45 replies to this topic

[Utnapishtim]

BBC NEWS
Tuesday, 31 December, 2002, 02:17 GMT
Ageing process 'key' pinpointed

Scientists believe the 'retirement' of a specific gene may go a long way to explaining why the human body deteriorates with age.
They have discovered that a gene called FoxM1B plays a crucial role in helping the body's tissues to heal and replenish themselves.

This is a knack that we all gradually lose as we get older and leads, among other things, to progressive weakening of the muscles and bones, saggy skin and slower healing of wounds

A team from the University of Illinois at Chicago has shown that failure of the FoxM1B gene to work properly damages the body's ability to replicate its own cells.

And it seems that the older we get, the more likely are malfunctions in the gene.

Gene therapy

The researchers used gene therapy to created mice with liver cells lacking the FoxM1B gene.

They then measured how quickly the organ was able to regenerate itself following injury.

Regeneration was much faster in animals whose cells carried FoxM1B. Without the gene, regeneration was slow.

Cell division requires two basic steps: first a doubling of DNA, the genetic instructions inside a cell, and then a process called mitosis, in which the duplicated DNA is separated into two new daughter cells.

Lead researcher Dr Robert Costa said: "If the cells had no FoxM1B gene their DNA often failed to make a copy of itself, and they had trouble dividing."

Protein

The key appears to be the pile up of a specific protein - called p21Cip1 - in the cells which not only blocks DNA division, but also appears to trigger genes linked to diseases of old age, such as cancer and Alzheimer's.

Dr Costa believes that FoxM1B probably controls production of an enzyme that breaks down this protein and prevents it building up in the cell.

The researcher team also found that FoxM1B controls a key enzyme needed to help cells pull apart at the end of mitosis, the final step in cell division.

Dr Costa said: "These results clearly link FoxM1B with the failure of tissues to mend.

"And in old age, when the FoxM1B gene is essentially out of action, we see the results."

The research is published in the Proceedings of the National Academy of Sciences.

[Lazarus Long]

The reason I posted the article above is that it might represent an approach for modifying the process without HAVING to alter gene structure, just alter the programming. There is a biochemical switch that appears to override the gene during the stem cell phase of the blastomere that resets the gene function back to normal zygotic phase even when the gene has already mutated to the cancerous phase.

Get it?

Something about about this period is possiblibly reproducible as a drug that could tell all the genes to treat right now as the beginnning, instead of the end of the life cycle. I realize that this is not a very scientific form of expression and a gross oversmplification but I disagree that we should allow ourselves to get too fixiated on CHANGING our gene structure, if we could reset the genetic clock's biochemical mechanism.

As for the use of viral phages for transcriptase purpose I agree that there is a severe risk of an immunological overload particularly when we are trying to correct neurological concerns. I think Stem Cells, and frankly more likely to be fetal stem cells in this regard ( though I just posted an article to the contrary), are the manner to correct neurological damage in adults.

There are two separate issues, one keeping us alive, and second designing our offspring to be more capable and longer lived then we are by adjusting their genetics. I personally will worry seriously about gentic divergence later after I have lived for a few centuries and the latest generations are no longer viable candidates for reproduction. Of course that doesn't mean that we can't have any fun. And anyway there will always be recombinant techniques that can be applied in vitro to make babies when speciation has made the future so complicated.

Like I implied in the first place however we don't have to worry about this until we have lived so long.

[Aegist]

Approaching the final year of my UG degree, preparing myself to get into Honours, and then finally into my PhD project, where I am pretty confident my thesis will be on something to do with this topic.

This is the question which really drives me at the moment. I am less concerned with trying to identify all the thing which happen as the body gets older, and trying to combat them, and concentrating more on how the body registers its biolgocal clock. The discovery of what it is which allows the body to know its age will allow us to find a way to manipulate it, and thereby completely bystepping all age related genetic disease (Alzheimers, parkinsons etc). Since a large portion of age related issues are actually genetically triggered break downs or lapses into disrepair, being able to tell the body 'Hey, you're 25 years old' should reduce the problem of finding the fountain of youth considerably.

