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Wolfram
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Researchers zero in on a cause of aging
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Researchers zero in on a cause of aging
Experiment points to defect in cells
By Alice Dembner, Globe Staff | May 27, 2004
Taking a major step toward identifying one cause of aging, researchers have shortened the life of mice and created signs of old age by injecting a
small genetic defect in the mice's mitochondria, the tiny power plants within each cell.
The experiment in Sweden offers the first hard evidence of a decades-old theory that mutations in the mitochondria are one of the causes of
age-related illnesses. Earlier research had shown that such defects build up in people as they grow old, but scientists were not sure whether that was
a cause or a symptom of aging.
''What we have now is this clear-cut cause-and-effect relationship," said Dr. Nils-Goran Larsson, a genetics professor at the
Karolinska Institute in Stockholm and the senior author of the study. ''It will provide a completely new angle to treat aging-related
problems."
Other researchers, however, said the theory won't be fully proven until experiments extend the life span of mice by eliminating defects in the
mitochondria.
Larsson said the new results could lead to the development of drugs or procedures to ward off the changes to the mitochondria. A number of companies
are already working on other compounds, potentially related to mitochondria, to tackle the diseases of old age.
The study, published in today's issue of the journal Nature, comes as researchers are unlocking many of the mysteries of aging. Scientists have
identified a number of genes that affect aging in animals. They have linked the natural shortening of telomeres, the tail ends of chromosomes, to
shorter life spans. In addition, researchers have added years to the lives of mice by increasing their ability to disarm byproducts of metabolism
called free radicals, which can damage cells.
Since mitochondria also generate free radicals, the latest work may also propel work on the free-radical theory, researchers said.
A separate path of research is focusing on factors that regulate life span, rather than on the causes of aging. Altering the genes that control
insulin receptors can double the life span of worms, researchers have shown.
David Sinclair, a molecular geneticist at Harvard Medical School who works on the regulators of aging, said the Swedish experiment
''suggests -- but doesn't prove -- that mitochondria might really play an integral part in the aging process" and he suggests that
the regulators will prove more important in combating aging than the causes. ''We believe that manipulating the regulators of aging will
have a much larger effect on longevity because these regulators could potentially slow down all the causes of aging, not just one," Sinclair
said.
However, Dr. George M. Martin, a geneticist at the University of Washington in Seattle who wrote an article accompanying the Swedish study, said the
paper makes ''an important contribution because . . . changes in the mitochondrial DNA may be among the more important processes of
aging."
Mitochondria are the structures in each cell of the body that convert fat and sugar into usable energy. If they severely malfunction, humans
eventually die. The theory that damage to the mitochondria caused aging was first proposed in 1972, according to Sinclair. Evidence piled up that
these changes were common in older people and animals, but no one had attempted to prove the connection.
In the Swedish experiment, researchers genetically engineered the mice to have a defect in their mitochondria. They replaced a single amino acid,
which disabled the ability of the mice to find and correct errors in their mitochondrial DNA. As the mitochondria replicated themselves as part of
normal growth and development, errors built up.
Starting at young adulthood (24 weeks), the mice began to show symptoms of premature aging, including weight loss, hair loss, curvature of the spine,
osteoporosis, and enlargement of the heart. They lived an average of 48 weeks, and all had died by the age of 61 weeks. Normal lab mice can live up to
two years. Designing the experiment and carrying it out took a painstaking four years, Larsson said. ''I now know why no one had done it
[before]," he said.
Larsson said next steps would include researching the underlying mechanisms and figuring out how they relate to other possible causes of aging. In
addition, he said, the mice would be used to design ways to counteract the problem using drugs, diet, or genetic alterations.
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How could it be that you only get the mitochondria from your mother? Why aren´t the mitochodria already old when you get them and get older??
Which are the wonderfull mechanisms that prevent somatic cells from aging?
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Blind Angel
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for the first question, the answer is evident, the cell that you are made from are the one of your mother, actually the ovary of your mother, the
spermatozoide only give up is genetic code. For the second i don't know, i'm thinking on it.
/}/_//|//) /-\\/|//¬/=/_
My PGP Key Fingerprint: D4EA A609 55E4 7ADD 8529 359D D6E2 33F6 4C76 78ED |
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Geomancer
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The germ line cells use thier telomere-whatever-ase to enable infinite division. Individual germ line cells would age, but aging cells would kill
themselves, allowing undamaged ones to replace them. Additionally, germ line cells are likely to have much more active repair mechanisms, and so age
more slowly.
Edit: Note that this is just stuff I made up. The real world may be different.
[Edited on 28-5-2004 by Geomancer]
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Wolfram
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How about...
How about to engener this repair mechanisms to be activated in all cells? And make damaged cells in all the organism to kill themselves?
