Recently Adam Ford conducted a fascinating video interview with biogerontologist Aubrey de Grey (part of a long and wonderful series of video interviews by Adam). We are pleased to present you with both the video interview itself, and an edited textual transcript. Enjoy!
Adam: So we’ve mentioned about the delivery aspects, like of the seven deadly things… actually, can we start at Seven Deadly Things? So there are seven deadly things. One of the major ones you’re working with at the moment is LysoSENS. Is that correct?
Aubrey: That’s certainly correct, yes. LysoSENS is the introduction of non-human genes or enzymes into our cells, that will improve the ability of the lysosome to break down substances that currently it can’t break down. That’s why such substances accumulate slowly but inexorably in various cell types and in some of the most important diseases of old age.
Adam: Is there any secondary one which you think you’re going to target after LysoSENS?
Aubrey: We’re definitely not doing them in some order. We’re doing them all at the same time. I’m interested in making sure that none of these things are left behind. So actually, our main focus is on… well, I mean, the main reason why we prioritize certain things over others is simply if they are not being prioritized by the rest of the world.
At the moment, at our Research Center in Mountain View, we are working on LysoSENS, as you said, but we are also working on MitoSENS, the obviation of mitochondrial mutations in aging – ways to make those mitochondrial mutations harmless, essentially by putting copies of the mitochondrial genome into the nuclear genome. And in projects that we are funding in university labs around the country, we are doing a number of other things relating to other aspects of SENS. So yes, we are interested in focusing on all of these things in parallel.
Adam: Okay. So what are the seven deadly things, not sins, but things – that the SENS Foundation plans to research itself, or partner with other organizations to achieve its goals, as opposed to the types of things that SENS will look outside of itself to get the research done?
Aubrey: Well, really, the answer to that question will change over time. So at the moment, there are just a few areas within SENS that we are de-prioritizing because they are being funded quite well elsewhere. One of them is the elimination of amyloid, a type of garbage outside cells, that occurs in Alzheimer’s disease. And even there, it’s only sort of that one subset of that one deadly thing that we are not working on.
So we are working on something very similar, the accumulation of a similar type of garbage outside cells that occurs predominantly in the heart. It just turns out that even though Alzheimer’s work is well-funded and well respected and everything, nevertheless doing the same sort of approach for other types of amyloids, other types of extracellular garbage, is not being particularly enthusiastically pursued by other people, so we are doing our bit.
Similarly, in the case of lost cells where cells die and they are not automatically replaced by other cells, by the division of other cells – That is what stem cells are for. Stem cell Therapy is very real – People are working in lots of areas in that field, so of course we are not trying to duplicate that effort. But even there, we are doing one or two things. For example, we’re interested in a particular type of cell loss which is the shrinkage of an organ called the thymus, which is responsible for the creation of certain types of immune cells.
It turns out that restoration of the thymus to its youthful size is something that not many people work on. The approaches that have been tried have not been very successful. We are looking at some more ambitious but we think more promising approaches that have not been looked at by other people. And for all the other areas of SENS essentially we are doing everything.
Adam: Excellent. Okay. First of all, I wanted to ask you about, which isn’t quite directly related but what do you think the Future of Monitoring the Body for defects approaching dangers and thresholds will be?
Aubrey: Well, the good thing about the various types of accumulating damage that contribute to aging is that they are mainly caused by very intrinsic and non-negotiable, shall we say, aspects of metabolism like breathing, for example. As a result of that, the rate at which various different types of damage accumulate in the body is not all that different from one person to another. I mean there will be some difference always, but not more than, let’s say, a factor of two between any pair of people.
So that means actually that the motivation for monitoring people to see how much damage they’ve got of any particular type is a good deal lower than it is for most diseases. Ultimately if you don’t have that information then all that means is that you may end up having to administer certain therapies twice as often as necessary, and there’s really not much harm in that.
It may actually end up being easier in many cases, in most cases, not to bother with the monitoring and just to assume the worst case scenario for everybody.
Adam: Okay. So there are various techniques that have been sort of mentioned on the SENS website. There’s the Transplantation, Cell Therapy, Somatic Gene Therapy and Somatic Protein Therapy. They are the ones which tend to have some use with the SENS approach.
The Transplantation seems the easiest, but there are obviously rejection issues and issues of infection. But then you’ve mentioned something called Tissue Engineering.
Aubrey: Okay. So Transplantation, as you say if we think of Transplantation in its traditional sense, the taking of an organ from another individual and transplanting it in, then you do indeed have issues of rejection and also infection.
Tissue Engineering is all about creating organs that have never been in another individual and putting them in after having been created in the laboratory. So the actual Transplantation process is exactly the same as it is when the organ would come from another individual. But, first of all, the risk of infection will be very greatly minimized because the organ can be created in the lab in a sterile environment. Secondly, the immunity problem can be completely eliminated by creating the organ using cells that come from the individual that you are helping, that you’re going to be eventually giving the organ to.
