Re: News: Is Aging an Accident of Evolution?
- From: Vend <vend82@xxxxxxxxxxx>
- Date: Fri, 1 Aug 2008 09:49:47 -0700 (PDT)
On 1 Ago, 09:21, Vend <ven...@xxxxxxxxxxx> wrote:
On 1 Ago, 00:45, Ron O <rokim...@xxxxxxx> wrote:
On Jul 31, 6:40 am, Vend <ven...@xxxxxxxxxxx> wrote:
On Jul 31, 1:00 pm, Ron O <rokim...@xxxxxxx> wrote:
On Jul 31, 3:17 am, Vend <ven...@xxxxxxxxxxx> wrote:
On 30 Lug, 18:08, Ye Old One <use...@xxxxxxxxx> wrote:
Is Aging an Accident of Evolution? Stanford Scientists Say "Yes"
http://www.dailygalaxy.com/my_weblog/2008/07/is-aging-an-acc.html
"Everyone has assumed we age by rust. But how do you explain animals
that don't age? Some tortoises lay eggs at the age of 100, there are
whales that live to be 200 and clams that make it past 400 years."
Stuart Kim, PhD, Stanford University professor of developmental
biology and genetics
Prevailing theory of aging challenged by Stanford University Medical
School researchers. Their discovery contradicts the prevailing theory
that aging is a buildup of tissue damage similar to rust. The Stanford
findings suggest specific genetic instructions drive the process. If
they are right, science might one day find ways of switching the
signals off and halting or even reversing aging.
“We were really surprised,” said Stuart Kim, who is the senior author
of the research.
Kim’s lab examined the regulation of aging in C. elegans, a
millimeter-long nematode worm whose simple body and small number of
genes make it a useful tool for biologists. The worms age rapidly:
their maximum life span is about two weeks.
Comparing young worms to old worms, Kim’s team discovered age-related
shifts in levels of three transcription factors, the molecular
switches that turn genes on and off. These shifts trigger genetic
pathways that transform young worms into social security candidates.
The question of what causes aging has spawned competing schools, with
one side claiming that inborn genetic programs make organisms grow
old. This theory has had trouble gaining traction because it implies
that aging evolved, that natural selection pushed older organisms down
a path of deterioration. However, natural selection works by favoring
genes that help organisms produce lots of offspring. After
reproduction ends, genes are beyond natural selection’s reach, so
scientists argued that aging couldn’t be genetically programmed.
The alternate, competing theory holds that aging is an inevitable
consequence of accumulated wear and tear: toxins, free-radical
molecules, DNA-damaging radiation, disease and stress ravage the body
to the point it can’t rebound. So far, this theory has dominated aging
research.
But the Stanford team’s findings told a different story. “Our data
just didn’t fit the current model of damage accumulation, and so we
had to consider the alternative model of developmental drift,” Kim
said.
The scientists used microarrays—silicon chips that detect changes in
gene expression—to hunt for genes that were turned on differently in
young and old worms. They found hundreds of age-regulated genes
switched on and off by a single transcription factor called elt-3,
which becomes more abundant with age. Two other transcription factors
that regulate elt-3 also changed with age.
To see whether these signal molecules were part of a wear-and-tear
aging mechanism, the researchers exposed worms to stresses thought to
cause aging, such as heat (a known stressor for nematode worms),
free-radical oxidation, radiation and disease. But none of the
stressors affected the genes that make the worms get old.
Are they mistaking correlation for causation?
The fact that some genes are transcribed more frequently with age
doesn't mean that these genes cause aging.
Was the lifespan of the stressed worms reduced?
(I hope they measured it instead of putting all the stressed worms in
the blender to hunt for transcription factors).
So it looked as though worm aging wasn’t a storm of chemical damage.
Instead, Kim said, key regulatory pathways optimized for youth have
drifted off track in older animals. Natural selection can’t fix
problems that arise late in the animals’ life spans, so the genetic
pathways for aging become entrenched by mistake. Kim’s team refers to
this slide as “developmental drift.”
Why would a pathway optimized for the youth become disrupted in older
animals if there is no wear and tear?
“We found a normal developmental program that works in young animals,
but becomes unbalanced as the worm gets older,” he said. “It accounts
for the lion’s share of molecular differences between young and old
worms.”
Kim can’t say for sure whether the same process of drift happens in
humans, but said scientists can begin searching for this new aging
mechanism now that it has been discovered in a model organism. And he
said developmental drift makes a lot of sense as a reason why
creatures get old.
“Everyone has assumed we age by rust,” Kim said. “But then how do you
explain animals that don’t age?”
Some tortoises lay eggs at the age of 100, he points out. There are
whales that live to be 200, and clams that make it past 400. Those
species use the same building blocks for their DNA, proteins and fats
as humans, mice and nematode worms. The chemistry of the wear-and-tear
process, including damage from oxygen free-radicals, should be the
same in all cells, which makes it hard to explain why species have
dramatically different life spans.
I suppose that tortoises and whales have a slower metabolism than
humans, which in turn have a slower metabolism than mice.
It isn't as simple as metabolism. Some birds likely have a higher
metabolism than humans, but they live a lot longer. It is
maintenance. Some organisms place more resources into keeping things
fixed up than others. If our cells and tissues regenerated as well at
85 as they did at two years of age the life span of our brains would
be the limiting factor. It takes energy and resources to do this.
Is it possible to repair the extracellular matrix?
It should be possible, but you might have to replace the cells. They
would have to die, and be replaced. Some tissues like your liver does
this, but your brain tissue doesn't seem to be able to do it.
One of the most visible effect of ageing is the loss of tissue (skin
in particular) elasiticity.
If I uderstand correctly, this is mainly due to damage to collagen and
other extra-cellular proteins, which occours even if skin cells are
continously replaced.
It occurred to me that the longest living organisms are woody plants.
Instead of an extracellular matrix of protein/polysaccharide gels,
plants have cell walls mostly made of cellulose and lignin, highly
stable polymers capable of resisting for hundreds or even thousands of
years after the plant death (that's why we have ancient wooden
artifacts, paper and cloths).
Maybe this chemical stability is the key of the long lifespan of woody
plants.
.
- References:
- Re: News: Is Aging an Accident of Evolution?
- From: Ron O
- Re: News: Is Aging an Accident of Evolution?
- From: Vend
- Re: News: Is Aging an Accident of Evolution?
- Prev by Date: Re: Evolution is not a fact
- Next by Date: Re: News: Flatfish evolution was neither fluke nor turbot-charged.
- Previous by thread: Re: News: Is Aging an Accident of Evolution?
- Next by thread: Re: News: Is Aging an Accident of Evolution?
- Index(es):
Relevant Pages
|
