A Short Interview with George Church on Genetics and the Treatment of Aging

The Life Extension Advocacy Foundation volunteers recently interviewed George Church, one of the leaders in the research community who has come around these past few years to speak out in public as being very much in favor of treating aging as a medical condition. I point this out largely because they ask about some of his recent comments regarding timelines in the near future development of anti-aging therapies. He thinks that the first are only a few years away, which is indeed true from my perspective given what is happening in the development of senolytics to clear senescent cells, but Church doesn't have senolytics in mind when he says this. He is one of the luminaries of modern genetic biotechnology, and he sees the future through that lens.

Professor George Church - Turning Back Time to End Age-related Diseases

You recently said that you "predict we are about to end the aging process. In the next five years no less!" Whilst progress has indeed been rapid in the field of rejuvenation biotechnology, could you clarify, is this five years to achieving this in human cells, to clinical trials or what exactly?

Within five years it seems plausible to have some gene therapies in FDA approved clinical trials in dogs - aimed at general aging reversal, but quite likely, labeled for specific diseases (and in humans soon thereafter). This means combinations of gene therapies aimed at most of the known major aging pathways, though there are major challenges in efficient delivery.

Do you agree that epigenetic alterations as described in the Hallmarks of Aging are a primary driver of the aging process, and if so do you think we can safely use cell reprogramming factors OSKM (OCT4, SOX2, KLF4 and MYC) to turn back cellular aging?

Yes. Epigenetics are important drivers, but it are only part of the Hallmarks of Aging - and OSKM would, in turn, be only part of that. Other examples are factors behind heterochronic parabiosis. Efficacy may depend on the various tissue types.

DNA damage is proposed to be a primary reason we age. Can it be repaired by targeting TFAM (Transcription factor A, mitochondrial precursor) to increase NAD (a coenzyme in all living cells that facilitates the production of energy) levels that are known to facilitate DNA repair?

We have targeted TFAM and consequently raised NAD successfully. The NAD-facilitated repair is not the only route - we can prevent DNA damage (via the management of radical oxygen species), prevent the impact of such damage (e.g. duplicating tumor suppressor genes), favor specific types of DNA repair, or induce apoptosis in cells which appear to acquire potentially oncogenic mutations.

Cancer is caused by an unstable genome resulting from DNA damage and could be considered the poster child of aging diseases, can we use CRISPR to defeat cancer?

Genome editing (TALENs, CRISPR, etc.) and transgenic methods (CART) are being 'successfully' applied, but proof of generality and long remission is not here yet. Effective alternatives are preventative - vaccines against some of the 11 infectious, cancer-causing agents (e.g. HPV), inherited genome sequencing, genetic counseling, prophylactic surgery and avoiding environmental risk factors. Some strategies which work to preventatively reduce cancer in mice might benefit from engineering germline or more efficient delivery of gene therapies (since single untreated cells matter more for cancer than other diseases).

Do you think we can learn useful knowledge that can be applied to humans from the whole-genome sequencing of long lived species such as the 400-year-old greenland shark?

The most promising sequencing insights will probably come from genomes closest to average humans, such as naked mole rat, bowhead whales and human supercentenarians. Even more crucial is low-cost, high-accuracy testing of hypotheses flowing from those sequences, plus already hundreds of hypotheses from model organisms and cell biology (see the GenAge database).

Genetics is an enormous area, even when you narrow down the scope to genetic biotechnologies that can be used to build therapies relevant to aging. There are numerous different things going on, not all of which we should be equally enthused by. I'll draw some fairly arbitrary lines here to demarcate three classes of genetic therapy. The first broad class of work is very similar to existing pharmaceutical development: the construction of means to temporarily alter the level of a particular protein or interfere in one or more interactions carried out by this protein. Genetic technologies hold the promise of being able to carry out this task with far greater accuracy and control over the size of the outcome. The second class of work involves the creation of permanent effects by adding or removing DNA in a targeted fashion, such as to provide a functional copy of a gene that is broken as a result of an inherited mutation. This is not yet practical for therapies applied to human adults due to challenges in obtaining reliable, comprehensive cell coverage, meaning introducing the new DNA into enough cells, and especially stem cells, to produce a significant and lasting effect. But that goal lies very close in the near future.