But i guess the above is highly speculative since not much is known about how this mechanism work.
I have heard of some researchers that are aiming to create a mouse with some kind of genetic trigger built in so that aged cells can be whiped out
from the whole mouse by giving the mouse some chemical. Now thats mad science 
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Wolfram
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Look at this we have come to a point were serious scientist are aiming for actually find a Cure for Aging!!!!
Just the thing that there are sane people that have a such goal, and think it could be realisable is for me amazing and inceadible. I can not really
belive it..
And one day it will happen...ofcourse..
http://www.gen.cam.ac.uk/sens/
Here is some information about the mouse project which I was talking about and much more:
http://www.gen.cam.ac.uk/sens/IBGcase.htm#media
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unionised
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What, exactly, is "The deleterius effect of TIME passing by."?
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JohnWW
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The process of cell division results in the telomeres, the protective ends on strands of DNA, becoming progressively shorter. This is hastened by such
things as stress and free radicals, so I understand. It eventually results in cells becoming unable to reproduce by division, with tissue loss
following when the cells die without being replaced, after an average of roughly 50 divisions, much sooner than if bonding between DNA strands
resulting from reactions with free radicals was the only source of inhibition of DNA replication. The only exceptions are those cells in which the
telomeres are constantly repaired by the enzyme telomerase, but in nature the only cells in which telomerase is produced are reproductive cells such
as eggs and sperm, and cancer cells which can reproduce indefinitely. Research is being done into ways of "switching on" telomerase production in
ordinary cells. One firm that is doing such research is Geron Inc. of Menlo Park, California; see http://www.geron.com .
[Edited on 2-3-2007 by JohnWW]
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.torNO
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Growth Hormon protect cells from aging. Surely it's more elaborate,but that is a main factor.
[Edited on 2-3-2007 by .torNO]
U belin : the splendent. the shiny one.
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franklyn
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Cancer is the only known immortal mamalian living organism. It can in some
cases have hundreds of chromosomes not just the usual 46. Strains of it used
investigationally came from donors which have died half a century ago. In the
plant kingdom living Bristle pines and Sequoias 5000 years old are known. There
is even a Mesquite bush in the California desert that first took root an estimated
11000 years ago. Telomeres will determine the Hayflick limit which ultimately
figures when you're ripe for decrepitude. The deleterious effect of TIME passing
by could be interpreted as being late to meet your date  or just plain old
entropy.
As a chum of mine was fond of saying " sometimes you're the windshield, and
sometimes you're the bug ". To an actuary being runned over by a truck figures
into longevity.
U P D A T E
Clive of India's tortoise dies of liver failure, aged 255 March 22, 2006
http://www.timesonline.co.uk/tol/news/world/asia/article7445...
http://en.wikipedia.org/wiki/List_of_long-living_organisms
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solo
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Hayflick limit
Perhaps assisting the telomers to increase the Hayflick number by consuming Carnosine( beta-alanyl-L-histidine) is a dipeptide of the amino acids
beta-alanine and histidine. It is highly concentrated in muscle and brain tissues.)
The Hayflick limit[Note 1] (or Hayflick phenomenon) is the number of times a normal human cell population will divide until cell division stops.
Empirical evidence shows that the telomeres associated with each cell's DNA will get slightly shorter with each new cell division until they shorten
to a critical length.[1][2]
The Hayflick limit was discovered by Leonard Hayflick in 1961,[1] at the Wistar Institute in Philadelphia. Hayflick demonstrated that a population of
normal human fetal cells in a cell culture will divide between 40 and 60 times. The population will then enter a senescence phase, which refutes the
contention by Nobel laureate Alexis Carrel that normal cells are immortal. Each mitosis slightly shortens each of the telomeres on the DNA of the
cells. Telomere shortening in humans eventually makes cell division impossible, and this aging of the cell population appears to correlate with the
overall physical aging of the human body. Natural maintenance of the length of the telomeric region appears to prevent genomic instability and helps
to curb the development of cell mutations that may lead to cancer.
.......source,
http://en.wikipedia.org/wiki/Hayflick_limit
Carnosine can increase the Hayflick limit in human fibroblasts,[24] as well as appearing to reduce the telomere shortening rate.[25] This could
potentially favor the growth of certain cancers that thrive due to telomere preservation.[14] Carnosine is also considered as a geroprotector.
......source,
http://en.wikipedia.org/wiki/Carnosine
It's better to die on your feet, than live on your knees....Emiliano Zapata.
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Formatik
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There are other materials that lengthen telomeres like: astragalus, omega 3-polyunsaturated fatty acids. Aminoguanidine (of limited value). And
antioxidants lengthen telomeres since they reduce oxidative stress which accelerates telomere shortening by generating DNA single-strand breaks.
