and extend lifespan significantly. He believes human trials of telomerase-based therapies for extending lifespan will occur within the next 10 years. This timeline is significant because it coincides with the retirement of Baby Boomers in the United States and Europe.[citation needed] Some experiments have raised questions on whether telomerase can be used as an anti-aging therapy, namely, the fact that mice with elevated levels of telomerase have higher cancer incidence and hence do not live longer. In addition, certain premature aging syndromes have been associated with telomere shortening. Telomerase also favors tumorogenesis, leading to questions about its potential as an anti-aging therapy.[15] On the other hand, one study showed that activating telomerase in cancer-resistant mice by overexpressing its catalytic subunit extended lifespan.[16] The potential remains for telomerase activators to contribute to the development of cancer. Exposure of T lymphocytes from HIV-infected human donors to a small molecule telomerase activator (TAT2) retards telomere shortening, increases proliferative potential, and, importantly, enhances cytokine/chemokine production and antiviral activity.[17] A study that focused on Ashkenazi Jews found that those that live the longest inherit a hyperactive version of telomerase that rebuilds telomeres.[18] Mice engineered to block the gene that produces telomerase unless they are given a certain drug aged at a much faster rate and died at about six months, instead of reaching the average mouse lifespan of about three years. Administering the drug at 6 months turned on telomerase production and caused their organs to be "rejuvenated," restored fertility, and normalized their ability to detect or process odors. The finding raises hope for treatment of conditions such as progeria and other accelerated aging disorders, as well as possible organ regeneration therapies, such as repair of liver damage due to hepatitis or alcoholism.[19] A study published in the journal Nature in January 2011 found that Telomerase reactivation reversed tissue degeneration in older telomerase-deficient mice.[20][21]

OpenStudy (anonymous):

Telomerase has a proliferative effect on Telomere, they decide if more Telomere should be built on the end of the chromosomes. At each celldivision a bit of telomere is removed untill it reaches a end point where it cannot go through any more celldivision. Then the chromosome either goes into what i think was called G0 state, or Telomerase build up additional Telomere. If a it would go through celldivision nontheless, it would start to break down chromosomes in the divison and the end result would not be a copy of the cell but rather a randomly put together chromosome which may or may get taken care of the bodies autoregulating function that handles this kind of situation, if it does not. A proliferative function will occure by Telomerase on the defective Telomere and you got yourself a form of cancer most likely. |dw:1334942030197:dw| For illustrative properties i drew a rough scematic of Telomere Telomere is how you usually measure the age of the a tissue, note that it does not follow the same schematic globally, if a alcoholic has plenty of Telomere left on his skincells, it does not indicate the "relative age" of his Liver or any other tissue for that matter. I do recall reading a year ago in a journal i suscribe to about a Bloodtest coming up to determine what your relative age would be, and how long you pratically got left to live. It is finished and ready for clinical application, but many socioeconomic and political factors hindered its distribution, imagion your insurence cost depending on a bloodtest, jobbapplication, dating, etc.... It is practically possible to know within a 80% probability how many years +/- 2 years you have to live.

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