- IT has been a never-ending quest since
the dawn of humanity to stop the clock, to find the so-called fountain
of youth. What's different today is that the riddle of why we age has become
the focus of intensive scientific research across the globe.
-
- The research has even attained a strong
air of respectability, with some geneticists predicting an average life
span of 140 years by the mid-21st century, through the development of new
longevity drugs.
-
- Biotechnology is indeed the flavour of
the year. In the US, a ballooning number of commercial organisations are
dedicated to unearthing the mysteries of ageing.
-
- The Geron Corporation with 89 employees
is one of the more established pioneers in the area, attempting to introduce
potentially lucrative rehabilitative and diagnostic products for treating
cancer and other age-related diseases.
-
- The company has taken its research into
the microscopic world of the single cell. Theoretically, the scientists
believe, working on the parts that make up the whole could help the whole
to survive longer.
-
- Geron concentrates its cell investigation
on telomeres, tiny non-coding cuffs on the ends of chromosomes that act
like the plastic ends of shoelaces. Geron is building on research published
by anatomist Leonard Hayflick, who in the early 1960s discovered that telomeres
grow shorter as cells replicate until, after 100 or so cell divisions,
the cells themselves grow old. If we can get to the bottom of what causes
telomeres to shorten, then the secrets of ageing will reveal themselves
or so the theory goes. Ageing appears to be nature's way of bringing a
halt to cell mutation telomeres appear to act as a protector of reliable
genetic information. Aged cells do not die immediately; they are simply
no longer capable of reproducing daughter cells with replicated DNA. In
one of those quirks of nature, some cells such as sperm and cancer cells
don't suffer telomere shortening, and divide thousands, not hundreds,
of times.
-
- In 1984, Elizabeth Blackburn (an Australian)
and Carol Greider from the University of California used a single-cell
organism to find why telomeres shorten in some cells and not in others,
and detected an enzyme called telomerase responsible for sustaining telomere
length.
-
- Telomerase may be an exciting enzyme
for cancer researchers. To be able to switch telomerase output off in cancer
cells would halt mutated cells in their tracks. In April this year, Geron
announced that telomerase-deficient mice suffer a decline in tissue and
organ function when, after a certain number of cell divisions, telomeres
become critically short. Conversely, the presence of telomerase in reproductive
and cancer cells, for example, imparts a kind of immortality by rewinding
the telomere clock.
-
- This may bode well for those interested
in inhibiting telomerase as part of cancer treatment. Sydney's Garvan Research
Institute executive director John Shine paints a more realistic picture:
not all cancer cells produce telomerase. Cancerous cells proliferate because
of a spectrum of mechanisms and genes, he insists.
-
- Even if scientists could isolate the
parcel of DNA responsible for ageing, every cell in the human body would
have to be modified. The only way to circumvent this is to change genetic
information in an embryo. When the sperm has fertilised an ovum and before
any cell division has taken place at this miraculous point in nature
the DNA of the human could be changed to eradicate the ageing code. This
genetic manipulation would alter not just the cells of the foetus in question,
but every generation of offspring thereafter.
-
- Genetic changes of this kind which would
effectively mutate the human race create a minefield of ethical issues.
Perhaps that's why in Australia, research into ageing has concentrated
on improving the quality of life for the elderly. Hormone replacement therapy
in both men and women can slow down some of the symptoms of ageing despite
accompanying risk factors while synthetically produced human growth hormone,
available as a prescribed drug for children affected by dwarfism, can also
improve lean muscle mass and bone density in the elderly.
-
- However, research in the US has shown
that synthetic hormone treatments can set off serious side effects such
as diabetes and heart disease.
-
- Meanwhile, as the hunt for a "longevity
drug" heats up, two new theories on the genetic foundations of ageing
are being advanced:
-
- Gumming Up This theory holds that cell
ageing is triggered by sugar or food molecules gumming up the body's works
by forming complexes with proteins and other vital molecules. This backs
up another rather controversial theory: that eating less helps you to age
more slowly. George Roth from the National Institute on Ageing in Maryland
in the US found that mice reared on a draconian diet live 30 to 40 per
cent longer than other mice. The study's message: eat less, live longer.
As the average Western diet makes this a rather impractical aim, scientists
are working on a drug that tricks cells into thinking they are receiving
less food. Roth believes that with this sort of advance people could live
up to 120 years.
-
- Free radicals The by-products of cells
metabolising energy, free radicals, are thought to play a part in the ageing
process. The cells, unbalanced by one extra electron, run around the system
trying to redress their imbalance by bonding with other cells, causing
damage as they go. In one study, vitamin E was found to soak up free radicals
and expel them from the body's system.
|
Sightings HomePage