Exercise lengthens telomeres, and higher body fat (and abdominal fat) is associated with shorter telomeres.
Psychological stress (perceived stress and chronic stress) have been found to be associated with higher oxidative stress, lower telomerase activity
and shorter telomere length. Activities that reduce cognitive stress (e.g. meditation) are useful here.
To slow and milden effects of aging, it requires a multifaceted approach. Ingesting one single substance will not do much.
Things we can augment as individuals to slow aging down (and hinder aging-related pathologies) include mainly modification of glycation reactions,
telomere length, DNA damage, muscle wasting, etc.
The modulation being done through selective and healthy dietary modification, exercise, and stress reduction.
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gregxy
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Selegiline has been shown to extend the lives of rats and dogs by up to 30%. It is a MAOI which increases dopamine when taken at low doses. It is not
known how it extends life, but one theory is it reduces damage from free radicals produced by MAO.
I take 1-2 mg/day, it improves my mood and appreciation of music. It's mainly for those over 40.
http://www.selegiline.com/
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franklyn
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This man has lived in 3 centuries
http://gma.yahoo.com/blogs/abc-blogs/last-living-man-born-19...
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Polesch
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The idea that shortening of the telomeres might be a cause of aging has just been a hype, there's still no research to show think link. And animals
given telomerase show no signs of slower aging.
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franklyn
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He's lived in 3 centuries and is not bedridden.
<object type='application/x-shockwave-flash' data='http://www.reuters.com/resources_v2/flash/video_embed.swf?videoId=253072630&edition=BETAUS'
id='rcomVideo_253072630' width='460' height='259'> <param name='movie'
value='http://www.reuters.com/resources_v2/flash/video_embed.swf?videoId=253072630&edition=BETAUS'></param> <param
name='allowFullScreen' value='true'></param> <param name='allowScriptAccess' value='always'></param> <param name='wmode'
value='transparent'></param> <embed src='http://www.reuters.com/resources_v2/flash/video_embed.swf?videoId=253072630&edition=BETAUS'
type='application/x-shockwave-flash' allowfullscreen='true' allowScriptAccess='always' width='460' height='259' wmode='transparent'></embed>
</object>
Techniques to Disrupt, Deviate and Seize Control of
an Internet Forum In case you wonder W T F ! is going on here
?
www.zerohedge.com/contributed/2012-10-28/cointelpro-techniques-dilution-misdirection-and-control-internet-forum https://web.archive.org/web/20120814124000/www.washingtonsblog.com/2012/08/the-15-rules-of-internet-disinformation.html
___________________________________________________________________________________________________________________
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___________________________________________________________________________________________________________________
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franklyn
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http://www.telegraph.co.uk/science/science-news/10447117/Wor...
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bfesser
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Interesting, but wrong. Here's just one example of older living creatures:
<a href="http://en.wikipedia.org/wiki/List_of_oldest_trees" target="_blank">List of oldest trees</a> <img src="../scipics/_wiki.png"
/>
Some really old people:
<a href="http://en.wikipedia.org/wiki/Oldest_people" target="_blank">Oldest people</a> <img src="../scipics/_wiki.png" />
Photography of extremely old organisms:
<a href="http://rachelsussman.com/portfolios/OLTW/main.html" target="_blank">The Oldest Living Things in the World.</a> <img
src="../scipics/_ext.png" />
80,000 years—no, that's not a typo; 8×10<sup>4</sup> <em>annus</em>—clones:
<a href="http://en.wikipedia.org/wiki/Pando_(tree)" target="_blank">Pando</a> <img src="../scipics/_wiki.png" />
This blew my mind:
<a href="http://en.wikipedia.org/wiki/Endolith" target="_blank">Endolith</a> <img src="../scipics/_wiki.png" />
[Edited on 15.11.13 by bfesser]
Interesting:
<em><a href="https://en.wikipedia.org/wiki/Hydra_(genus)#Non-senescence" target="_blank">Hydra</a></em> <img
src="../scipics/_wiki.png" />
<em><a href="https://en.wikipedia.org/wiki/Turritopsis_dohrnii#Biological_immortality" target="_blank">Turritopsis
dohrnii</a></em> <img src="../scipics/_wiki.png" />
Attachment: hydra_senescence_paper.pdf (169kB)
This file has been downloaded 947 times
[Edited on 7.1.14 by bfesser]
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chemrox
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@Solo
So does the literature suggest ingesting carnosine will slow aging or have the experiments gotten that far? I wonder if the lab monkeys are taking
carnosine?
"When you let the dumbasses vote you end up with populism followed by autocracy and getting back is a bitch." Plato (sort of)
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Organikum
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Quote: Originally posted by gregxy  | Selegiline has been shown to extend the lives of rats and dogs by up to 30%. It is a MAOI which increases dopamine when taken at low doses. It is not
known how it extends life, but one theory is it reduces damage from free radicals produced by MAO.
