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Posted on 05/16/2003 11:17:48 PM PDT by Ernest_at_the_Beach
It's not the Fountain of Youth, but it is intriguing: a class of molecules that researchers have discovered prolongs life and prevents a debilitating age-related illness.
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These findings, announced by a team of University of California-San Francisco scientists in today's issue of the journal Science, are thus far confined to a lowly worm found in compost heaps everywhere.
But because worms, humans and all other creatures share the identical class of molecules -- called "small heat shock proteins" -- the implications of this work are far-reaching, applying to devastating diseases of the aging human population, such as Alzheimer's and Parkinson's.
"We think we've found an important physiological explanation for aging and age-related disease," said lead investigator Cynthia Kenyon, a professor of biochemistry at UCSF. "The hypothesis is that they may be involved in keeping the proteins of cells in good working order."
The discovery builds on a decade of work by a growing number of scientists, providing a better understanding of the fundamental mechanisms that regulate the march toward decrepitude. The pharmaceutical industry is already exploring ways to make use of the research, looking for ways to increase the activity of the heat shock proteins to prevent disease and slow aging. Any such medicine is years away from reaching patients.
The newly discovered class of molecules plays a crucial caretaking role in cells: maintaining the shape of cellular proteins, on which all life forms are built.
When proteins are damaged and misshapen, they clump together -- causing, it is thought, diseases such as Alzheimer's and Huntington's. This class of molecules comes to the rescue, binding to the damaged proteins so they are unable to clump together and cause disease, Kenyon said.
Other researchers have found that when these molecules fall down on the job -- perhaps because of environmental stressors such as extreme heat, toxins or yet-unknown factors -- it appears aging accelerates and illness sets in.
Commenting on Kenyon's research, Gordon J. Lithgow of the Buck Institute for Age Research in Novato said, "It's very well to have general ideas about aging, but this offers concrete examples linking longevity to disease."
Kenyon found that cells of long-lived worms had an abundance of this special class of molecules.
To be sure, old age is a different experience for a worm than a human. The creature, a millimeter-long translucent nematode called Caenorhabditis elegans, matures in a few days -- and perishes in two weeks.
But the nematode's simple biology makes it possible for scientists to probe the animal in the finest possible detail, molecule by molecule, gene by gene. Because so much of life's most fundamental systems have remained unchanged over millions of years of evolution, the worm can help shed light on humans.
Scores of scientists in the United States and abroad are turning to the worm to address the problems of aging.
Ten years ago, Kenyon created a stir by creating a genetically mutated worm that lives twice the normal life span.
These long-lived worms were found to accumulate disabling proteins later in life than normal worms. Predictably, they have not just increased lifespan but delayed onset of age-related disease.
What contributes to their longevity?
The worm genes make proteins similar to those in humans. These hormones speed up aging in normal animals. But in genetically altered animals, the hormones are damaged, so animals live longer.
Kenyon figured out the presence of these heat shock proteins was needed for these worms to live longer. Then, Lithgow's lab showed that increasing levels of these proteins could extend lifespan in normal worms, as opposed to those that had been genetically altered. Kenyon took the next step, showing that these proteins could delay the onset of disease.
Thus these proteins link aging to age-related disease, she said.
And the worms with higher protein levels are probably enjoying these extra days.
"Aging is slowed down," said Kenyon. "When the normal worms are in the nursing home, really, these guys are out on the golf course or backpacking in the woods. . . . They're vigorous and active."
Oh no, my brother-in-law will be around forever.
Does that mean he'll eventually read your post on this thread?
You probably won't have to worry about him being around forever unless he is very wealthy or unless he is a worm.
Roy: Why not?
Tyrell: Because by the second day of incubation, any cells that have undergone reversion mutations give rise to revertant colonies like rats leaving a sinking ship. Then the ship sinks.
Roy: What about EMS recombination?
Tyrell: We've already tried it. Ethyl methane sulfanate as an alkalating agent and potent mutagen. It created a virus so lethal the subject was dead before he left the table.
Roy: Then a repressive protein that blocks the operating cells...
Tyrell: Wouldn't obstruct replication, but it does give rise to an error in replication so that the newly formed DNA strand carries the mutation and you've got a virus again. But, uh, this-- all of this is academic. You were made as well as we could make you.
Roy: But not to last.
Tyrell: The light that burns twice as bright burns half as long. And you have burned so very very brightly, Roy.
...
Roy: I've seen things you people wouldn't believe. Attack ships on fire off the shoulder of Orion. I watched C-beams glitter in the darkness at Tan Hauser Gate. All those moments will be lost in time like tears in rain.
Time to die...
Probably not, since most organisms (as opposed to cell cultures) don't die because of the Hayflick limit. If humans were killed by the Hayflick limit, their lifespans would be at least 150 years (according to the latest estimates.)
But in any case, the Hayflick limit is not an absolute constraint: cells can be made to divide forever, blasting the Hayflick limit out of the water.
Depends on whether any of your worms have been given life extension treatments---and whether or not you want the worms you've got to live longer than normal :-)
Keep in step!
"That seems to be a good general framework for thinking about cellular senescence in cells grown in the laboratory," agrees Cech. But he predicts that the mechanisms that dictate cellular life span will inevitably turn out to be more complex. For example, he notes that other researchers have found that other cells with an added catalytic subunit gene will not divide beyond their normal limit unless they are also lacking p53, a well-known tumor suppressor gene that is mutated in many human cancers.
Wasteful.
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