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Health
See other Health Articles

Title: Slowing aging with telomerase
Source: [None]
URL Source: http://www.bbc.co.uk/news/science-environment-12207953
Published: Jan 30, 2011
Author: Neil Bowdler
Post Date: 2011-01-31 00:20:48 by Tatarewicz
Keywords: None
Views: 120
Comments: 11

Related stories

* Do we all want to live to 100? * Genes reveal 'biological ageing' * Vitamin D 'may help slow ageing'

Scientists are slowly unlocking the secrets of ageing, and some suggest treatments may soon be at hand to slow or even reverse the ageing process.

But what can science really achieve, and what are the dangers of meddling with our biological clocks?

Could such treatments induce cancers in humans, for example, and what about the world's burgeoning population and the West's "pension time bomb"? Chromosome tips

The ageing process is a complex one, and for long remained an impenetrable mystery, but progress is now being made.

Late last year, a team at the Dana-Farber Cancer Institute in Boston published a Nature paper in which they detailed the reversing of the ageing process in mice.

They targeted the chromosomes that reside within the nuclei of all cells, and specifically telomeres, caps at the tips of chromosomes. The telomeres protect the chromosomes from damage, but also shorten with age, until the cells are no longer able to replicate.

By understanding the ageing process, we can help combat arthritis, diabetes and heart disease”

End Quote Professor Tim Spector King's College London

Professor Ronald DePinho and colleagues manipulated the enzyme that regulates these tips - known as telomerase - and witnessed dramatic results. Mice engineered to lack the enzyme aged prematurely, but when the enzyme was replaced, the mice appeared to rewind the clock.

"What we were expecting was a slowing or stabilisation of the ageing process," he told the BBC. "Instead we witnessed a dramatic reversal in the signs and symptoms of ageing."

"These animals had their brains increase in size, they improved their cognition, their coat-hair was restored to a healthy sheen and their fertility was also restored."

Of course, this was a story of mice, not men, and applying such principles to humans could be an altogether bigger challenge. Telomerase has been linked with cancer, and there are likely to be many other mechanisms involved in ageing.

Many believe mitochondria may play a bigger role - genetic material contained within the cell but outside the nucleus. Mitochondria are the "power houses" of cells, but have also been seen to generate harmful chemicals linked with aging.

Then there is the role played by free radicals, highly reactive atoms or molecules that attack our bodies. Anti-ageing drug

But even though a comprehensive picture of how we age is still to be constructed, there are scientists who are already testing anti-ageing treatments on humans. Chromosome with telomeres at tips Telomeres (in red) are found at the ends of each chromosome, and shorten with age

Professor David Sinclair also works in Boston at an ageing laboratory at Harvard Medical School. He and his colleagues have been working on synthetic drugs called "Sirtuin activating compounds" or STACs.

Animal studies have indicated STACs can restore the health and life prospects of obese mice and early-stage trials in humans are now underway.

The research follows earlier work on resveratrol, a naturally-occurring ingredient of red wine. Both resveratrol and STACs appear to mimic the effects of restricting calorie intake, which has been seen to slow ageing in animals.

"This isn't going to be an excuse to eat French fries all day and watch TV but is a way to augment your healthy lifestyle and give you the ultimate benefits of perfect health which your body is capable of," Professor Sinclair told the BBC.

"It doesn't change food intake - the mice eat just normally or they get fatter, but their body doesn't seem to know they're fat and their organs and even their longevity is as good as a really healthy mouse."

But should we be experimenting with something so fundamental as ageing in the first place? And what of the ethical issues?

Professor Tim Spector of King's College London, who also works on the ageing process, says the focus is not on extending life, but on extending good health.

"If it means by living a long time you're crippled by arthritis and can't get out of the house that's not much use to anyone."

"But by understanding the ageing process, we can help combat arthritis, diabetes, heart disease, all these things which are age-related."

Professor James Goodwin, head of research at Age UK, believes access will quickly emerge as a key issue, should effective anti-ageing medical treatments be developed.

"Will everybody be able to get this technology which will give them a longer healthier life, or will it be restricted to the rich and wealthy?" he asks.

"Or how will the poorer countries regard the richer countries of the world where everyone is living well and living longer?" Œ79;

Click for Full Text!


