X-Message-Number: 25397
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 
dividing, so they can keep telomeres from shortening as fast as in the somatic 

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 
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 

development then there would be a lot more variability in age of puberty, etc. 
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"


Rate This Message: http://www.cryonet.org/cgi-bin/rate.cgi?msg=25397