So, does anyone have any idea how the body determines its biological age? Telomeres are a reasonable option, since they definately have a 'counter' mechanism in them. But then different parts of the bodyt would record different ages (arteries for Eg divide much more than brain cells because arteries are under constant stress and dmg, so need constant repair.)

Other consideration: The body is a decentralized system. It is highly unlikely that any organ would act like a biological clock...so it is probably a cellular thing. (pointing back to telomeres)...i just can't think of anything else.

Can anyone else think of something?

[Bruce Klein]

The more I read about it, the less convinced that telomeres are that imoprtant... I'm looking at telomeres as more of a cancer fighting defence than anything else. The skin produces skin stem cells that replace these cells. So, i don't thinking aging is a matter of less and less cells.

Rather, I believe it's more a problem of accumulated defects in the genetic code.

I do agree that the body does have a count somehow.. it knows when to enact the hormones for puberty etc.

I believe it's probably going to boil down to a few hundred genes.

[Aegist]

Well, we can work from the fact that the Body releases certain chemicals (hormones, enzymes..whatever) as it needs them. More testosterone, less estrogen etc at specific ages. The body knows, as u said, when it is in puberty. It knows when to go through menopause (though that may be simply triggered by the end of Eggs.) It knows when to harden you rbones (from the softer, more numerous Baby bones), it knows when to make u grow. It knows when to make u stop growing. It knows when to get hairy.

So, obviously the body knows how old it is. No doubt, at these particular ages, genes are turned on, and those genes cause hormones to be produced in excess (or, some genes are turned off, and some hormones etc are stopped being produced). But....BUT....what is it that figures out when it is time to turn on/off those genes?

There MUST be a biological clock. Perhaps it is a slow build up of a particular chemical (but surely such a thing would be detectable? Take a cellular sample from a baby and a cellular sample from an octagenerian and look for the difference in chemical composition), perhaps it does have to do with genetic dmg? (But such a thing really isn't....definite enough. Some cells get dmgd, some don't. There is no simple, exact clock built into the random bombardment of genetic dmg.)

While genetic dmg, cellular dmg etc (as result of Free Radicals, radiation etc) is most definately a part of aging, I am not convinced that this is the sort of method that something would evolve to use as a determination of age. As should be made clear by all the examples of age related phenomenon above, it is vitally important for the body to know how old it is. An organism as advanced as Mammals MUST (tentatively) have a definate biological clock with which to measure this advancement through time.

I WANNA KNOW WHAT IT IS!!!! *stamps feet* [wacko]

Edited by Another God, 10 January 2003 - 07:34 AM.

[Cyto]

Well your just in time for some papers of how poorly we understand a lot of signaling pathways and chromatin 'activation.' But on a lighter note...

All I can say is that since peoples biological clocks all operate at different times it must be an somewhat wavering biological clock. Both my parents were very late 'bloomers' and I was very very eary.

So would have to be a global genomic trigger, I would say it safe to point to the endocrine system like you were talking about. Course, to refute myself somewhat. I have less hair on one side of my face then I do the other, so this can also point to maybe something in the neurological field? Or Im just really really messed, heh.

Dont know too much how to answer your question (dont know the development field) but I can try and add to the focusing of the question.

If you dont already have them I would highly recomend Deveopmental Cell from cellpress.com or Genes & Development from Genes and Devel. The Genes and Development are also good for stem cell research (great!).

And here be a intro to Indocrine functions, neat site and seems to say stuff.
The Site


And I agree with BJK 100% on the damage but I would link that to stem cell genetic damage and loosing the 'providers' is whats screwing it all up...even if most do hide in the bone marrow.


Sorry if I didnt help at all

*shrug*

Edited by XxDoubleHelixX, 10 January 2003 - 09:14 AM.

[Sophianic]

Welcome back, Another God.

Although it's been a while since I read it, Michael Fossel, Ph.D., M.D., discusses what he calls "the telomeric clock" in chapter 3 of his book "Reversing Human Aging." The book also contains an extensive bibliography.

