Accelerated Aging Gene Identified

bradbury writes "A host of news sources are carrying news that the gene responsible for Progeria, otherwise known as Hutchinson-Gilford Syndrome, has been identified as Lamin A (LMNA). Sources include a Eureka Alert article, a Science Daily article and a Nature Science Update article. Of interest is the fact that the gene causes at least 6 other genetic diseases. For the hard core science people, an extended discussion of LMNA can be found in the OMIM database here."

Comments

First post

[Anonymous Coward]

First Post!

Now what?

[Blaine Hilton]

Okay they think they have the gene isolated, but now what? How many more years will it take to use this information effectively? It seems like these discoveries are happening faster, but when you are dealing with accelerated aging the people do not have much time to wait.

Re:Now what?

[Ashran]

+0 Obvious

They have to start somewhere - as always.

Re:Now what?

[bradbury]

The logical therapy process is to first isolate the gene, then figure out what it does and/or what goes wrong with it. This may involve determining its 3-D structure. After that one can pursue either computer aided drug design to correct the "function" of the gene, or gene therapy to offset malfunctions or even replace the gene with its normal versions.

One of the real problems with this is that we do not currently have reliable methods for removing the broken genetic code and replacing it with corrected genetic code. But the drug therapy approach may function as an intermediate stopgap measure.

In addition, knowing the gene allows for genetic testing for such defects, so the number of individuals plagued by the disease may decrease in the future.

Re:Now what?

[gene_tailor]

>knowing the gene allows for genetic testing for such defects, so the number of individuals plagued by the disease may decrease in the future.

This is true in principle, but not really applicable in this case because the mutation is 1) very very rare... (one in four to eight million newborns ) so it's unlikely to be worthwhile to reccomend such a test to prospective parents 2) often spontaneously mutated in the patient (the parents didn't have the mutation)

However, this development will let a diagnostic test be developed, so the doctors can figure out if a possible patient actually has this disease or not.

Re:Now what?

[bradbury]

Though the mutations are very very rare, parents would presumably pay not to have a child which would suffer from them. Since in the not so distant future one would presume that all of these genetic tests will be done using chip based technology, having an additional test on the chip for Progeria isn't going to increase the cost significantly. There is obviously a market for a test set for the most "severe" genetic defects which cause birth defects, kill a child prematurely, cause developmental problems, etc. One could consider that it might be a form of cruel punishment or torture to allow a child who would suffer from these conditions to be born.

It is going to be a sticky issue in society to deal with this knowledge.

So does this mean we are gonna invade Progeria?

[Anonymous Coward]

It seems like such a nice little place, really old.

Accelerated Aging Gene

[valkraider]

Spelled: "Children". Having just one is enough to accelerate anyone's aging. Results are directly proportional to the number of kids. Your rate of acceleration may vary.

Re:Accelerated Aging Gene

[SmartGamer]

Well, it is genetic. If your parents didn't have any kids, you aren't likely to have any either.

Identifying Genes...

[teutonic_leech]

... means establishing a roadmap to develop treatments. Many beancounters are wondering how mapping genes is every going to benefit anyone - well, it's like drawing a map, over time you discover relationships which were previously unknown... Once you understand the mechanisms behind those relationships, you are able to design treatments and establish a better understanding of the genesis of genetic deseases.

so...

[The Lynxpro]

Dick Clark has Lamina B???

In my day...

[JDWTopGuy]

Voice: Wheezy old man

In my day, we didn't blame disease and gettin' old on genes and DNA. Heck, we didn't even know what DNA was. Probably thought it meant something dirty. You darn youngsters with all your excuses for everything... da... what was I talking about? Get off my lawn!!!!

This story is missing from the home page

[bobbozzo]

Why are this and other science stories not showing up on the Slashdot home page?

It's now 4/17/03 23:43 GMT

Re:This story is missing from the home page

[knowledgepeacewi]

because slashdot is a fearmongering sensationalist media conglomerate that caters to the lowest common denominator of the nerd community at the behest of the corrupt Republican Regime of the Bloodthirsty Imperialist American Nation.

Accelerated Aging Gene Identified?

[Feztaa]

And when will we see the cure for old?

Re:Accelerated Aging Gene Identified?

[gene_tailor]

First, we have to understand what old IS. No, really -- I'm serious -- we have to figure out what the underlying things are that happen in cells to make them old, before we can try to stop them or reverse them. Unfortunately, as another person already mentioned, this is such a bizarre disease, causing defects in the nuclear membrane, that understanding how it works probably will not tell us much about regular aging. Werner's syndrome, on the other hand, might help....

It's bad enough...

[lowmagnet]

That most of the companies with product placements in BladeRunner were killed by 'The BladeRunner Curse', but now you are telling me that J. F. Sebastian may be cured by then? OK, time to re-make the movie!

Interesting - but not helpful to aging problem

[Muhammar]

Progeria is genetic disorder, patients have defective gene that messes up the nuclear membrane. Hence DNA deffects acumulate fast, cells apoptose and the whole picture is similar to accelerated aging. Understanding the problem will help with the affliction diagnosis, but the underlying mechanism of the damage will probably turn out to be something common, even banal - like oxidative stress that does not get repaired quickly enough.

