LONGECITY

So if ultra-short telomeres are associated with arthritic tissue, then could telomerase help to cure arthritis?

http://www.eurekaler...c-ust011312.php

So if ultra-short telomeres are associated with arthritic tissue, then could telomerase help to cure arthritis?

Good question. Something made the telomeres get short, so even if you lengthened the telomeres and rescued the senescent cells, there would still be a problem. However, it sounds like telomere extension could be a way to dial back the disease. It might form part of a multi-pronged approach to treatment.

I am thinking that it is a problem with inflammatory signals - at least in part. So lengthening telomeres might not help all that much. If telomere shortening is not the source of the problem, but just a symptom (of cells being in a chronic inflammatory environment around the joint), then increasing telomerase might not help as much as you would otherwise expect.

Another telomere length correlation, adding data to a relationship known for some years: "A process linked to natural cell aging has now also been associated with knee osteoarthritis, researchers say. Telomeres - lengths of DNA on the ends of chromosomes, sometimes described as being like the plastic cap on a shoelace tip - naturally shorten with age, but can also shorten due to sudden cell damage. Abnormally short telomeres have been found in some types of cancer and preliminary research has suggested that the average telomere length is also shortened in osteoarthritis. In this new study, Danish researchers used new technology to closely examine the telomeres of cells taken from the knees of osteoarthritis patients who had joint replacement surgery. The cells had abnormally shorted telomeres and the percentage of cells with ultra-short telomeres increased with proximity to the damaged area in the knee joint ... The telomere story shows us that there are, in theory, two processes going on in osteoarthritis. Age-related shortening of telomeres, which leads to the inability of cells to continue dividing and so to cell senescence [deterioration], and ultra-short telomeres, probably caused by compression stress during use, which lead to senescence and failure of the joint to repair itself. We believe the second situation to be the most important in osteoarthritis. The damaged cartilage could add to the mechanical stress within the joint and so cause a feedback cycle driving the progression of the disease."
Link: http://health.usnews...d-to-cell-aging

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Good question. Something made the telomeres get short, so even if you lengthened the telomeres and rescued the senescent cells, there would still be a problem. However, it sounds like telomere extension could be a way to dial back the disease. It might form part of a multi-pronged approach to treatment.

+1 what niner said.

The way I choose to see it, a disease is like a row of dominoes falling. One can't pick up just one of the pieces and expect it to return to the way it was before.

AFAIK osteoarthritis involves overproliferation of bone tissue, which is consistent with telomere shortening as the cells approach their Hayflick limit at which point further cell division halts. If one were to reset the telomeres, one might just be encouraging further proliferation and make things worse.