The third class of work involves more complicated use of genetic machinery. The production of programmable DNA machines that can read cell state, react, and carry out logical operations to produce different outcomes for different circumstances, for example. The Oisin Biotechnologies approach to targeted cell destruction is one such early, simple machine. Far more complex machinery is obviously possible, given the existence of cells in the first place. This class of more complicated uses also include applications of gene therapy that achieve a more devious and multi-layered goal than just inserting a gene that will result in proteins being produced. For example, allotopic expression of mitochondrial genes involves inserting altered versions of mitochondrial genes into nuclear DNA, their usual sequences wrapped in such a way that cellular transport machinery will pick it up these altered proteins, move them back to the mitochondria, and then import them into mitochondria, ending up with a copy of the original protein at the end of that process.

Now, much of the first category of genetic engineering, tinkering with levels of specific genes, will be just as marginal for the treatment of aging as the pharmaceutical approaches that preceded them. That is inherent in the proteins and genes being targeted. When the goal is mimicking the response to calorie restriction, or increasing autophagy, or similar alterations shown to modestly slow down aging in laboratory animals, then the small size and lack of reliability in the outcome is as much inherent in the target as it is in the method used to manipulate the target. These mainstream efforts are only slightly increasing resistance to the consequences of molecular damage in aging, or slightly slowing the accumulation of that damage. They are not truly effective means of addressing aging.

We should nonetheless expect to find that some targets accessible to genetic methods are a lot better than those that can be or have been manipulated via drugs. There are some promising genetic variants that exist in the wild and have far larger effects on human cholesterol levels than the best drugs, such as statins, for example. There is myostatin and follistatin, that can be targeted to increase muscle growth to a far greater degree than any pharmaceutical method, and thus resist age-related loss of muscle mass. But these are still not repair therapies. They are only ways to better compensate somewhat for the losses and damage of aging. The damage will still win if it is not addressed.

So what George Church describes in the short term is really just the application of genetics to the ongoing pharmaceutical tinkering with metabolism that has achieved little of any practical use in the past few decades. All that has been gained is knowledge. What he describes in the longer term is the much more ambitious project of rebuilding the human genome, one small step at a time, to create packages of changes that result in slower aging, greater resistance to the consequences of aging, and other enhancements to the human condition. This is an immense project of vast scope and complexity. It will happen in the fullness of time, but it cannot possibly produce anywhere near as good an outcome in the next few decades as the alternative approach of keeping the present baseline human genome unmodified, and focusing on periodic repair of the molecular damage that arises as a side-effect of the normal operation of metabolism. The research community has a far better roadmap for this goal, there is far less to achieve, and it is a much easier set of projects, where far more is known of what must be done. Genetics with the goal of improving humanity is seductive, as the long-term potential is truly amazing - but unless we address the damage first, we'll all be long dead before that potential is reached.


I typically agree with you Reason but I think when it comes to this your argument starts to lose clarity.

Let's think about stem cell therapies. One of the most important branches of SENS even though Aubrey neglected it for 15 years (until very recently) - well, we know allogenic sources of stem cells are simply not applicable to what we want to achieve.

So we need therapies making use of autologous stem cells, that and a receptive environment, and the right signals on top of it all - those can only be achieved with the use of genetics. Furthermore if there is a way to reprogram cells in vivo and it's safe I think the quite sizable problem of delivery - something which is mentioned only as a passing note in SENS and not considered a legitimate strand, but is a well know and quite serious problem - will become irrelevant.

Secondly, George Church did mention killing cells which are too far gone to be of use - that's even more ambitious than clearing senescent cells - I think he would have said senescent cell if he thought of those in that instant. Senescence is a good measure of cell quality currently but if we could clear the bad cells before they become senescent then we'd be doing one better.
You pointed out yourself Oisin is basically doing genetics...

I don't value one plan over the other. Both have their high points, for stem cells direct reprogramming is - with all the information we have currently - the superior one. Injecting stem cells in a gel or some other emulsion is pretty good if you want to get a ton of cells of ONE type inside the body fast, but that's only good for treating a disease. How would we do that for every stem cell type? On what schedule? In what clinic? How much would it cost? How would the healthcare system handle this crazy load of constantly manufacturing personalized cells?
Quite honestly - it's impossible.

If anything direct reprogramming IS THE FAST WAY TO RepleniSENS. Not the other way around. I think Aubrey should seriously consider making the use of reprogramming factors a recognized and preferred method for RepleniSENS at this point - if the aim is SENS being finished by 2025 that's about the only option he has I think.

