211 replies to this topic

[Karomesis]

as a layman, I see the battle against aging similar to investing. the biggest risks seem to provide the biggest payoffs. is this true in a general sense with aging?

from what I understand, gene therapy/engineering provides massive benefits or catastrophic disaster depending on which gene is affected, wouldn't it be easier to test and retest a bunch of genes to get to escape velocity that much faster? and wouldn't the speed of computation assist in this research?

[Aegist]

Because 'testing genes' is not a binary action. With the many thousands of genes in humans, there is no simple 'test' for each of them. There are about a billion permutations of every gene which could yield better or worse results, plus there is an infinite number of potential new genes which could be created from latent DNA and pseudogenes which could help or hinder ageing.

Gene therapy is only helpful when you have a gene manipulation which you know will help, once you ahve that information, then you can worry about implementing it.

[John Schloendorn]

Like everywhere, is is hard to get a payoff without a risk, and easy to get a risk without a payoff..

[Karomesis]

Because 'testing genes' is not a binary action. With the many thousands of genes in humans, there is no simple 'test' for each of them. There are about a billion permutations of every gene which could yield better or worse results, plus there is an infinite number of potential new genes which could be created from latent DNA and pseudogenes which could help or hinder ageing.

isn't there a catalog of genes, a database that essentially points us in the right direction as far as what to test? and likely outcomes of it's efficacy.

I guess that's what I should've said initially. I'm not saying to test every permutation that could exist.

[Aegist]

Because 'testing genes' is not a binary action. With the many thousands of genes in humans, there is no simple 'test' for each of them. There are about a billion permutations of every gene which could yield better or worse results, plus there is an infinite number of potential new genes which could be created from latent DNA and pseudogenes which could help or hinder ageing.

isn't there a catalog of genes, a database that essentially points us in the right direction as far as what to test? and likely outcomes of it's efficacy.

I guess that's what I should've said initially. I'm not saying to test every permutation that could exist.

The Human Genome allows us to predict where genes are by virtue of appropriate promotor sequences, initiation sites, start stop codons etc. So we do have a 'catalogue' of every gene, but we have no idea what the vast majority of those genes do. Nonetheless, as i said originally, it isn't a binary action. pick any one gene...what do you want to do with it? Disabling it may be a binary sort of action, and easy enough to do, but it is very unlikely that disabling any number of genes will ever yield any great solutions to ageing. (maybe i'm wrong...but it seems very unreasonable to me) more likely you will ahve to manipulate the bahaviour of genes, which could be done any billion number of ways. The outcomes of which we still ahve no method of predicting.

[Karomesis]

what are the theoretical limitations of stem cells, specifically ESC?

i.e. if we had ESC treatments for every single cell type in humans, how long would we live and why?

How much damage can ESC reverse? I apologize if my question is too broad, I'll narrow it down depending upon the responses from you pros. [glasses]

[John Schloendorn]

Not necessarily too broad, but unanswerable without doing the experiment ;-)

[Karomesis]

Not necessarily too broad, but unanswerable without doing the experiment ;-)

haven't we already seen some studies with late stage heart disease being treated with ESC? and the outcome was an increase in LVEF from what I remember.

[John Schloendorn]

No cells derived from ESC in vitro have ever been used in humans. Even they had been, that wouldn't tell us anything about how much longer we would live if hypothetical ESC were applied "for every single cell type", because we don't know what these hypothetical treatments would be like.

How much damage can ESC reverse?

In theory, well screened ESC should be almost free from age-related damage, because a biologically young generation of new organisms develops from them without terribly much further selection.

[Karomesis]

http://www.telomolec...lomolecular.asp

as I understand it, they're saying that repairing telomeres will alleviate many age realted diseases and even are so bold to declare that they would like to do away with the aging process itself.

are there any nanotech pro's here who would care to elaborate on the feasibility/science behind the company's stated objectives.

the whole things seems almost too simple, but I may in fact be completely wrong as I have no expertise in this area.

[caston]

Is mitochondrial transfer between humans possible?

for example during sex

[Brainbox]

The Human Genome allows us to predict where genes are by virtue  of appropriate promotor sequences, initiation sites, start stop codons etc. So we do have a 'catalogue' of every gene, but we have no idea what the vast majority of those genes do. Nonetheless, as i said originally, it isn't a binary action. pick any one gene...what do you want to do with it? Disabling it may be a binary sort of action, and easy enough to do, but it is very unlikely that disabling any number of genes will ever yield any great solutions to ageing. (maybe i'm wrong...but it seems very unreasonable to me) more likely you will ahve to manipulate the bahaviour of genes, which could be done any billion number of ways. The outcomes of which we still ahve no method of predicting.

No one said this explicitly, but as far as I'm understanding (layman extraordinaire), there are also lots of dependencies between the action of genes? So, the predictability of manipulating one gene is additionally complex since it depends on the presence of other genes as well?

