Hey y'all.

Paterson the mad parkie poster is back. I haven't found many news
articles recently that 'reached out' to me, but suddenly, there were
several in the Health and Science section of the Nando Times last
night.

Number One:

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Scientists hope newly found gene will provide clues to aging process
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Copyright © 1996 Nando.net Copyright © 1996 Seattle Post-Intelligencer

SEATTLE (Apr 11, 1996 11:41 p.m. EDT) -- Seattle scientists have
discovered an "aging gene," a finding they hope will lead to better
understanding of the aging process and age-related diseases, such as
coronary artery disease, diabetes, osteoporosis and cancer.

The identification of a gene that causes the rare disorder known as
Werner's syndrome, in which people suffer from what appears to be a
rapidly accelerated aging process, is the first gene ever found to be
associated with aging.

"This is an important step for scientists to begin to figure out how
people age and how aging leads to aging-related disease," said Dr.
Gerard Schellenberg, principal author of the report announcing the
finding in Friday's edition of the journal Science.

Schellenberg, a geriatric specialist at the Veterans Affairs Puget
Sound Health Care System in Seattle and a research professor of
medicine at the University of Washington, said the search for clues to
aging using Werner's syndrome was launched years ago by scientists
like the UW's Dr. George Martin.

"George has been working on the biology of Werner's for almost 30
years," Schellenberg said.

Werner's syndrome, identified in 1904 by a medical student named Otto
Werner, is a rare disorder first recognized because of physical
symptoms in young adults typically associated with the elderly --
wrinkled skin, loss or graying hair and a much higher risk of
age-related diseases like osteoporosis, cataracts, cancer and
diabetes.

In 1966, Martin was part of a group of researchers led by Dr. Charles
Epstein (the Nobel Prize-winning California geneticist injured in 1993
by the Unabomber) that described key features of tissue cells in
patients with Werner's and confirmed the cause as a genetic disorder.

Martin, a co-author of Friday's Science article, said they took skin
biopsies from patients who had the disorder and tested the tissue
cells to see how many times they could divide and replicate.

They found young people with Werner's syndrome had cells that were
able to replicate much less, similar to what is typically found in the
cells of elderly people. The patients' family histories were studied
and the researchers were able to show that this disorder was
genetically linked.

"It's not the gene for aging," Martin emphasized Thursday. What it is,
he said, is a gene that causes a disorder which may or may not provide
us with better understanding of the typical aging process and
age-related diseases.

Dr. David Galas, a molecular biologist and chief scientist for the
Bothell-based biotechnology firm Darwin Molecular Corp., agreed. But
Galas said it seems likely the genetic changes in Werner's syndrome
will provide insights into the degenerative genetic changes in aging.

"The fact that DNA metabolism is implicated in this kind of syndrome
strongly suggests that normal aging involves at least some of the
consequences of mishandling DNA information," he said.

DNA, deoxyribonucleic acid, is the molecule in the cells of nearly all
living creatures that contains an organism's genetic code --
"blueprints of life." Finding a gene requires sequencing, or
"reading," the code by identifying the basic units, called base pairs,
in a section of the DNA.

Scientists at Darwin worked with Schellenberg, who also collaborated
with researchers from Japan and from Yale University, and used
computerized DNA sequencing technology to track down and clone the
one (called WRN) for Werner's syndrome. Darwin has applied for a
patent on the discovery.

"We are now working to identify the best initial medical targets
related to the Werner's gene," Galas said.

The gene produces an enzyme (called a helicase) that unwinds the twin
strands of the DNA double helix when repairing or replicating genetic
material in cells. How this leads to the accelerated aging process in
Werner's syndrome remains unclear, the scientists said.

"But now we have the gene so we're closer to understanding," said
Schellenberg, adding that he's convinced this will also provide
insights into the normal aging process.

The UW's George Martin, however, said he'll remain skeptical for now
as whether what's learned about this gene can be applied to the
routine aging process.

"There are things you see in Werner's syndrome you don't see in
'normal' aging," Martin said. For example, he said, autopsied patients
with Werner's show no degenerative changes in their brain or central
nervous system.

Galas and Schellenberg acknowledged the possibility that the
appearance of symptoms that look like accelerated aging in people
Werner's syndrome could mask a fundamentally different biochemical
process that occurs in normal aging.

"We may find that this gene is just part of a complex pathway, and it
may not be directly related to longevity in most people," Galas said.
But it's also equally possible, he said, that the gene will point to
common genetic changes that take place in many of the degenerative
changes we now attribute to aging.

Should that be the case, Schellenberg and Galas said, the next step
will be to exploit this genetic knowledge to develop new therapies
aimed at preventing or at least reducing the risk of the diseases and
ailments we now accept as inevitable consequences of getting old.
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janet
the parkie in paradise
where the oleander hedges are bursting into pink.

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