Posted by: Anonymoose at August 1st, 2017 9:11 PM

@Anonymoose: What I'm saying here is that, (a) gene therapy approaches to targeting e.g. mTOR are not going to be all that different from pharmaceutical approaches in their upside, despite being potentially more effective at achieving that goal, because the goal of adjusting metabolism to slow aging is the problem, not the method by which you do that, and (b) there are a range of compensatory approaches to aging that become practical with genetic technologies, such as myostatin knockout, that will be better than those presently available, but they aren't a replacement for SENS because they don't repair damage, and (c) there are genetic technologies that are a part of the overall SENS-like damage repair approach, and (d) there is this glowing future of an edited, improved humanity with a reworked genome that is a very long-term project and shouldn't even be on the radar right now, (e) I think Church appears to my eyes to be overly supportive of work that falls under (a), overestimating its potential, or similar.

Posted by: Reason at August 1st, 2017 9:27 PM

@Anonymoose - the only reason the SENS RF would have to fund stem cell work would be if no one else was funding it, and that is not the case.

Yes stem cell delivery looks like a problem every bit as difficult as delivery in gene therapy has turned out to be, but again, plenty of research is already being done on this problem.

Posted by: Jim at August 1st, 2017 9:38 PM

He seems to be much more concentrated on parabiosis than MTOR from the few interviews I've read. If anything he'd probably put myostatin knockout as a very high priority.

If gene therapies are to be accepted we probably will have to start with something simple and well known like MTOR inhibition. Scientists have been working on it for 40 years. If we have a gene therapy that directly does that people like Barzilai won't have an excuse to waste money on developing drugs for it.

I see many indirect positives to what Church is doing. As well as the obvious direct ones.

Posted by: Anonymoose at August 1st, 2017 9:38 PM

Absolutely no research is being done on delivering multiple cell types continuously. I don't think anyone in the field even considered it a possibility, or indeed - a sane thing to do.

Posted by: Anonymoose at August 1st, 2017 9:44 PM

@Anonymoose wouldn't it be amazing to deliver multiple cell types continuously? How else are we going to use stem cells for comprehensive rejuvenation!? The human body has many different cell types and i think we might have to rejuvenate all cell types. Am i wrong?

