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No Single Gene for Ageing

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#1 dangerousideas

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Posted 13 September 2005 - 04:02 AM

I spotted the following news release on www.eurekalert.org, which may be of interest to some here...

No single gene for ageing

According to professor Thomas Kirkwood of the University of Newcastle, there is no single gene for ageing. Throughout time, Humans have used energy to get food, produce offspring and survive danger – not to repair and maintain cells. So the maintenance system in the body slowly breaks down.

This topic was of great interest at the seminar for ageing at the conference "Functional genomics and disease" taking place in Oslo, Norway. Thomas Kirkwood is the director of the internationally recognised Institute of Ageing and Health (IAH).

Developmentally it has been more important for humans to invest energy in reproduction and not in maintenance or repair of the body over time.

But genetic factors do exist. "Approximately 25 percent of how a person ages is inherited from parents," says Kirkwood. "Stress, environment, nutrition, lifestyle and immunity play an additional role. Great variation between individuals can be seen in organisms such as round worms – and in humans."

Studies of ageing also give insight into the causes of cancer, because cancer and ageing have the same background causes, thinks Vilhelm Bohr, professor at the University of Baltimore in the United States.

"Cancer is more frequent with age. We must understand the causes of ageing to be able to understand why we have cancer," points out Bohr during his presentation at the conference.

Kirkwood's paper was presented at the "Functional genomics and disease" conference - Genetics Conference, Oslo, Norway, University of Oslo and European Science Foundation .

Contact: Prof. Kjetil Taskén
The Research Council of Norway

#2 Infernity

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Posted 13 September 2005 - 09:17 AM

Aging is a genetically disease that always overtook with, in all part of evolution so it seems. We started from dead elements, matters with no living mechanism of energy gathering.

We stop aging, we stop many many many other illnesses that aging causes.
The smart thing to do is heal aging and automatically solve other problems rather than solving each separately. And always deal with more and more.

I wish I had a scientific background in genetics so I could be clear and sure, unfortunately I yet do not have.


#3 John Schloendorn

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Posted 13 September 2005 - 10:11 AM

The smart thing to do is heal aging and automatically solve other problems rather than solving each separately

That is the idea Infy, very well said.

#4 olaf.larsson

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Posted 14 September 2005 - 09:31 AM

According to professor Thomas Kirkwood of the University of Newcastle, there is no single gene for ageing.

No Really!!?? I guess you have to be professor to find out that.. LOL

#5 dangerousideas

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Posted 14 September 2005 - 10:54 PM

Yes, most here will not be too shocked by that particular observation!

That said, I think that the idea that the biomechanics inherent in our genetic heritage appears to favor reproduction over maintenance is interesting - even if on reflection it also appears to be rather obvious and perhaps even a matter of common sense. A lot of things seem obvious after you hear someone say them out loud...

For me, (not my field) the observation raises a couple of interesting secondary questions:

1. Does the metabolic emphasis (repair vs. reproduction) vary with age? When a child is growing and maturing (aging in a positive context), how does the activity profile differ from when an adult is passing from maturity to decline (aging in a negative context).

2. Presumably, there are some metobolic processes that support repair - even if they don't necessarily do so at the expense of reproduction. Can these be identified, isolated, and stimulated - and what happens when they are?

3. Is there anything interesting that happens in terms of life extension when puberty is delayed/extended? Menopause?

Each of these questions could be old hat to someone knowedgable (which I am not), but its a bit of data to file away in case something interesting and related comes up later....

#6 John Schloendorn

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Posted 15 September 2005 - 09:26 AM

1. Sorry, we need better definitions there. If aging is the accumulation of cell damage, then in many respects kids age as much as adults do. The major difference is that kids have been doing so for a shorter time and thus have accumulated less total cell damage. For example, atherosclerotic lesions can sometimes be detected as fatty streaks before puberty, while they gradually become larger and more oxidized until eventually reaching dangerous levels in late adulthood.
I guess what you refer to as "positive aging", i.e. organ formation, growth, ect. is normally called development and to my knowlege mechanistically independent from any types of age-related cell damage.

2. Most of our data on enhancing repair processes comes from germ-line engineered, transgenic animals. Very broadly speaking, enhancing cellular repair (division) can often attenuate the rate of accumulation of age-related tissue damage, while on the other hand it also tends to promote cancer (which is thought to be a disease of hyperactive cellular repair pathways). As a result, and presumably also because it is difficult to measure directly, experiments that enhance cellular repair often do not address cancer at all.
Enhancing molecular repair, too, can sometimes extend health and life span. Selective molecular repair of one specific type of cell damage can sometimes be ineffective, when other types of damage are limiting factor in causing aging. Some believe this is the reason that overexpressing genomic DNA repair enzymes has so far been of limited phenotypical benefit.
Given the enormous time frame over which age-related damage accumulates in humans, one might consider interventions that target the damage itself, rather than the rate of its accumulation.

3. There is a positive correlation of age of onset of puberty and life-span between species, but I'm not sure about within species. (bear in mind that correrlation is not causation) I do not know about menopause.

