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Telomere-Lengthening Procedure Turns Clock Back Years In Human Cells

Zothecula writes Researchers at the Stanford University School of Medicine have developed a new procedure to increase the length of human telomeres. This increases the number of times cells are able to divide, essentially making the cells many years younger. This not only has useful applications for laboratory work, but may point the way to treating various age-related disorders – or even muscular dystrophy.

3 of 183 comments (clear)

  1. Interesting approach by Chikungunya · · Score: 5, Interesting

    Making the treatment directly with mRNA sidestep a lot of dangers of promoting cell replication, the immune system would not have any foreign proteins to recognize and so multiple doses are feasible, the RNA is degraded over time so the replication goes back to normal instead of keeping forever in an artificial state and it was demonstrated that the cells grow "old" again after the treatment.

    Still, it feels like its going to be much more a lab tool than a anti-aging treatment for a few more decades, RNA treatment is very tricky to do in vivo and even the most promising candidates for treatment (vaccines and so on) only produce very limited success, unless some revolutionary vector is invented in the near future it will pass a lot of years before this can be safe and efficient enough to be commercialized.

  2. Re:Expensive by ShanghaiBill · · Score: 5, Insightful

    I suspect that this will be one of the most expensive treatments ever.

    There is no particular reason to believe this will be expensive. It is just some RNA, which can be inexpensively replicated. Even if it is patented, it is likely that someone else can some up with a similar technique, making it a competitive market, and driving down prices.

    If you really want to be a pessimist, you should instead focus on how this is going to bankrupt Social Security. People are going to retire at 65, and then collect benefits for the next 55 years.

  3. Re:cancer by Doubting+Sapien · · Score: 5, Interesting

    Not offhand in any good laymen's literature I know of. But the process is described in a bunch of molecular biology textbooks I don't have access to at the moment. When chromosomes are not protected with telomere caps on the ends, the cellular machinery is likely to mistakenly treat them as DNA double strand breaks. What happens in such situations is that proteins involved in DNA repair will try to join the "naked" end to the nearest other piece of DNA, even if it belongs to another healthy chromosome. Fused chromosomes are always bad news for cellular health. The problem is amplified in what is called a breakage-fusion-bridge (b/f/b) cycle as cells try to continue dividing with abnormal chromosomes that now doesn't separate as they should.

    The presence of healthy telomeres suppresses this process. Even if your chromosomes get messed up through the infrequent snags that still happens occasionally, a damaged chromosome that is able to restore the presence of telomeres at the end by one means or another (there are several) will stop undergoing b/f/b cycles. Mind you, the chromosome is still damaged to some degree, but it doesn't get worse.

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