Posted by: Akschith at August 1st, 2017 11:48 PM

Hi ! Great interview,

Just my 2 cents,

The more I hear about stem cell, the more I'm lost, it'S so all over the place. But, one thing (I feel) seems to come out; stem cells are health improvers and Median Lifespan determinants - not Maximal lifespan (That's the domain of replicative senescence and telomeres). How so ? Well for example, one study found that aging is accompanied by MicroRNA loss and that some miRNAs dictate/orchestrate all of this, some miRNAs are elevated in aging while some are lost; guess which ones are good and bad ? Exactly, the ones that are good are the ones that control genetic pathways relating to IGF/Insulin/mTOR and anti-inflammation (they increase IL-10, TGbeta and anti-inflammatory genes), while the bad ones which increase - activate TNF-alpha and IL-6 inflammatory cytokines). This was found in the CSF (cerebro spinal fluid) of elders whose miRNAs in it were different from in young people (said good ones lowered and said bad ones increased). But, now for the kicker, this was in the Hypothalamus, the hypothalamus contains stem cells which control aging (supposedly) in the entire body (since the brain is the key player here to longevity and aging slowdown (from neurons control)), I think the right word would be control 'inflammation' and thus, oxidative stress from said inflammation; and thus, Median average liefspan - Not maximal lifespan. Why ? Because another study done on centenarians showed that they kept the 'stem cell niche' longer (mor quiescent) and with less damage (they did not run out of stem cells and they were less damaged to being with 'Younger'...taller telomeres). Thus, centenarians had longer 'tissue homeostasis' (longer 'health') which helped to reach over a 100 years old - but why do they die at 122 or 140 (I read a south american man supposedly lived 140, doubt it but it could be possible if unlikely; it stops mostly at 120-150 (because telomeres are too low - replicative senescence)). I put faith in RepliniSENS but not too much, for health definitely, I mean stem cells - it's all over the place - and now, if we might remove the niche altogether it could change something (most likely not), instead of doing 'stem jell injeciton' (it's almost futile is mouse so far, always gives about 20% helath extension that's it). But of course that's just for stem cell, if combines with the others it becomes more powerful so we'll have to see what the other therapies (LYso SENS, and the others, will do, allotopic expression, I'm not sure about this; I mean studies have increased ATP (like the ATP allotopic gene success) and it makes almost no difference. Like it said here, it sesms damages just Win altogether, I wonder how SENS will circumvent the problems like DNA admage, SSBs, DSBs, replicative senescence, telomere loss, histone loss, lamina messing up, chromosome decompacting, methyl loss, and so forth. No answer.
CR is still the way to go (funny because one miRNA 'Activates' CR, litterally). ANd studies that have 'boosted' miRNA that are anti-inflammatory in mice and reduced the 'inflammatory' miRNA - made barely 20% avg. lifespan extension - in mice that were already progeric. IT means that CR, by metabolism slowing, can't stop aging (evidently); and repairing damage could be the only solution (as gene reprogramming (iPSCs and yamanaka Sox Oct Nanog carry cancer danger and not that strong in effect either - again all of this ends up being health boost but not driving the 'intrinsic aging' process - which is different (and is controlled by replicative senescence/Hayflick limit; and telomere loss thatregulates entry/conversion to replicative senescence once cell cycle arrest happens). Here's one more demonstration that aging and health are different (yet the same, but different thus not Exactly the same and identifiable as two things (and the 'same pseudo' thing). One study compared centenarians with anemia and without anemia; and it showed that the anemia ones had lower hemoglobin levels, were unhealthy, and - were Centenarians Too. Just like those 'healthy' centenarains with higher hemoglobin levels. So no, health is not the determinant of Intrinsic Aging, is the second state that is to bekept in 'homeostasis' for tissue homeostasis and 'normal aging to death' of it. It has a threshold (too much damage and you die - Now), if you keep healthy you cuold live a 100; if you keep sick you could Die younger - Or, Live To A 100 Years Old Frail just like these anemia ones (lenghty period of 'frailty/decrepetidue/unhealthyness' - yet Outliving other 'healthy people' who die suddenly, Before You). Of course SENS therapies will make a 'morbidity compression' (it's almost assured but not a certainty), where people 'Stay Healthy' until they are 122 and then in 1 month it 'goes (from) bad to worse (to Final)' and they die at 122 +1 month. We so Optimized - that we can Live a 100 Years SICK. Of course, these people that do reach that are the micro %, the Rest of the pop. 85-90% Die from being sick/unhealthy because they don't have the magic genetic to protect them from the onset of diseases with time and thus, inflammation (that centenarians/super-centenarians had the genes - remember, elders lost microRNAs that are anti-inflammatory because they activate CR and IL-10/TGb and other protection; they got more inflammatory ones; while the centenarians kepth the ones found in 'young people'. This was in the hypothalamus; brain degenerescence is impossible with Longevity; the hypothalamus houses stem cells - they control 'health homeostasis' (not 'intrinsic aging')) - keep a solid brain and a solid hypothalamus and you slow aging because more anti-inflammatory miRNA in CSF. But, not that won't make you live above 122 either because it is not the intrinsic aging mechanism. So stem cell is iffy). :)

Just my 2 cents.

Posted by: CANanonymity at August 2nd, 2017 1:33 AM

Ps :''The more I hear about stem cell, the more I'm lost, it'S so all over the place. But, one thing (I feel) seems to come out; stem cells are health improvers and Median Lifespan determinants - not Maximal lifespan (That's the domain of replicative senescence and telomeres).'' If All stem cells could replace nearly or All Cells, continuously (like forever), I guess then, the problem would be solved. But, therein lies the problem, the stem cells themselves - that are bound by the same mechanism (replicative senescence and telomere loss, they lose them too and one day, stem cells can't do replace cells, like they did long ago; that's when you run out of 'tissue renewal'). Continous stem cell replacement has given healthspan improvement but not much in terms of MLSP, because it was not enough (or Enough/Type/All stem cells to Replace All/Types of cells in tissues - to make Total Reversal of Aging)). Perhaps that's what is lacking, it being capable of delivering everytype of cell possible to replace Everything (or nearly), then this would be enough to keep the tissue Renewal/homeostasis 'frozen' (not lowering, thus non-aging). But, seeing it's so difficult just for 'some stem cells'; I think All Cells/MANY type of stem cells cocktail delivery is just too demanding right now. As such, it is still, 'certain' type stem cells are delivere, yielding 'certain' poorer results. And perhaps, also, not enough of them. So it's a Diversification, Quantity and Quality Thing to Cover the whole Thing in the body. Even then, I hold certain doubt that all the types of (billion) stem cells will mobilize and do magic to reverse us to 20 years old. I want to believe that it is possible because it could very well be. I just also hope that indeed, instrinc aging could be twarthed by this stem cell renewal concept, but hold doubt. Let's hope.

