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Medicine Science

Aging Reversed In Mice 554

Hugh Pickens writes "The Guardian reports that scientists claim to be a step closer to reversing the aging process after experimental treatment developed by researchers at Harvard Medical School turned weak and feeble old mice into healthy animals by regenerating their aged bodies. 'What we saw in these animals was not a slowing down or stabilization of the aging process. We saw a dramatic reversal – and that was unexpected,' says Ronald DePinho, who led the study. The Harvard group focused on a process called telomere shortening where each time a cell divides, the telomeres are snipped shorter, until eventually they stop working and the cell dies or goes into a suspended state called 'senescence.' Researchers bred genetically manipulated mice that lacked an enzyme called telomerase that stops telomeres getting shorter causing the mice to age prematurely and suffer ailments, including a poor sense of smell, smaller brain size, infertility and damaged intestines and spleens. When the mice were given injections to reactivate the enzyme, it repaired the damaged tissues and reversed the signs of aging raising hope among scientists that it may be possible to achieve a similar feat in humans – or at least to slow down the aging process."
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Aging Reversed In Mice

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  • Cells do not normally produce telomerase on their own because not producing it protects against cancer. Turning on the gene that makes telomerase is one of the hurdles pre-cancerous cells have to cross on their way to becoming cancerous.

    Also, as someone else pointed out, telomeres are just one aspect of aging. You can induce mice to age prematurely by restricting embryonic expression of telomerase, but that doesn't necessarily mean that mice that age normally will be similarly completely restored by adding it.

    There are a number of degenerative diseases (macular degeneration and probably alzheimers) that happen because of inadequate waste removal. No amount of telomerase is going to cause all the little protein fragments lying around to be magically cleaned up and excreted.

  • Re:Old news (Score:3, Informative)

    by ByOhTek ( 1181381 ) on Monday November 29, 2010 @08:29AM (#34373266) Journal

    Not really - mice, unlike humans, normally have telomerase functioning throughout their entire lifespans. Telomere shortening is not an issue for them.

    Actually, if I remember my undergrad genetics correctly, unless you know people living to around 800 years old, it's not an issue for people either.

  • Re:Old news (Score:5, Informative)

    by ByOhTek ( 1181381 ) on Monday November 29, 2010 @08:39AM (#34373312) Journal

    Telomerase activation shouldn't give you cancer. First of all, your telomeres won't be a problem untill you are in the 700-800 year range (if I remember my undergrad genetics courses correctly). At least, outside of the white blood cell lineages, those will probably go for most people in the first 100 years - they could probably use some telomerase. OK, so lets say you would normally get cancer by the time you were 150, thankfully, your white blood cells stop functioning so well around age 90 and you die of pneumonia instead. Now, lets assume the other causes of aging are fixed, so, that's pretty much the standard.

    Insert telomerase. You now live to 150, and die of cancer. Did the telomerase give you cancer? No, it just allowed you to live long enough for the factors that did give you cancer to take hold.

    You do have cells in your body producing telomerase - the gamete producing lineage. You can trace telomerase back to the development of successful linear DNA from that lineage - without break. No cancer. Telomerase is a DNA stabilizing agent, not a mutagen.

  • Re:Old news (Score:2, Informative)

    by mibe ( 1778804 ) on Monday November 29, 2010 @12:01PM (#34374984)
    On the contrary, the vast majority of human cancers have telomerase (are "immortal"), perhaps what you're thinking of is the ability to grow in culture, which is a relatively rarer phenomenon (HeLa cell line!) but nowadays can be artificially induced. This makes sense because a cancer's rapid growth rate would be unsustainable in the long term without some way of getting around telomere loss. The rapid division combined with most cancer's predisposition to mutation results in natural selection for these specific kinds of mutations - the first cell to express telomerase, for example, will out-compete his shorter-lived brothers in the long run, so inevitably all cancers wind up circumventing the telomere issue in one way or another. If you've got access, you can read this nice review article: http://www.ncbi.nlm.nih.gov/pubmed/9282118 [nih.gov]

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