[Lazarus Long]

As has already been noted, there are two essential components to every time bomb, first a clock, and second a trigger. This is both elegant and basic, but there are other components in the theoretical model that are essential that are often overlooked when thinking too mechanically; the measure for example.

The measure is a critical subcomponent, both in an abstract sense (a rate) and a mechanism (a pendulum). The measure in this case may be manipulable. The trigger also has subcomponents that should be identifiable, such as the fuse.

I have used a metaphore intentionally, because the principle is the same as diffusiving a bomb. Break the sequence and you may prevent the result. But is there another way? Probably, in fact I would bet there are a number of ways.

Regardless.

Other consideration: The body is a decentralized system. It is highly unlikely that any organ would act like a biological clock...so it is probably a cellular thing. (pointing back to telomeres)...i just can't think of anything else.

This is probably true. What if the nature of this clock is multiphasic, as it most apparantly seems?

A conceptual example is the function of am/pm, for a species it would be a "seasonal measure". Almost all life forms on this planet have adapted an internal biological meter for preparing the body for seasonal adaptive characteristics, fat storage, hair growth, hibernation, migratory instinct, mating, etc.

There is likely to be a complex, residual, cumulative, or isommeric molecule that functions to establish this longer term periodicity. We know that hormonal triggers are more imediated so what we should look for are the presence of complex hormone "like" substances that don't at first appear to correlate to any immediate or specific physiological change. And I would suggest focusing on the brain itself for such chemical signitures. As per the pineal and pituitary glands.

These chemical markers are probably not present in any great quantities but are closely associated with other aspects of neurophysiology and general physiological development. Also I would reinvestigate the role of the hypothalumus in this regard.

It clearly has biological functions during prepubescent development that are replaced after maturity and it has a memory related set of functions. Don't just think minute to minute when thinking about the clock, think about the phases of development, the seasons of our youth, and the dark night of our future: should we fail.

Opinions?

[Aegist]

*nodz*
Yep, thanks alot everyone. Particularly for the links. I will do some reading and come back with more thoughts....

AG

[Lazarus Long]

A simple organ that is often overlooked in this discussion, is also the thymus. It is a source of T Cells and seems to influence development but after puberty disappears of its own accord; (an example of a clockwork in motion?)

Interestingly enough it appears that the organ can be synthethized, I wonder what would happen if the function of this organ were returned to an adult in the post reproductive phase. Rat experiment anyone?

It is also a candidate for cloning and can promote T Cell production and perhaps Stem Cell's if prompted.

LL/kxs

Henry Gray (1821–1865). Anatomy of the Human Body. 1918.

4c. The Thymus

The thymus
(Fig. 1178) is a temporary organ, attaining its largest size at the time of puberty (Hammar), when it ceases to grow, gradually dwindles, and almost disappears. If examined when its growth is most active, it will be found to consist of two lateral lobes placed in close contact along the middle line, situated partly in the thorax, partly in the neck, and extending from the fourth costal cartilage upward, as high as the lower border of the thyroid gland. It is covered by the sternum, and by the origins of the Sternohyoidei and Sternothyreoidei. Below, it rests upon the pericardium, being separated from the aortic arch and great vessels by a layer of fascia. In the neck it lies on the front and sides of the trachea, behind the Sternohyoidei and Sternothyreoidei. The two lobes generally differ in size; they are occasionally united, so as to form a single mass; and sometimes separated by an intermediate lobe. The thymus is of a pinkish-gray color, soft, and lobulated on its surfaces. It is about 5 cm. in length, 4 cm. in breadth below, and about 6 mm. in thickness. At birth it weighs about 15 grams, at puberty it weighs about 35 grams; after this it gradually decreases to 25 grams at twentyfive years, less than 15 grams at sixty, and about 6 grams at seventy years. 1





FIG. 1178– The thymus of a full-time fetus, exposed in situ. (See enlarged image)