Posted by: CANanonymity at August 2nd, 2017 2:42 AM

Its an interesting perspective CANanonymity - I read a paper discussing how inflammation helps normal cells become more stemlike, so they can respond to damage, and also spurs stem cells into action - but inflammation needs to go back down unless stem cells remain locked in undifferentiated state, and normal cells in the inflamed area stay stem-like too, which heightens chance of cancer, etc., if left too long.

So we can start to see the picture here of how we need to control inflammation and senescent cells in order to have our stem cells work properly (we need this inflammation in an acute response, but it needs to resolve quickly, which it can't do if the background level is too high). This will keep us healthy.

But yes, it appears you are right, even with nice low levels of background inflammation stem cells will not be able to proliferate forever, due to loss of telomeres - hence the success of (intermittent) inhibition of MTOR with rapamycin, which not only limits cell geroconversion to senescence, and controls inflammation, but also slows down proliferation so you can get a MLSP extension. Incidentally you wouldn't want to inhibit MTOR genetically - as it needs to be intermittent, otherwise the fast proliferating cells of the immune system, gut, etc., can't do their job - plus if done too young (before adulthood) it would screw up development.

So for all these reasons we are going to have to use some kind of compete body comprehensive telomere extension or cell rejuvenation in situ to beat MLSP.

Posted by: Mark at August 2nd, 2017 5:00 AM

I though we already went over this.

First off what do you mean by stem cell therapy is the question?
Are you thinking getting old cells from an old body and forcing them to divide rapidly and put them to even more stress making them older and putting them back in?
That's not going to make you younger.

Do you mean taking stem cells from a younger individual and putting them inside an older one? Still not going to make you younger because generally your immune system will hunt those down and eliminate them so you'd only get the short lived benefit of the signals they produce. Not to mention it's not a sustainable method anyway.

Are you thinking reprogramming your own stem cells ex vivo? That process does in fact reset telomere length. But then the problem is you have to put all the stem cells back in, and besides it's easier to reprogram cells which are closer to the type of cell you want to yield and then you have to put them all back. Technically feasible, practically impossible.

Doing the reprogramming in vivo, if it is safely possible, will make it something we can achieve in the foreseeable future.

There are further methods that can be used - somatic cell nuclear transfer can be used to create embryonic cells with your own DNA ex vivo. But that is a burdensome process like all the other ex vivo methods, not to mention it's considered of questionable ethical standing and to top it off it's just as unsustainable as any other embryonic stem cell therapy.

And finally something for the future - synthesizing cells completely artificially - in this case we would still require to put them back in, but considering we'd be able to make these cells cheaply, with greater QC than any other method and free of any stressors that they are put through to expand for a therapy - whether they expand inside or outside your body, there is benefit so it's something to consider. Maybe at that point we'd have figured out how to deliver them safely and efficiently.

Since we are currently stuck on the first method which is also the worst method even if there is another hurdle to overcome, the bigger one right now is the cells we use are not better than what is already in the patient be it animal or human and our method of taking the cells out, expanding them and putting them back in probably makes them worse than they were to begin with - direct reprogramming is definitely a step from this if we can make it work.

Ultimately we might need to include some sort of a signaling cocktail with the cells or maybe modify them genetically for them to work perfectly. But that's a long way from where we are now. We need to get good stem cells inside a body first to see what the hell happens and find a way of doing it consistently. Hard to build theories without robust data - we might or might not need a forced whole body cell turnover like I proposed last time - but we have no way of knowing that currently.

As I said last time, we are making the first steps on a long path. SENS was not meant to make you non-aging. It's meant to give you 30 years and if you're lucky you'll get an extra 30 years by the time those 30 years are gone - that has always been the deal. If you give up on the starting line you will obviously not make it beyond that line.

Posted by: Anonymoose at August 2nd, 2017 8:02 AM

BTW direct reprogramming is quite possibly more than enough to get you to your highly vaunted 120 because it emulates having centenarian genes.

Of course if you have good genes in general, because there is damage beyond stem cell exhaustion you have to contend with. But with reprogramming more people will reach centenarian age and I would not be surprised when we overcome the current record.

Breaking beyond that barrier is currently a meaningless thing to think about. If we can get most people to 120 then think about the beyond. You people constantly try to jump over the hardest part which is getting most people to 120 in the first place.

Pace yourself. You can't sprint a marathon.

