X-Message-Number: 25397 From: Date: Fri, 24 Dec 2004 09:08:19 EST Subject: telomeres don't regulate early stages of aging >Thus the telemere aging hypothesis just like the other aging theories can not explain from a biochemistry point of view why different animal species age at a different rate. That's right. And you won't find any telomere researcher claiming that there is a direct correlation between telomere length and aging rate. (Bowhead telomeres are roughly the same length as human, yet they live twice as long). Remember that stem cells do have a low level of telomerase activity while they are dividing, so they can keep telomeres from shortening as fast as in the somatic cells. Telomeres have nothing to do with aging in rodents or lagomorphs; their telomeres don't shorten but they age even faster than animals with telomere shortening. In longer-lived mammals, telomeres have little to do with the initial phases of aging (unless you believe in Telomere Position Effect as a developmental control system, which I certainly don't; if TPE were used to control development then there would be a lot more variability in age of puberty, etc. Plus, we evolved from rodentlike creatures, who can't use TPE). Telomere shortening in large, long-lived mammals is probably a cancer-control strategy; it makes it harder for one cell to grow without limit. The most important short-term medical use for telomere modification is to develop better drugs that turn telomerase off; this might eliminate 95% of cancers (or at least the remnant cells after conventional treatments). Or it might just force the cancer to switch to ALT (we saw that happen once in our lab... my suspicion is that most cancers aren't smart enough to do it), but IMHO at least it would slow the disease down for years. However, after the other causes of aging in large mammals are dealt with, telomere shortening does add an additional complication. If you want to make a human that lives over 120, you're going to have to solve the telomere shortening problem. It is even possible but not proven that some of the deficiencies of 80-year-olds (thin skin, artery walls, blood cell counts) are due to cell senescence from telomere shortening. Content-Type: text/html; charset="US-ASCII" [ AUTOMATICALLY SKIPPING HTML ENCODING! ] Rate This Message: http://www.cryonet.org/cgi-bin/rate.cgi?msg=25397