Development.—The thymus appears in the form of two flask-shaped entodermal diverticula, which arise, one on either side, from the third branchial pouch (Fig. 1175), and extend lateralward and backward into the surrounding mesoderm in front of the ventral aortæ. Here they meet and become joined to one another by connective tissue, but there is never any fusion of the thymus tissue proper. The pharyngeal opening of each diverticulum is soon obliterated, but the neck of the flask persists for some time as a cellular cord. By further proliferation of the cells lining the flask, buds of cells are formed, which become surrounded and isolated by the invading mesoderm. In the latter, numerous lymphoid cells make their appearance, and are agregated to form lymphoid follicles. These lymphoid cells are probably derivatives of the entodermal cells which lined the original diverticula and their subdivisions. Additional portions of thymus tissue are sometimes developed from the fourth branchial pouches. Thymus continues to grow until the time of puberty and then begins to atrophy. 2


FIG. 1179– Minute structure of thymus. Follicle of injected thymus from calf, four days old, slightly diagrammatic, magnified about 50 diameters. The large vessels are disposed in two rings, one of which surrounds the follicle, the other lies just within the margin of the medulla. (Watney.) A and B. From thymus of camel, examined without addition of any reagent. Magnified about 400 diameters. A. Large colorless cell, containing small oval masses of hemoglobin. Similar cells are found in the lymph glands, spleen, and medulla of bone. B. Colored blood corpuscles. (See enlarged image)


Structure.—Each lateral lobe is composed of numerous lobules held together by delicate areolar tissue; the entire gland being enclosed in an investing capsule of a similar but denser structure. The primary lobules vary in size from that of a pin’s head to that of a small pea, and are made up of a number of small nodules or follicles, which are irregular in shape and are more or less fused together, especially toward the interior of the gland. Each follicle is from 1 to 2 mm. in diameter and consists of a medullary and a cortical portion, and these differ in many essential particulars from each other.

The cortical portion is mainly composed of lymphoid cells, supported by a network of finely branched cells, which is continuous with a similar network in the medullary portion. This network forms an adventitia to the bloodvessels. In the medullary portion the reticulum is coarser than in the cortex, the lymphoid cells are relatively fewer in number, and there are found peculiar nest-like bodies, the concentric corpuscles of Hassall. These concentric corpuscles are composed of a central mass, consisting of one or more granular cells, and of a capsule which is formed of epithelioid cells (Fig. 1179). They are the remains of the epithelial tubes which grow out from the third branchial pouches of the embryo to form the thymus. 3

Each follicle is surrounded by a vascular plexus, from which vessels pass into the interior, and radiate from the periphery toward the center, forming a second zone just within the margin of the medullary portion. In the center of the medullary portion there are very few vessels, and they are of minute size. 4

Watney has made the important observation that hemoglobin is found in the thymus, either in cysts or in cells situated near to, or forming part of, the concentric corpuscles. This hemo globin occurs as granules or as circular masses exactly resembling colored blood corpuscles. He has also discovered, in the lymph issuing from the thymus, similar cells to those found in the gland, and, like them, containing hemoglobin in the form of either granules or masses. From these facts he arrives at the conclusion that the gland is one source of the colored blood corpuscles. More recently Schaffer has observed actual nucleated red-blood corpuscles in the thymus. The function of the thymus is obscure. It seems to furnish during the period of growth an internal secretion concerned with some phases of body metabolism, especially that of the sexual glands. 5

Vessels and Nerves.
—The arteries supplying the thymus are derived from the internal mammary, and from the superior and inferior thyroids. The veins end in the left innominate vein, and in the thyroid veins. The lymphatics are described on page 698. The nerves are exceedingly minute; they are derived from the vagi and sympathetic. Branches from the descendens hypoglossi and phrenic reach the investing capsule, but do not penetrate into the substance of the gland. 6

*****************

Man-made thymus churns out immune cells.(Brief Article)
Author/s: J.T.
Issue: July 22, 2000

In the thymus, so-called T cells mature into full-fledged immune system sentinels. Seeking better ways to grow these white blood cells in the laboratory, David T. Scadden of Massachusetts General Hospital in Boston and his colleagues have built an artificial thymus by seeding a three-dimensional carbon matrix with tissue from the immune organ.