#7 dangerousideas

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Posted 30 September 2005 - 07:01 PM

Development, the Process that Gives Rise to an Adult Organism also Causes Aging

Research, published July 25

URL: http://www.hmnews.org/article2599.html

In “Genomes Optimize Reproduction: Aging as a Consequence of the Developmental Program,” appearing in the August issue of the journal Physiology, Joao Pedro de Magalhaes and George Church assert that the aging process is driven by the same genetic processes that drive development.

The idea that development is linked to aging has been frowned upon by scientists for decades, but new evidence demonstrates the two are not only linked but that aging and development are regulated by the same genetic mechanisms. “We now know of several animals that can delay development and as a result delay aging as well,” said lead author de Magalhaes. “Even in mammals there is growing evidence that aging is a consequence of developmental mechanisms. For instance, the pace of development influences the pace of aging, suggesting that the timing of developmental mechanisms determines the timing of aging in mammals.” Hence, the researchers argue that the same genes that regulate the way children grow and develop will later be responsible for their degeneration.

While the same genes drive development and aging, the researchers do not consider that aging is an intentional product of evolution like development. “I don’t think aging is under strong selection,” de Magalhaes said. “What happens, at least in higher organisms like mammals, is that evolution is not about selecting for long life. Evolution is about optimizing developmental mechanisms for reproduction. Once an organism has passed its genes to the next generation evolution gives up on it and the same genes responsible for the growth and maturation of that organism will inadvertently end up killing it. Examples include cell proliferation genes that are crucial in embryonic development but at older ages become harmful and can cause cancer and other age-related diseases.”

One optimistic aspect of this new work is that scientists already know a number of genes regulating development and aging. “Some hormones like growth hormone and genes involved in insulin-like signaling appear to do just that: they regulate growth and development early in life and later contribute to aging. Still,” de Magalhaes warned, “there is a lot of work to be done before we know all the genes involved. Development and aging are so complex that it will be some time before we fully understand them.”

Source: Harvard Medical School

#8 dangerousideas

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Posted 30 September 2005 - 07:07 PM

Study Finds Cell Mutations That Lead To Apoptosis May Contribute To Aging In Mammals

Cells, published July 14

URL: http://www.hmnews.org/article2562.html

A University of Florida study has found that mutations in the mitochondria caused by obesity and lack of exercise -- not oxidative stress from free radicals -- may be a key factor in the aging process.

The study, published in this Friday’s issue of Science magazine, finds that accumulation of mitochondrial mutations that promote apoptosis, or programmed cell death, may be a central mechanism driving aging and may be unrelated to the release of free radicals, previously thought to cause aging. This may be because of an accumulation of DNA mutations in the mitochondria, the cellular powerhouse that converts food to energy.

Results from the study may lead to more effective methods to prevent aging and stress the importance of a healthy lifestyle, said Christiaan Leeuwenburgh, an associate professor in the department of aging and geriatric research in the College of Medicine and contributing author of the study. He estimated that average maximum human lifespan could be increased from the current 70 years to more than 100 years with exercise and a proper diet.

“All the therapies have been targeted to reduce the free radical production in the mitochondria, and now it looks like that doesn’t make complete sense,” he said.

By breeding mice with the inability to detect and repair mistakes in the DNA replication process, researchers discovered there was no increase in oxidative stress despite an increased mutational load. However, there was a significant increase in apoptosis, said Leeuwenburgh.

In mammals, uncorrected mistakes can cause genetic disorders, aging or even death, said doctoral student Asimina Hiona, who was instrumental in the biochemical analysis of free radicals and apoptosis in the study. In the mutated mice, that ability was impaired so the cells could not repair themselves.

The finding disproves the previously believed mitochondrial “vicious cycle” theory of aging, which states that increases in mitochondrial mutations increase oxidative damage, which is one cause of aging.

“It was previously believed that the more mitochondrial mutations you have, the more free radicals you’re going to produce,” said Leeuwenburgh. “But that’s one thing this paper shows, that that’s not necessarily the case.”

The mice used in the study were bred by Thomas Prolla, an associate professor and lead investigator of the paper, and Greg Kujoth, an assistant scientist, both of the genetics department at the University of Wisconsin.

“Mice with accelerated aging may be a useful system to discover compounds that improve function in aging individuals and perhaps retard or prevent some of the diseases associated with aging,” Prolla said.

The researchers discovered that on average, the mutant mice lived a third as long as normal mice. At just nine months of age, they experienced significant loss of hair, hearing, bone mass, intestinal lining and overall weight, conditions similar to those of an aging human. Unaltered, the same mice normally live 30 to 32 months.

Also, no programmed cell death was observed between mutant and control mice at 3 months of age. However, by the time the mice reached 9 months, significant levels of programmed cell death were found in the testes, heart, thymus and other organs.

Although the mice were considered a “good model” of aging, they lacked a chronic inflammatory component which can cause cardiovascular disease, Alzheimer’s and other health problems that affect individuals as they age. Chronic inflammation is associated with the increased production of free radicals produced by other sources, such as white blood cells.

“As we get old, we become stiff and have pains and processes that have inflammation,” Leeuwenburgh said. He added that inflammation may be prevented by maintaining an ideal body weight through caloric restriction and exercise.

If people practice a healthy lifestyle, then stem-cell therapy, nanotechnology and special exercise and dietary interventions will be even more beneficial, he said.

Source: UF

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