This may emulate aging, but not explain how to prevent aging.

*BSD is dying

[Anonymous Coward]

It is official; Netcraft now confirms: *BSD is dying

One more crippling bombshell hit the already beleaguered *BSD community when IDC confirmed that *BSD market share has dropped yet again, now down to less than a fraction of 1 percent of all servers. Coming on the heels of a recent Netcraft survey which plainly states that *BSD has lost more market share, this news serves to reinforce what we've known all along. *BSD is collapsing in complete disarray, as fittingly exemplified by failing dead last in the recent Sys Admin comprehensive networking test.

You don't need to be a Kreskin to predict *BSD's future. The hand writing is on the wall: *BSD faces a bleak future. In fact there won't be any future at all for *BSD because *BSD is dying. Things are looking very bad for *BSD. As many of us are already aware, *BSD continues to lose market share. Red ink flows like a river of blood.

FreeBSD is the most endangered of them all, having lost 93% of its core developers. The sudden and unpleasant departures of long time FreeBSD developers Jordan Hubbard and Mike Smith only serve to underscore the point more clearly. There can no longer be any doubt: FreeBSD is dying.

Let's keep to the facts and look at the numbers.

OpenBSD leader Theo states that there are 7000 users of OpenBSD. How many users of NetBSD are there? Let's see. The number of OpenBSD versus NetBSD posts on Usenet is roughly in ratio of 5 to 1. Therefore there are about 7000/5 = 1400 NetBSD users. BSD/OS posts on Usenet are about half of the volume of NetBSD posts. Therefore there are about 700 users of BSD/OS. A recent article put FreeBSD at about 80 percent of the *BSD market. Therefore there are (7000+1400+700)*4 = 36400 FreeBSD users. This is consistent with the number of FreeBSD Usenet posts.

Due to the troubles of Walnut Creek, abysmal sales and so on, FreeBSD went out of business and was taken over by BSDI who sell another troubled OS. Now BSDI is also dead, its corpse turned over to yet another charnel house.

All major surveys show that *BSD has steadily declined in market share. *BSD is very sick and its long term survival prospects are very dim. If *BSD is to survive at all it will be among OS dilettante dabblers. *BSD continues to decay. Nothing short of a miracle could save it at this point in time. For all practical purposes, *BSD is dead.

Fact: *BSD is dying

How good this is.

[azav]

This is really good news and for many reasons.

Progeria is a very sad disease. Imagine having the chance to live and knowing that you'll die at 15 not even being able to be accepted into society. The poor kids look like a big headed child character from the first Star Trek series.

Also, this is evidence that the decoding of our geneome had great benefits for the future. Once we can identify where defects (that cause many dieseases) lie within the DNA and RNA, the next step of finding out how to address them can be approached. It'll take some time but this is a damn good thing for the health of our kids and their friends.

This is a major problem.

[c_jonescc]

Hurry, we need to save Jack

Re:Interesting - but not helpful to aging problem

[bradbury]

An interesting comment. While there isn't yet a direct tie between a defective nuclear membrane and an increased rate of DNA damage defects it seems a reasonable hypothesis. That oxidative stress that doesn't get repaired quickly enough has some merit but doesn't go far enough. It appears that that would lead to an increased number of DNA double strand breaks and that may be the real source of the problem. That is because a significant fraction of double strand breaks are repaired by a process called non-homologous end joining (NHEJ) and that process may actually delete DNA in the process of doing the repair. (For the technical people, this is because the repair process uses exonucleases such as the Artemis protein or the Werner's syndrome protein.)

So, for the programmers on /., its a really simple perspective -- over time the code becomes corrupted.

And next?

[Rubyflame]

When will they find the regular aging gene? We need a cure for that too.

Re:And next?

[Anonymous Coward]

There's already a cure for regular aging. Just get bitten by a vampire, and you'll be immortal. Of course, you'll be a bloodthirsty demon, but you'll look good!

Clearing misconceptions...

[robslimo]

Regarding the statements:
Accelerated Aging Gene Identified
and
the fact that the gene causes at least 6 other genetic diseases

Genes do not exist to "cause disease". Genes have a function and genes which have mutations or inherited flaws can cause disease by not performing their intended function properly.

The gene LMNA codes for Lamin A which is a protein that is a component of the nuclear membrane. When the gene is flawed, the protein is flawed and so are the cells' nuclear membranes. This leads to poor tissue strength and widespread cell death.

Also, I contend that the disease "Progeria" is misnamed. Afflicted persons have symptoms that mimic some symptoms of ageing, but are marginally related. I further believe that while many bio-medical insights may be found in the pursuit of a cure or treatment for Progeria, the results will have little or no impact on treatments for true ageing.

Still, any new knowledge about our genetic makeup and processes is good.

Re:Now what? (clarification)

[gene_tailor]

>all of these genetic tests will be done using chip based technology

OK, Bradbury, you are probably right when you are looking ahead some number of years and suggesting thousands of tests will go on a single chip. In that case LMNA defects will surely make the list. I was looking at the short-term case, where each test is still done individually at a cost of several humdred bucks, through a genetic counselor, and thinking that the rarity of this one makes in uneconomical to even bother to develop such a test for this individual disease.