Wednesday, February 17, 2010

Secret of Aging

The real news appears to be that the role of telomeres has been overstated.  Cellular aging appears be a response to ongoing DNA damage or other damage and not particularly programmed.

My own conjecture is that our high metabolic rate out runs our ability to produce enough stem cells to replace cell losses on a timely basis.  This a mechanical explanation that largely fits the apparent facts.

I have observed a small but bad scar on my knuckle, caused when I was a teenager slowly transition back to mostly normal skin tissue.  Any inherent weakness has dissipated over the decades.  Yet this strongly suggests that the only restraint from rapid rejuvenation is merely mechanical capacity.

That suggests that stem cell augmentation can hugely restore a large part of the aging body.  It is little wonder that such optimism exists around the subject of stem cells.

As an aside, healing is sharply enhanced by taking doses of condriten sulphate.  This was shown to reverse heart attack damage to the point of eliminating EKG evidence long after the event.  This obviously applies to any and all internal damage needing to heal up properly.

At least we clearly know the pathway that induces well known aging effects.

Scientists discover the secret of ageing

By Clive Cookson in London

Published: February 15 2010 23:00 | Last updated: February 15 2010 23:00

One of the biggest puzzles in biology – how and why living cells age – has been solved by an international team based at Newcastle University, in north-east England.
The answer is complex, and will not produce an elixir of eternal life in the foreseeable future.
But the scientists expect better drugs for age-related illnesses, such as diabetes and heart disease, to emerge from their discovery of the biochemical pathway involved in ageing.
The Newcastle team, working with the University of Ulm in Germany, used a comprehensive “systems biology” approach, involving computer modeling and experiments with cell cultures and genetically modified mice, to investigate why cells become senescent. In this aged state, cells stop dividing and the tissues they make up show physical signs of deterioration, from wrinkling skin to a failing heart.
The research, published by the journal Molecular Systems Biology, shows that when an ageing cell detects serious damage to its DNA – caused by the wear and tear of life – it sends out specific internal signals.
These distress signals trigger the cell’s mitochondria, its tiny energy-producing power packs, to make oxidising “free radical” molecules, which in turn tell the cell either to destroy itself or to stop dividing. The aim is to avoid the damaged DNA that causes cancer.
The Newcastle discovery plays down the role of telomeres, the protective tips on the ends of human chromosomes, which gradually become shorter as we grow older.
“There has been a huge amount of speculation about how blocking telomere erosion might cure ageing and age-related diseases,” said Tom Kirkwood, director of Newcastle’s Institute of Ageing and Health. “The telomere story has over-promised and the biology is more complicated.”
He added: “Our breakthrough means that we stand a very much better chance of making a successful attack on age-related diseases while at the same time avoiding the risk of unwanted side-effects like cancer.”
His colleague Thomas von Zglinicki emphasized caution in the research’s next stage – to investigate ways to prevent cellular senescence.
“It is absolutely essential to tread carefully in trying to alter processes that cause cells to age, because the last thing we want is to help age-damaged cells from breaking out to become malignant,” said Mr von Zglinicki.

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