[AdamSummerfield]

I have a question on my mind,
At the magnifications that reveal the details of organelles, we can see a 2-dimensional slice of the cell. We can also see many monocoloured dots filling the cell-space. Each molecule or ion will reflect light at a specific wavelength (or reflect an electron that will give us a specific wavelength to be converted into a visible image on a computer). Does each dot seen in TEM images denote one molecule each? I have also found a sentence in Wikipedia stating that

"spherical aberration has allowed the production of images with sufficient resolution to show carbon atoms in diamond separated by only 89 picometers"

which shows that we do observe matter at this level.

[pyre]

what would bulk deubiquination cause, or bulk decitrullination since modifying acetylation causes a large beneficial change here are guesses

ubiquinone labels things to be labelled as junk

citrullination causes things to be labeled "make inflammation" wikipedia says: get citrullinated during cell-death and tissue inflammation
that sounds like decitrullination chemicals might be a longevity candidate drug

I don't know a whole lot about citrullination, but in studying immunology I've run into ubiquitin a lot.

I worry about mass ubiquitination, because we are realizing that ubiquitination can act as an activating or deactivating enzyme-substrate reaction just as phosphoryllation/dephosphoryllation can. For example, the NFkB pathway-regulating enzyme A20 deubiquitinates at one Lys residue to increase its function and at another to be marked for destruction. The proteins that it takes the polyubiquitin chains from are important immune modulators such as NEMO and TRAV6. (Boone et al. 2004)

Your thought about using 'clean-up' markers to reduce intra- and extra-cellular junk is interesting, and perhaps is worth looking into, perhaps a mouse with a KI Ubiquinone, Citrullinataion protein, or a deacetylase inhibitor as a better marker of possible longevity increase.

Thanks for your thoughts.

[fly0]

Hi,

how many mitochondria does a human ovum contain? And how many different mitochondrial genomes?

Thanks in advance for answers!

[kent23]

Hi fly0,

According to Shoubridge and Wai (2007), "Mature oocytes contain at least 100,000 copies of mtDNA, organized at 1-2 copies per organelle. " So that would be 50,000-100,000 mitochondria per "mature oocyte", by which I think they mean "ovum" in the strict post-meiotic sense.

See:
http://www.ncbi.nlm....Pubmed_RVDocSum

Why do you want to know? (I'm curious.)

[fly0]

Thank you kent23,

I'm asking just out of curiosity. What I really want to know is how many different mitochondrial genomes a human possesses, not counting minor (possibly somatic) mutations. From the article you quoted it couldn't be more than about 10-20 since about 10 mitochondria are contained within a primordial germ cell.

[RCollins]

What animal is considered to have the longest lifespan? Whales, lobsters, albatross, or something else?

[Lazarus Long]

Of the 3 you list I actually think it is lobsters assuming they don't become someone else's food but sea urchins can live longer. Some whales can live over 100 years as well as some birds but some lobsters and turtles can live centuries.

Recently a whale over 120 years was killed a lobster at around a 100 but it is estimated that before they became a staple diet of humans that some lived to 150.

http://www.seasabres...obsterfacts.htm

Sea urchins also live to 100 years on average but it is estimated that they could live to 200 without us messing up their environments.
http://oregonstate.e...ov03/urchin.htm

According to the age of the harpoon tip found in this bowhead whale it appears he was at least 115 and up to 130 years old.
http://www.usatoday....-12-whale_N.htm

The albatross by comparison is only about 50 years on average but there are parrots, macaws, and cockatoos that live from 80 to about 100 and sometimes over.

http://en.wikipedia.org/wiki/Albatross

[Lazarus Long]

While I was looking up some references for that reply I found this recent study studying senescence characteristics in the grey headed albatross

Senescence effects in an extremely long-lived bird: the grey-headed albatross Thalassarche chrysostoma
http://www.pubmedcen...i?artid=1634918

What I found interesting in the study is toward the end when they do a comparative analysis of aging in the birds versus humans.

Also this one that studied telomere shortening in longer lived birds and mammals finding it to be less than in shorter lived ones.

Telomeres Shorten More Slowly in Long-Lived Birds and Mammals than in Short-Lived Ones
http://links.jstor.o...2...>2.0.CO;2-6

[Epsilion]

I have a question.

I have read many articles in many journals talking about telomerase.
We know that it is widely use for cells immortalisation. Some researcher argued in their articles that activated
telomerase in immortalised cells could possibly lead to malignant phenotype (tumor) but without proof of their claims.
Many paper shows that these claims were unfounded and that experiments has no showed any evidence of
tumor formation linked to activated telomerase in somatic cells [1]. This said, we can agree that telomerase could be
something that could be use to extend lifespan.