I take 1-2 mg/day, it improves my mood and appreciation of music. It's mainly for those over 40.
http://www.selegiline.com/ |
Very high daily doses of GHB/GBL prolong rats life also by 20% or more. I would not recommend such a regime to humans nevertheless.
The wish to live forever is something what I see as strange at least, IMHO most people wo want this so very much are the last I want to see even
longer hanging around.
The goal is not to live longer just for being not dead, but to live say 70 or max. 80 years in good health and then drop dead all of a sudden. Thats
perfect and worth to wish for. The hordes of demented wrecks are the very last this world needs and thats what modern medicine actually gave us. Thank
you very much. Thats cruel and inhuman and I seriously hope somebody kills me before I turn into a salivating vegetable. If I should not be able to do
this myself.
/ORG
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franklyn
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http://www.gizmag.com/aging-reveresed-mitochondria/30209/
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Chemosynthetic
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Mitochondrial biogenesis is real big where I work. I have extremely mixed feelings on the subject.
A lot of cancer pathways alter metabolism, cell cycle checkpoint receptors, and telomerase expression, by the way. I know researchers who claim in
casual conversation that they induced model organism cancer with TERT vectors. I never asked much about it as it seems in line with one of the
prevalent oncogenesis pathways I research.
http://www.nature.com/nature/journal/v469/n7328/full/nature0...
http://m.jco.ascopubs.org/content/18/13/2626.long
I could cite a lot more, but don't want to clutter the thread with niche oncogenics.
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AJKOER
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| Quote: Originally posted by Formatik | There are other materials that lengthen telomeres like: astragalus, omega 3-polyunsaturated fatty acids. Aminoguanidine (of limited value). And
antioxidants lengthen telomeres since they reduce oxidative stress which accelerates telomere shortening by generating DNA single-strand breaks.
Exercise lengthens telomeres, and higher body fat (and abdominal fat) is associated with shorter telomeres.
Psychological stress (perceived stress and chronic stress) have been found to be associated with higher oxidative stress, lower telomerase activity
and shorter telomere length. Activities that reduce cognitive stress (e.g. meditation) are useful here.
To slow and milden effects of aging, it requires a multifaceted approach. Ingesting one single substance will not do much.
Things we can augment as individuals to slow aging down (and hinder aging-related pathologies) include mainly modification of glycation reactions,
telomere length, DNA damage, muscle wasting, etc.
The modulation being done through selective and healthy dietary modification, exercise, and stress reduction. |
Researchers outside of the pharma complex have promoted the anti-aging ability of Vitamin C (a free radical scavenger), reference Gary Null, for over
forty years. So the research out of Sweden is not news, it is more of an affirmation of prior research that is now deemed fit for consumption.
For the longest time there has been major impediments, correct me if I am wrong, as there is no money in staying young or promoting health for the big
pharmaceutical companies (no billions in blood pressure, anti-cholesterol, weight loss,..., medicines) via non-patentable natural substances or
healthy living and eating.
Doctors in the USA have been locked into only being able to write prescriptions, for whatever has been legally declared a disease, and not, for the
most part, in promoting healthy eating, life styles or other preventative healthcare. Their primary job, often with bonuses, appears IMHO, to be
acting as field marketing agents for big pharma.
Sad, but with more universal healthcare, there may be changes coming and not just for healthcare with an increase focus on anti-aging and preventative
care, but for the bad food business as well, another big payer.
[Edited] By the way, the big fus in Washington over a viable universal healthcare law, is in my opinion, that most likely with time, to reduce cost,
the government could become more active in removing bad food products that are suspected to cause illness, environmental toxins and even look to
promoting cures over maintenance drugs. This could cost multiple billions to some of the most powerful special interest groups.
[Edited on 16-8-2014 by AJKOER]
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gregxy
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This company in the UK
http://www.antiaging-systems.com/
Sells 100s of anti-aging drugs. Some are schedule 4 in the USA.
Most of course don't work but it is a valuable resource if you want to experiment with this stuff.
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aga
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A simple observation is that we generally no longer live according to our design parameters.
No other Ape eats processed or concentrated foodstuffs, and tends to Graze while moving around a lot.
It is Incredible that we live as long as we do.
Unlikely that we evolved to be McApes and exist as we do.
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stoichiometric_steve
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| Quote: Originally posted by aga | | A simple observation is that we generally no longer live according to our design parameters. |
if organisms lived according to their "design parameters", there would be no evolution, and you wouldn't even be able to write down such whimsy since
you'd still be a microbe.
we're not designed for anything beyond successful reproduction.
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