When precursor T cells are added to this matrix, mature cells emerge within 2 weeks, the investigators report in the July NATURE BIOTECHNOLOGY. This artificial thymus "has the potential to generate not only normal T cells to replace cells lost as a result of infection, chemotherapy, radiotherapy or aging, but also cells that can be manipulated to treat a number of diseases," David L. Porter and Stephen G. Emerson, both of the University of Pennsylvania in Philadelphia, say in an accompanying commentary.

COPYRIGHT 2000 Science Service, Inc.
COPYRIGHT 2000 Gale Group


Footnote by LL,

Another overlooked aspect of the design of a clock is:
How is it read?

Think of the difference between analogue and digital information. The body's ability to recognize its own memory is important. Another place to find the clock is to look for and then follow the connection of the trigger. Examine the diurnal/nocturnal chemical signatures and where these lead.

We don't even know where in the body this information is stored, or the true medium. I suspect the answers will come together.

[Lazarus Long]

Another few thoughts:

When thinking of the face of this clock it would be better to visualize the natural analogue of radiactive half-life. That is NOT to say that the substance(s) we seek is necessarilly in the process of radiactive decay (though this should not be overlooked as possible) but that such things as isomeres can chemically mimic the process of isotopes in this regard as reflects such physical phenomenon as crystal growth.

Never forget the presence in the body of complex trace heavy molecules. We don't fully understand why many of these are needed but many substances that are toxic in large quanities are critically necessary to metabolic functions in trace amounts.

As a parting comment, there is one critical aspect of a Time Bomb that we also should never overlook and haven't yet mentioned, the explosive itself.

What starts aging?
And why is it necessary to the body?
Why can trauma and stress effect the rate of aging?

[Lazarus Long]

Postscript:

Another subject with regard to the biological that should be closely re-examined in light of the new investigative tools we now possess is the pediatric illness Progeria.

It is a genetic disorder (lights should start flashing) that causes a rapid acceleration of the aging process. Children live through the entire life cycle by the time they should instead be finishing puberty.

I first saw a case of this when I was a child, my father had to treat a patient suffering from the syndrome. The impression of seeing an seven year old girl dying of old age stuck with me for life. My father described how helpless he felt because there was literally nothing at all that could be done at that time. There is still all too little.

The child's biological clock was broken he told me, and like a watchwork that is broken the child's metabolism was going through all the phases of development in a hyperaccelerated rate.

We now have good reason to believe that the condition is genetic and all too little else because very little research has gone into the disorder since it is so rare. This is a heart wrenching illness that causes small children to basically die of old age.

I suggest a review for starters of some of the pages found here: Progeria Search

And here is an overview. LL/kxs


BY: Crystal Ward

Shannon Jackson

Period 5

WHAT IS PROGERIA?
Progeria is a rare genetic condition characterized by an appearance of accelerated aging in children. Its name is derived from the Greek and means "prematurely old." The classic type is the Hutchinson-Gilford Progeria Syndrome which was first described in England in 1886 by Dr. Jonathan Hutchinson and again in 1886 and 1904 by Dr. Hastings Gilford.

HOW COMMON IS PROGERIA?
The classic syndrome has a reported incidence of about 1 in 8 million newborns, and the total incidence is estimated to be about 1 in 4 million. It affects both sexes equally and all races. Since first described, more than 100 cases have been identified around the world. In this decade, children with progeria have been reported in Algeria, Australia, Austria, Canada, China, England, France, Germany, Mexico, Puerto Rico, South Africa, South America, Switzerland, Turkey, the United States, Venezuela, and Vietnam.

WHAT ARE THE FEATURES OF PROGERIA?
The general characteristics are dwarfism, baldness, a pinched nose, small face and jaw relative to head size, delayed tooth formation, aged-looking skin, stiffness of joints, hip dislocations, generalized atherosclerosis, and cardiovascular problems. The children have a remarkably similar appearance, despite racial background. At present, there is no cure or specific treatment available.

