The important thing to recall here is that BioTime is the current home of Michael West, who is a superbly skilled publicist.
In terms of the science, this isn't by any stretch of the imagination a reversal of aging in cells. It is what it is, which is generating useful cells with longer telomeres - if you want to define age as the length of telomeres, then sure, let's say you've reversed aging. But that isn't a useful definition.
The question of how telomeres fit into the bigger picture of aging is still very much debated. Their average length in some tissues decreases with age, but that might be a secondary result of other processes such as accumulated mitochondrial DNA damage. Lengthening telomeres with telomerase in conjunction with cancer suppression genetic engineering has increased mouse life span by 50% - but here again there is the possibility that the telomerase isn't extending life by extending telomeres, but by doing something else.
There's a theory that since telomeres decrease in size every mitosis that they are the reason for the Hayflick limit (the max number of times a cell can divide). The theory then says that as cells reach the limit you 'age'.
The article says they figured out a way to increase telomeres in the lab, this is not very new though there are known telomerase inducers out there.
I'm not sure how revolutionary it is though the article has very little info and I've read about this topic since more than 10 years ago.
EDIT: Found this from 2007:
"Since 2007, several compounds have been discovered that cause somatic cells to express higher levels of telomerase than usual. In April 2007, Geron Corporation licensed New York-based company TA Sciences to conduct human trials on a molecule called TA-65, a derivative of Astragalus propinquus, that acts as telomerase activator"
It is impossible to tell from their website what they did. My institution does not have a subscription to "Future Medicine" so the best I can get is the abstract.
It sounds like they've altered the expression of 3 key developmental genes (none of which are telomerase, but may be upstream of it). These genes transform the cells into an induced pluripotent stemcells (iPS). They created 6 lines, five of which showed telomere shortening to similar levels of that seen in other iPS lines. However, one of the iPS lines they created the TRF (dna that telomerase acts on) continued to lengthen for 60 days.
The flowchart picture is science fiction - they haven't done anything like that in this study.
Telomeres are on the ends of every chromosome (strand of dna). They contain no genetic information themselves. Every time your cell splits, special enzymes attach themselves chromosome, copying everything as they go, including the telomere. However, the enzymes, due their shape, can't actually travel all the way down a dna strand; they don't actually copy the last little bit of dna. If there were genetic information on the end of the dna strand, it would be lost. However, there are telomeres which act as a protective buffer and it just so a little bit of the telomere is lost instead of genetic information. However, because a little bit of the telomere is lost with every split, eventually the telomere shrinks and vanishes. At that point, the cell can no longer copy itself without losing information, and so it doesn't.
This company seems to have found a new way to regrow the telomere in young cells.
>At that point, the cell can no longer copy itself without losing information, and so it doesn't.
I was under the impression that the cell can no longer copy itself because the telomeres are 'caps' that hold the chromosome together, and without them, the chromosome unravels.
The key text is in the first paragraph of the boxed, italicized paragraph. "Induced pluripotent stem cells" can be generated from ordinary human tissue. People have been doing that for a while. However, the stem cells produced this way senesce after surprisingly few generations. Biotime researchers have shown that by overexpressing telomerase, they are able to delay this sencescence substantially. This validates the hypothesis that telomere degradation was the cause of the senescence.
This is important basic science, but unlikely to lead to a silver bullet for aging any time soon.
Unfortunately, diigo did not save the item for me, but I recall reading several months ago that telomerase was no longer thought to be a central aspect of anti-aging. So I can't reconcile that with this new item. Anyone?
I'm not a bio geek. The main thing I'd guess is that since this feat is done on single cells in the test-tub, it's not going to have an immediate medical impact.
In terms of the science, this isn't by any stretch of the imagination a reversal of aging in cells. It is what it is, which is generating useful cells with longer telomeres - if you want to define age as the length of telomeres, then sure, let's say you've reversed aging. But that isn't a useful definition.
The question of how telomeres fit into the bigger picture of aging is still very much debated. Their average length in some tissues decreases with age, but that might be a secondary result of other processes such as accumulated mitochondrial DNA damage. Lengthening telomeres with telomerase in conjunction with cancer suppression genetic engineering has increased mouse life span by 50% - but here again there is the possibility that the telomerase isn't extending life by extending telomeres, but by doing something else.
Biology is complicated.