Posted by: Anonymoose at August 2nd, 2017 8:15 AM

How do you keep the hypothalamus healthy and give it longevity. It may be rather simple, you need the right kind and amount of FOXO3a and FOXO6 (longevity genes), which are found in the hypothalamus and confer to it longevity properties. But you must have the right SNP's and alleles of each SNP. I am homozygous for the longevity alleles of at least 12 FOXO3A SNP's that researchers from around the World have shown to confer longevity benefits. So now why don't we use CRISPR to give people a block of these longevity SNP's. It will reduce aging in the hypothalamus and all over the body, because that is what the FOXO3A gene does. In 2011, there was a Boston study comparing 25 longevity SNP's throughout the genome for a 114 year old man and a 114 year old woman. The man who was the second oldest verified man ever in the World (a Japanese man has since died at just over 116) had was homozygous for the 5 FOXO3A SNP alleles, and was probably mostly responsible for his long life. He may have been homozygous for a dozen other FOXO3A SNP alleles but only 5 FOXO3A SNP's were used in the study. The woman did not have any of the FOXO3A longevity alleles, so maybe women are more dependent of FOXO1A as various researchers have shown.

Posted by: Biotechy at August 2nd, 2017 8:25 AM

Anonymoose - why are we spending so much time agonizing over stem cell rejuvenation methods, when Blasco et al have done such great work rejuvenating aged mice with AAV HTERT therapy? Surely this is a better short term fix: get telomerase expressed for a short period in many cell types.


Also looks like the worries about cancer were unfounded. I believe Blasco has more to publish on this soon.

Posted by: Mark at August 2nd, 2017 9:32 AM

Because, Mark, mice are not humans.

Mice have telomerase active in differentiated somatic cells.
So really, they never truly face replicative senescence caused by the Hayflick limit - they don't. Even if they didn't have telomerase active somatic cells, their stem cells are very much telomerase active and to top it off the telomere length of lab mice is 10 times greater than the ones of a human. Their telomeres are so long, telomerase knock out mice live just as long as normal mice. It literally has no negative effect on them.

As early as 2000 people were making observations their telomeres do no shorten visibly in culture and yet their cells enter replicative arrest - which led to the discovery that senescence is very rarely actually caused by replicative exhaustion. Even in humans.

So why and how telomerase made those specific mice live slightly longer is not something I highly concern myself with.
It has also made mice live shorter by making them more prone to cancer.

Also something of interest, Blasco very much supports reprogramming as a therapy:

Reprogramming has a benefit over simple telomerase induction - it's a mechanism with inbuilt safeties. As long as you do it intermittently you're probably safe. Probably.

Posted by: Anonymoose at August 2nd, 2017 10:22 AM

I wish that I could be in one or more of those upcoming clinical trials. (I'm 61 years of age.) But I get the impression they are going to be indicated for exotic diseases that I don't have, and therefore I won't meet inclusion criteria. My guess is that people like me will have to wait for FDA approval and off label use. It be nice of SENS approach can beat them to the punch.

Posted by: NY2LA at August 2nd, 2017 4:21 PM

By "exotic", I facetiously mean uncommon diseases. Maybe that wasn't apparent.

Posted by: NY2LA at August 2nd, 2017 4:24 PM

@NY2LA, you could do medical tourism down the road instead of waiting up to 10 years for FDA to give their stamp of approval. You would still would need to wait until the clinical studies are done, though. Myself, I would wait at least of few years AFTER it is available in medical tourism to try in case something negative comes up with the treatments. I am 57, so not much younger.

Posted by: Robert at August 2nd, 2017 6:59 PM

@Anonymoose - you need to do some more reading around Blasco's work as you don't appear to actually understand it.

Telomerase induction does not depend on having already active telomerase in somatic cells.

You are correct that replicative senescence is not a problem in mice, nevertheless telomerase induction was highly beneficial in them as shown in the link I provided. There are many reasons why this may be the case but in any case it is a reason for optimism - YES MICE ARE NOT HUMANS WHICH IS A GOOD THING AS HUMANS MAY WELL BENEFIT MORE FROM THIS THERAPY (humans are effected by replicative senescence).

The argument that telomere extension causes cancer is also very tired despite Reason's continued use of it, and looking increasingly unlikely (see same paper).

In any case the fact of the matter is that stem cell reprogramming is far away from being ready for trials in humans, telomerase therapy is pretty much ready to go. If it's tried and it doesn't work fair enough, we'll fall back on stem cell reprogramming. But until that time kindly stick to the science in your comments.

Posted by: Mark at August 3rd, 2017 3:04 AM

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