In article <Exrt8x.813 at world.std.com>, sphinx at world.std.com says...
You have received some excellent replies to the first part of your question,
particularly from Aubrey de Grey.
You have also picked up on a very exciting line of research into the
"telomeric theory of aging", but the popular press has not given you a
completely accurate picture of the research and its' potential.
>Another theory that seems to have some currency these days (it made the
>pages of The Economist's "Science and Technology" section, for example)
>is that aging is caused largely by damage to the "telomeres", which are
>end-segments of the DNA molecule which fail to get reproduced at the
>outer ends each time the DNA splits.
The telomeres do get shorter during mitotic division of reproducing somatic
cells but this is not "damage" but rather a normal result of the chromosomes
being unable to reproduce a small portion of the telomeres during each
reproduction.
> After many cell divisions,
>the telomeres are used up and what fails to reproduce correctly is "live"
>nucleotides at the ends of the DNA molecule, i.e. the information-bearing
>portion of the DNA starts to be modified. This process continues as
>further cell divisions occur, and pretty soon the DNA becomes so corrupted
>that subsequent cells in the line can't function properly or even remain
>alive.
When cells have reached what is called their "Hayflick Limit", their
telomeres are so short that mitosis cannot be initiated and the cells enter a
stage called senescence. The cells can remain in this stage for quite a long
time until cellular damage or programmed apotosis cause the cell to enter a
crisis stage. At this point the telomeres on numerous chromosome are
completely gone and the chromosome itself falls apart or combines
inappropriately with other chromosomes usually resulting in death of the
cell.(see information on the enzyme telomerase below).
>And there's research on an enzyme called "telomerase" which supposedly
>is able to rebuild the telomeres. I've seen speculation (probably in
>the aforementioned Economist article) that possibly telomerase will
>serve as the "Fountain of Youth" drug that everyone who's not tired of
>living has always wanted. Unfortunately, this particular FOY drug
>wouldn't rejuvenate somebody who was very far along in the aging process,
>but COULD halt further degeneration by saving those cells that had not
>lost any of their information-bearing genetic material.
>>-John Sangster
> Wellesley Hills, MA
The enzyme telomerase is a naturally occurring enzyme that helps to maintain
telomeric length in various cells of the body, most noticeably the germ and
stem cells. In most other cells telomerase is active during embryonic
development but is "shut off" when the cell terminally differentiates.
Telomerase has been shown to be active in the majority of cancers and its'
ability to add or maintain telomeric length on the chromosomes allows cells
to by-pass the senescent and crisis stages mentioned above. It is also the
most likely reason that cancer cells are immortal.
Recent research has shown that adding telomerase to normal reproducing cells
allows those cells to live beyond their expected Hayflick Limit with no loss
of cellular functioning. The implications of this research are exciting and
there is no theoretical reason the process couldn't rejuvenate numerous
bodily systems regardless of age.
Lifeline Laboratories, under the user name Excelife, will be posting a
statement of the "telomeric theory of aging" to several newsgroups over the
next week or so and you can get a good idea of the state of the research and
it's potential from these posts.
Between the telomeric theory of aging for dividing cells, the possible
mitochondria theory of aging for non-dividing cells and the use of various
growth factors for cellular prolification we are well on the way to
understanding and possibly controlling the process of aging.
Thomas Mahoney, Pres.
Lifeline Laboratories, Inc.
http://home.earthlink.net/~excelife/index.html
