>Telomerase seems to be the hot topic around here. It would certainly be an
>easy solution to the aging problem, if only it were that simple. I think
Personally, I think aging is a LOT more than just a problem. I think
it is an awful, dreadful, and horrible disease that needs to be cured
as quickly as possible.
>the evidence supporting the role of telomere shortening leading to in vitro
>senescence is overwhelming and people take this as a given now. Most
I agree. Telomere shortening has indeed been proven beyond a
reasonable doubt to be the sole cause of the *VAST* majority of
in-vitro cellular aging.
>academic researchers (see Martin J. of Gerontology: Biological sciences,
>vol 48, No 5, B171-172) however, that is researchers who do not depend on
>gulible investors for funding, do not share the believe that in vitro
>senescence, hence telomere shortening, has anything to do with organismal
>aging.
So you think someone that believes that telomere shortening could
indeed be one cause (of probably several) of the human in-vivo aging
process is a gulible person?
>I reviewed the evidence 2 years ago, and I did not find any compeling
>argument supporting the statement that in vitro senescence has any
>relationship to in vivo aging.
>Perhaps data has come out to support this point within the last 2 years. In
>this case, will anybody please enligthen me!
First of all, thank you very much for your post. I appreciate it.
Personally, I think we can be very certain that telomere shortening
DOES INDEED cause some ammount of in-vivo human aging during a
person's normal lifespan (lets just say someone under the age of 100).
Telomere shortening may only cause 1% of the human aging process or
for all we know perhaps 50% or more, but like I have previously
stated, we can be sure it is at least ONE CAUSE of at least SOME
ammount of the human aging process, here is why:
1) As all normal human cells divide they *age*. This is cellular
aging. Telomere shortening is the cause of this aging. Everytime a
cell divides, it has less replicative potential, and does not function
quite as well as it did previously. Telomere shortening causes this
lack of funcionality by various mechanisms.
2) It has been PROVEN that in-vivo human cells do indeed divide.
3) Since these human cells are dividing, they are gradually growing
older and older, becoming less functional, and their telomeres are
shortening.
4) It has been proven that during the *normal* human lifespan more
than a tiny ammount of cellular aging does indeed occur in-vivo.
So you see, it is really simple:
Our cells are dividing from the day we are born (and before). They are
gradually growing older. So in my opinion it is VERY clear that at
least to SOME degree, whether it is a large or small degree, cellular
aging does indeed effect us and cause in-vivo aging.
What we need to do now is try and determine both in animals and humans
how MUCH of the aging process is caused by cellular aging which is
caused by telomere shortening. For all we know, it is possible that
telomere shortening does not even effect us significantly until we are
VERY old (perhaps over 100 years of age). But eventually, if not
reversed, it would kill us. So I think finding ways to reverse
cellular aging and telomere shortening are VERY important.
You see, quite frankly, I want to live FOREVER in a human form. For
that to be possible, telomere enlongation therapies MUST be perfected,
among probably MANY other therapies to reverse OTHER causes of the
aging process such as perhaps AGE/Crosslink accumilation.
Hey, wait a moment... ALT-711 might already be a drug to help reverse
AGE/Crosslink accumilation. :-)
Best Regards,
William