My question is : Is there any papers about geneticaly modifying an organism (mouse, drosophila, c elegan or else) to have telomerase expressed in all their somatics cells? If so, I would like to have the reference. I have search a lot for this kind
of paper but I could'nt find any. I am eager to see what would be the results of an organism with full telomerase activity on all cells.


[1]Jiang, Xu-Rong; Jimenez, Gretchen; Chang, Edwin; Frolkis, Maria; Kusler, Brenda; Sage, Marijke; Beeche, Michelle; Bodnar, Andrea G.; Wahl, Geoffrey M.; Tlsty, Thea D.; Chiu, Choy-Pik. Telomerase expression in human somatic cells does not induce changes associated with a transformed phenotype. Nature Genetics (1999), 21(1), 111-114.

[maestro949]

as a layman, I see the battle against aging similar to investing. the biggest risks seem to provide the biggest payoffs. is this true in a general sense with aging?

from what I understand, gene therapy/engineering provides massive benefits or catastrophic disaster depending on which gene is affected, wouldn't it be easier to test and retest a bunch of genes to get to escape velocity that much faster? and wouldn't the speed of computation assist in this research?

Here's a more optimistic reply. I started babbling on so I just decided to make it a blog post...

[John Schloendorn]

Is there any papers about geneticaly modifying an organism (mouse, drosophila, c elegan or else) to have telomerase expressed in all their somatics cells?

Try this: Gonzalez-Suarez E, Geserick C, Flores JM, Blasco MA. Antagonistic effects of telomerase on cancer and aging in K5-m TERT transgenic mice. Oncogene 2005; 24(13):2256-70.

[Ben]

I had a look on Google and I'm having difficulty pinning down information on c-reactive protein and its relation to SENS and inflammation.

Can anyone help me out? Some links to good resources would be great.

[Anthony_Loera]

I have a question.

I have read many articles in many journals talking about telomerase.
We know that it is widely use for cells immortalisation. Some researcher argued in their articles that activated
telomerase in immortalised cells could possibly lead to malignant phenotype (tumor) but without proof of their claims.
Many paper shows that these claims were unfounded and that experiments has no showed any evidence of
tumor formation linked to activated telomerase in somatic cells [1]. This said, we can agree that telomerase could be
something that could be use to extend lifespan.


[/size]

Maybe you have already seen this... but I find it fascinating:
UCLA PowerPoint (3.5 Megs)

Unfortunately I don't have an audio recording of this, but look at the powerpoint attached for a Pathology postdoc at UCLA who now has gone to work full time for Cal Harley at Geron Corp. in Menlo Park, CA.

I was given this by a prof that stated:
New clinical data from AIDS patients at UCLA is available that discredits the notion that telomere elongation will increase the risk of cancer. Look especially at the Conclusion Slide (No. 99; fourth bullet).

A

[brokenportal]

What are the best peer reviewed journals for aging, sens, engineering and relevant stuff? And are they free or not?

[Nova]

Nano the robot gets into a brain bark, of the robot get out àxon and is attached to àxson neuron a brain and nano the robot gives out itself for same neuron as well as all others. The brain does not see a difference between àxson own neuron and àxson shoots nano the robot. Commands on thinking arrive both to neuron own and to nano to the robot which writes down the information on the computer and receives the answer from a database. The additional library for the young man where the information is loaded into library from the old person thus turns out. In a similar way the information can be downloaded in the computer where downloading goes with àxon constant memory.

It is possible to create the molecular computer for such robot?

[tachyon]

Hi everyone,

I'm a "newborn" imminist member and I was wondering what currently known nootropic is to be taken when one desires to increase his/her memory.
I have already checked some posts concerning this matter and I found that reversatrol, piracetam and modafinil are the ones that are focussed on this site.
Are these the only ones that have shown to benefit cognitive functions? I am well aware that reversatrol is mainly an "anti-aging" nootropic.

Thanks in advance.

[elvis1]

I would like to know what I should ask my doc to give me : i currently have pramipexol 0.25 mg 2-3 hours before sleep as I have RLS and I take it together with 1 mg of ezopiclone (before sleeping). During the day I have 100-200 mg of modafinil and I feel just as If I am getting used to it and with no energy at all ( moda gives me concentration for only 2 hours at max). I feel tired during a normal day. What should I do? Is there anything else I should input for you to help me?

[Tungsten]

Greetings, all!

As indicated by my post count, I'm rather a newbie to the Institute. I've known about the place for some time, but never really got into the forums (obviously). Anyway, here's the deal. I want to be one of the persons assisting in anti-aging research, and as I understand it genetic engineering is probably the best way to go about it at our current technological level. Obviously this will require a good deal of education before I'm ready for it.

So my question is this: what schools in the U.S. have the best programs for an aspiring bioengineer? I'm sure a Google search would lend some promising results, but I think the members of this forum would know which ones cater to our, ah, particular goals.

Thanks in advance,
Tungsten