WHAT IS THE CAUSE OF PROGERIA?
The exact cause is unknown, but it is believed due to a single abnormal (mutant) gene. A gene is the fundamental unit of heredity and human beings have about 80,000 of them. For each gene there are two copies: one from each parent. Progeria is considered to be the result of a dominant mutation because the gene in question has one normal copy and one abnormal copy, as opposed to a recessive mutation in which both copies are abnormal. Because neither parent carries or expresses the mutation, each case is believed to represent a sporadic new mutation which happens at the time of conception.

Observations suggesting the dominant mutation include (1) brothers, sisters and non-identical twins are almost never affected in the same family, (2) the parents are seldom related such as first cousins, and (3) the average difference in ages between father and mother is about six years as compared with the national average of about two years.

Research indicates that a chemical (hyaluronic acid) may be found in greatly elevated levels in the urine of Hutchinson-Gilford Progeria Syndrome patients. The same abnormality has been found in Werner Syndrome, which is sometimes called "progeria of the adult."

Few other diseases are known in which elevated levels of this chemical are found, suggesting that hyaluronic acid may prove to be a useful test for progeria.

HOW IS PROGERIA DIAGNOSED?
Because of the lack of a specific laboratory test at this time, the diagnosis must be based on the physical appearance of the individual. The diagnosis is usually made in the first or second year of life when skin changes and failure to gain weight become apparent.

Footnote by LL

Find the cure for these desparate children and their families and perhaps you will find the information that we all seek. Call it a win/win scenario.

[Socrates]

Socrates, Ever hear of cryonics?

Yeah, BJKlein, I heard about cryonics... but maybe it's better to discuss that in the appropriate place like caliban is suggesting us, huh?

[Lazarus Long]

I think it would be better to understand the full sequence of chemical interactions between the telomers and the cell. If cloning can reprogram the cell WITHOUT carrying the mutated gene then there must exist a biochemical filter that can select critical information. Not to push the analogy too far but analogous to the way a registration file works on the computer to rebuild the operating system.

Why do we have to replace genetic information if we can get a reboot.

What needs to be diciphered is why the cloning process causes the gene to return to normal. For example, if the nucleus is from the cancerous tissue then is the substance present in the cytoplasm of the fertilized zygote?

Or is it (whatever this substance X is) appearing after the nucleus starts dividing into the blastophere?

My point is that there may be a side door approach to this problem. Instead of changing the gene itself alter the way the gene expresses itself by modifying the chemical instructions that go out during cellular reproduction. This won't initially address neuron deterioration but it will sustain general body health.

Also as a separate approach:
Why can't we turn the process by which the mutation forming cancer occurs into the means for changing the gene? Mutation causes cancer because of the deterioration of the genetic program and the resulting information gets altered irreversibly. But what if we could get the gene to mutate in a controllable fashion during this process by introducing new information that in turn usurps the cancer.

Once the mutation has already destroyed the cells ability to properly reproduce, it hasn't in fact destroyed the cells ability to reproduce, just the outcome. What if we could then cause an additional mutation that takes cell growth in a specified improved direction.

A place to test this approach would be with pancreatic cancer in mice, Suppose the cancer could be reversed and the pancreas mutated into an improved model, one for example with perhaps a greater ability to produce insulin?

This approach to infusing mutations into ourselves would be slower but have the advantage of allowing a mutation to be organ specific, selected and therapeutic. The process of integrating the mutation into the species genome would then have to be followed in the manner that the introductino of GM foods would have to. To see if it is dominant, recessive, causes infertility in offspring, parent, etc.

Regarding the ontology of viruses my old profs and I had a very interesting discussion once. Viruses came into existence long after bacteria according to prevalent evolutionary models, and I argued that the explanation for this may lie in an episome that encrypted mutational ability into the bacteria in order to enhance environmental adaptive ability.

In other words this may have been a good thing gone bad. The episome survived outside the bacteria and became the first true bacteriophages in the later generations after its positive mutational character was lost. But if the concept of a gene that turns mutational ability on is true then it wouldn't be necessary to use a virus to introduce the new genetic program, it may only be necessary to preface the genetic instruction with this genetic key. The way your pin code gets you into your bank account. Then you have to decide the nature of the transaction, Is this a deposit? Or a withdrawl?