"Will everybody be able to get this technology which will give them a longer healthier life, or will it be restricted to the rich and wealthy?" Restrict it to those who are productive enough to be of a net benefit to the community, particularly doctors, food, shelter producers.

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#1. To: Tatarewicz (#0)

* Do we all want to live to 100?

No, 1000 sounds better. Of course since heaven is so much better, short lives might be a blessing.

God is always good!

RickyJ  posted on  2011-01-31   1:23:37 ET  Reply   Trace   Private Reply  


#2. To: Tatarewicz (#0)

"These animals had their brains increase in size, they improved their cognition, their coat-hair was restored to a healthy sheen and their fertility was also restored."

Lucky little mice. Hope it works on humans too.

God is always good!

RickyJ  posted on  2011-01-31   1:29:31 ET  Reply   Trace   Private Reply  


#3. To: Tatarewicz (#0)

Restrict it to those who are productive enough to be of a net benefit to the community, particularly doctors, food, shelter producers.

Naw. Any jagoff with a credit card can get it.

A people unwilling to use force, once diplomatic efforts have been exhausted, in order to preserve or obtain their liberty deserves the tyrants that rule over them.

mirage  posted on  2011-01-31   4:22:41 ET  Reply   Trace   Private Reply  


#4. To: mirage (#3)

Don't know if oral ingestion/digestion of "reneuve" would have much of an effect. IV administration should be be better. Nevertheless might be worth trying on some old geezer about to croak.

Tatarewicz  posted on  2011-01-31   5:17:15 ET  Reply   Trace   Private Reply  


#5. To: Tatarewicz (#4)

I don't know if it will be effective using an oral application either, but its out there already for those with a credit card.

Its not like we can stop people from buying syringes either if that becomes the "preferred method" of delivery either.

A people unwilling to use force, once diplomatic efforts have been exhausted, in order to preserve or obtain their liberty deserves the tyrants that rule over them.

mirage  posted on  2011-01-31   19:41:33 ET  Reply   Trace   Private Reply  


#6. To: RickyJ (#1)

deleted

The relationship between morality and liberty is a directly proportional one.

"Only a virtuous people are capable of freedom. As nations become corrupt and vicious, they have more need of masters." - Ben Franklin

Eric Stratton  posted on  2011-01-31   22:16:10 ET  Reply   Trace   Private Reply  


#7. To: Eric Stratton (#6)

On the other hand, if this life sucks for you, then you don't want to hold on to it that much. So many people judge one another when they aren't any better. Rodney King was a drunk and drug addict but he was right when he said, "can't we all just get along?" The answer to that of course is no, we can't all get along because many people love evil more than they love good.

God is always good!

RickyJ  posted on  2011-01-31   22:46:03 ET  Reply   Trace   Private Reply  


#8. To: RickyJ (#7)

deleted

The relationship between morality and liberty is a directly proportional one.

"Only a virtuous people are capable of freedom. As nations become corrupt and vicious, they have more need of masters." - Ben Franklin

Eric Stratton  posted on  2011-02-01   0:15:14 ET  Reply   Trace   Private Reply  


#9. To: mirage (#5)

Could be just another snake oil scam in that the telomerase in the potion has one universal chemical structure whereas everyone's DNA which codes for this protein has slight variations in base pairs meaning that any such added telomerase could be different and subject to attack as a foreign body by one's immune system. In which case each individual would have to have telomerase synthesized from his own DNA.

Shortened telomers predispose people to early heart attacks:

http://www.springerlink.com/content/w35551tu7p626257/

Abstract Shorter telomeres have been reported in premature myocardial infarction (MI) patients. Our work aimed at confirming the association of shorter telomere with MI in two case–control studies and in familial hypercholesterolemia (FH) patients with coronary heart disease (CHD). The HIFMECH study compared 598 white male patients (<60 years) who survived a first MI and 653 age-matched controls from North and South Europe. Additionally, from the UK, 413 coronary artery bypass graft (CABG) patients and two groups of 367 and 94 FH patients, of whom 145 and 17 respectively had premature CHD, were recruited. Leukocyte telomere length (LTL) was measured using a real-time polymerase chain reaction-based method. In HIFMECH, LTL was significantly shorter in subjects from the North (7.99 kb, SD 4.51) compared to the South (8.27 kb, SD 4.14; p41;=41;0.02) and in cases (7.85 kb, SD 4.01) compared to controls (8.04 kb, SD 4.46; p41;=41;0.04). In the CABG study, LTL was significantly shorter (6.89 kb, SD 4.14) compared to the HIFMECH UK controls (7.53, SD 5.29; p41;=41;0.007). In both samples of FH patients, LTL was shorter in those with CHD (overall 8.68 kb, SD 4.65) compared to the non-CHD subjects (9.23 kb, SD 4.83; p41;=41;0.012). Apart from a consistent negative correlation with age, LTL was not associated across studies with any measured CHD risk factors. The present data confirms that subjects with CHD have shorter telomeres than controls and extends this to those with monogenic and polygenic forms of CHD.

--------------------------------------------------------------------------------

Findings make sense in that heart muscle, etc. weakens when cells run out of regenerative steam.

Tatarewicz  posted on  2011-02-01   2:43:00 ET  Reply   Trace   Private Reply  


#10. To: Tatarewicz (#9)

Early attempts to cash in like this usually are snake oil scams.

However, if the body really is able to assemble from raw materials precisely what it needs for self-repair, then it shouldn't matter what order the enzyme is in if it can be broken down and reassembled properly.

So we need some more information before proceeding to a conclusion. However, the lab testing indicated a "generic" form worked fine.

We also know that the tail ends of DNA strands are made of "junk" DNA that breaks off as cells divide, thus providing the time-ticker for aging.

If "any" enzyme works to just throw a few more "junk" base pairs on the ends that are not read, used, or expressed, then it wouldn't matter what form the enzyme was in. The body would just use it.

A people unwilling to use force, once diplomatic efforts have been exhausted, in order to preserve or obtain their liberty deserves the tyrants that rule over them.

mirage  posted on  2011-02-01   2:49:08 ET  Reply   Trace   Private Reply  


#11. To: mirage (#10) (Edited)

Looks like telomerase is assembled inside the cell from three bases: adenine (Purine) adenine and uracil (pyrimidine)on a protein template so there should be lots of these molecules from food we eat. I don't know if the entire enzyme would be able to enter through the cell wall. How it works:

* Telomerase is found in the nucleus, where DNA replication takes place. Not all cells, however, show evidence of telomerase activity. Expression of TERC, the gene for the RNA component of telomerase, is widespread, but the expression of the protein component's catalytic subunit, TERT, is restricted to locations of telomerase activity. Telomerase activity was found to be almost absent in the majority of normal adult tissues, including cardiac and skeletal muscle, adipose tissue, lung, liver, and kidney (Kolquist et al, 1998).

* Because of this curious lack of telomerase activity, a theory arose connecting telomere length to aging and cell senescence. According to this theory, human somatic cells are born with a full number of telomeric repeats, but the telomerase enzyme is "turned off" in some tissues. The cells of those tissues would lose about 50 to 100 nucleotides from each chromosome end each time they underwent replication and division. Eventually, the telomeres would cease to exist and the chromosomes themselves would start losing nucleotides, carrying genetic defects into their next division so that neither daughter cell would be viable and would consequently undergo senescence (Alberts et al, 2002). Thus after a certain number of divisions a cell has "aged" and died.

* This theory has been tested using human fibroblasts grown in tissue culture. Human fibroblasts normally divide around 60 times before dying, and like most other somatic cells, they do not produce telomerase. Their telomeres gradually shorten as they continue dividing. When the telomerase gene is added to the cells' genomes, however, they maintain their telomere length, and some of the cells are able to proliferate indefinitely.

* If telomere length is a cause of human aging, then, might exposure to telomerase lengthen one's life?

* A control on cell division certainly seems important, however, in light of the fact that approximately 85% of all tumors show evidence of telomerase activity (Kilian et al, 1997). If telomerase is provided to maintain telomere length, a cell's life may be prolonged indefinitely, causing genetic instabilities that in turn lead to variant, cancerous cells. Figure 5 compares telomerase gene expression in normal human tissue and concerous tissue, suggesting the correlation.

www.bio.davidson.edu/Cour...g2003/Parker/protein.html

Tatarewicz  posted on  2011-02-02   6:22:44 ET  Reply   Trace   Private Reply  


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