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Telomeres


Mr Rayon

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  • 2 months later...

I think that this is a fascinating subject that needs opening up for further discussion. If it is true (and I may be wrong here) that telomeres are often shortened more as cells age, is it not possible to extend the life of these cells by using telomerase enzymes?

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I think that this is a fascinating subject that needs opening up for further discussion. If it is true (and I may be wrong here) that telomeres are often shortened more as cells age, is it not possible to extend the life of these cells by using telomerase enzymes?

 

Yes it's possible and evident in different cancers.

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Now that is interesting. Presumably what you are saying here is that cancer cells induce immortality by preserving the length of their telomeres. I wonder if immortalised cell lines show the same features as cancer cells?

 

Also, can the time come when humans can also use the correct chemical cocktail to extend their lives? After all, who really wants to consider their own death?

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The source of immortalized cell lines are cancer cells, like HeLa cells dervived from a woman with cervical cancer.

 

Anyway, if you look at our recent past, we've actually been able to extend our lives quite a bit via medical advances. But such a feat comes with a cost. For instance, we are now seeing an unprecedented rise in cases for heart disease and cancer not known to our ancestors. Whether it's better die or live as a vegetable is up for debate.

 

Also, you should look at the different theories on the causes of aging, like the DNA damage theory already published out there. It's thought that each has its own merit, so it's reasonable to think that immortality cannot be achieved until all of the potential causes of aging are addressed.

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Moreover telomere length are also a form of cell regulation. As already pointed out, loss of such a regulation can result in cancer.

 

And also to nitpick, not all immortalized cells are from cancer lines. But all cancers cell lines are immortalized.

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Progeria seems to be due to accelerated ageing and I wondered if an elucidation of the molecular processes taking place in accelerated ageing could be slowed down to decrease ageing in others. I know this is simplistic but in the factors that affect ageing, I am sure that all do not have an equal bearing on the ageing processes.

 

HGPS is caused by a mutation in the gene called LMNA (pronounced, lamin - a). The LMNA gene produces the Lamin A protein, which is the structural scaffolding that holds the nucleus of a cell together. Researchers now believe that the defective Lamin A protein makes the nucleus unstable. That cellular instability appears to lead to the process of premature aging in Progeria.

 

http://www.progeriaresearch.org/about_progeria.html

 

http://commons.wikimedia.org/wiki/File:Hutchinson-Gilford_Progeria_Syndrome.png

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For Progeria, let's say there's a way to induce a mutation to the gene encoding Lamin A which not only restores the structural integrity of the nucleus, but enhances it to the point that nothing can break it down. How does that help solve problems related to shortening telomeres and other aging factors?

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It doesn't affect progeria or shortening of telomeres but I am suggesting that if you look at all the factors that are affected during ageing, there may be one factor that will caue age to elongate - e.g. a restricted calorie intake. I think I have read that restricted calorie intake contributed to the delayed senescence of laboratory animals but someone would have to find a suitable reference for me.

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