[Lazarus Long]

Another broad category of analysis that could yield the fruit of understanding is to do long term studies on individual genetics over the full life cycle.

I do not think that a truly in depth analysis has yet to take place and because of the long term aspects of this most investigators would shy away from this kind of study. However, it may be possible to piggy back this study now upon previous studies for such things as the long term Cardiac Studies, and others that have been using large population studies begun in the 1950's and meant to be ongoing still.

Various governmental research institutes and Universities have been taking blood samples that might be useful for establishing a baseline for analysing natural mutation rates and possible "Markers" for the aging process in a single generation.

By taking this long term approach the genetics for both a reasonably large population and specific individuals in that population can be compared over a significant period, to include preteen, adult, and even seniscent.

I also think that a review of Geriatric medical studies is called for when looking for indicators of how the Bio-Clock operates in the body.

I am writing this to you AnotherGod, but also to all that have expressed interest in this avenue of study. Different individuals here represent different methodologies and interests that can be integrated to overlap in a constructively synthetic manner to promote our common goal.

I realize that there is a myriad of loosely related data out there and what is called for is a kind of epistomological filter that grants the investigator a means of correlating the necessary studies and approaches in a meaningful way.

For example the Progeria studies can yield constructive genetic information in a relatively short time and I suggest that if you look you will find underfunded studies in progress that already have some data collected. Identifying the specific genes controling this process is absolutely a prerequisite to undertanding how the gene(s) functions and integrates with the whole body's metabolism. And of course that is needed before we can offer any kind of therapeutic alternative.

And again realize that these children have little chance of survival and it would be vital to figure out simply how to "Normalize" their genes, but that processofers the tantalizing prospect that it may also yield significant result in our common quest.

[Lazarus Long]

And here is research and data to support the words above so that I can both eat and digest them.

Which is better to accurately predict the future a hundred years hence and be considered irrelevant or predict the outcome of endevors that will uhnfold in the present only to find that you can't alter the outcome of serious long term hazardous paths?

Monday, 20 January, 2003, 14:36 GMT
Secrets of Ageing Revealed


Telomeres stop genetic material unravelling

Scientists have found a way to measure the tiny mechanism within the body's cells which many believe may hold the key to the ageing process.

The researchers believe the technique will help efforts to pin down the causes of disease such as cancer that become more common as we get older.

It is widely thought that the number of times a cell can divide - and thus reinvigorate tissue - is controlled by the length of a microscopic structure called a telomere.

These structures are found on the end of our chromosomes and in effect stop them from unravelling, acting in the same way as the shiny bit at the end of the bootlace.

However, they get shorter each time a human cell duplicates.

At a certain length the cell stops duplicating altogether.

It is thought that this failure may be behind the ageing process as cells which can no longer divide change the way they work and are capable of actively degrading the tissue/organ in which they reside.

Therefore, it is an advantage to have longer telomeres, as this means cells will keep dividing for longer.


Single cells

Previously it has only been possible to establish an average telomere length from hundreds of thousands of cells.

The new technique, called STELA, can measure telomere length in a single cell from any tissue sample - and pinpoint the shortest ones which are most likely to cause trouble.

It is developed from a technique used in forensic science, where often only a very small amount of DNA is available for analysis.

Using the technique Dr Duncan Baird, of the University of Wales, has shown that telomeres are considerably shorter than previously thought at the point that the cell stops dividing.

He has also shown that there are large differences in the length of telomeres passed on from each of our parents - suggesting that genetics plays a significant role in longevity.

Dr Baird told BBC News Online: "Essentially STELA will allow us to find out whether telomere erosion has anything to do with ageing in humans."

"It may also be of use in analysing the early stages of cancer-early pre-malignant situations."

Mike Lake, Director General of Help The Aged, said: "This is a huge step forward for understanding illness in later life.

"Research into what is happening to our bodies as we get older is vital to enable improvements in medical treatments for older people now and in the future."

Details of the research are published in the journal Nature Genetics.

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