Now, for those reasons, Tissue Engineering has been a very big goal in biomedical technology for a long time now, at least for twenty to thirty years. But progress in actually making it work has been patchy, pretty slow – and the number one reason for that has been ‘Vascularization’. In other words, the requirement to actually create this organ with a blood supply that goes sufficiently thoroughly throughout the organ so that every cell in the organ is very close to a blood vessel, same as it happens in the natural body. People have tried the most extraordinary number of very creative approaches to making that happen but none of them have really panned out. What has really changed over the past few years is the development of a new approach to doing all of this, which involves taking the organ from another individual, as per a regular transplantation, but rather than putting it as it currently exists into the patient, what one does is, first of all, one gets rid of all the cells that belong to the organ. So that sounds crazy – but what it involves is basically getting rid of the cells but not getting rid of the vasculature. Because the vasculature is defined by proteins called the Extracellular Matrix which are not removed by this process. So the vasculature is still there. And then what you do is you take cells from the prospective patient and you basically just infuse them into this denuded vasculature, so that they can take up residence in the place of the cells that you got rid of.
That means you end up with an organ that is not going to be rejected because the Extracellular Matrix itself is the only part that’s foreign and it is not very immunogenic. And yet, the vasculature is really there because it comes from a regular organ that’s developed in another individual. Perhaps not even the organ of a human, maybe a pig or something like that. And so this is a very exciting area and people are working on it hand over fist across the world in many different organizations and in many different laboratories.
Adam: Wow. So what about mechanical and artificial body parts, will they have the same issues with rejection and infection?
Aubrey: Mechanical solutions to… let’s call them Non-Biological Solutions to medical problems, are certainly another very big deal in this whole area. In some cases, they are looking very promising already. So one that’s often talked about and a very important one in this area is the Cochlear Implant, which is as many people know the replacement of the inner ear by something that works purely on non-biological mechanics.
Cochlear Implants are still pretty primitive but they’re getting better awfully fast. In fact, I’ve heard it said by experts in this area that we could be as little as five years away from Cochlear Implants actually overtaking natural hearing in terms of their performance! So that’s pretty cool.
There are plenty other examples and I think this is going to actually become much more important as time goes on, especially as we increase the miniaturization of these things. So yes, this is absolutely very important! And as you say, it’s another way of avoiding the immune reaction problem.
Adam: So artificial or non-biological components won’t be rejected as easily as other tissues but they still may have infection problems?
Aubrey: Well, of course, whenever one does any kind of surgery on individual, one has always got the problem of infections getting in there at the same time. But the infection problem in the case of a transplant is a bit bigger, a lot bigger actually, because in a transplant you’ve got the problem of the infection maybe preexisting in the actual organ that they took out of the original body. So that problem certainly is eliminated when you do either this decellularization approach that I mentioned or a replacement with a non-biological organ.
Adam: Okay. But you need an existing organ in order to do the vascularization?
Aubrey: Well, not necessarily, because as I mentioned, the organ doesn’t necessarily come from a human. It can come even from a pig. And so, you know, animals could be grown for the precise purpose of supplying such organs.
Adam: Okay. All right. Cell Therapy, the introduction of modified cells, removal of the original ones or the failing ones if they are existing… it seems quite difficult. How do you do that?
Aubrey: Well, first of all, the removal of the existing ones is a separate issue. In general, removal of cells which are getting in the way, that are not functioning any more but they’re not dying, is something that’s in principle a good deal easier than replacement of cells because one can do a lot of different tricks. For example, one can actually immunize against these things. Typically cells that are not behaving look different – they have different protein on their surface and that can be used as a signature to get rid of these cells. I’m not saying it’s easy but that’s the sort of approach that can be taken.
The replacement of cells, well, that depends. It turns out that in research in stem cells, we’ve discovered an awful lot over the years about how different cells arise from other types of cells. In other words, basically the Phylogenetic Tree, the lineage of how the original embryonic zygote, the first cell of the body, divides and differentiates into a whole bunch of different other cells.
We’ve also discovered ways to take cells that have already been differentiated into a specific cell type and to de-differentiate them back into a more primitive form. So what this all adds up to is that we’re pretty close now to being able to create any cell type that we like, again, without the rejection problem, without the problem of the DNA being different, and therefore the immune system getting active when you put the cells into the body.
So that means that we have the potential to be able to replace any cell that we like into the body by introducing cells surgically that are precursors of the cells that we don’t have enough of any more. And then the cells will differentiate to replace the cells that have gone missing. That’s what Stem Cell Therapy is all about. And yes, it sounds pretty technical and in many cases we’re a long way from making it work. But in some cases we’re not very far away. There are already clinical trials out there for a number of different problems caused by loss of cells, including problems related to aging. Parkinson’s disease is probably the best example of that.
Adam: Nice. Okay. Excellent. So there are already roadmaps in place to deal with some of the issues that aren’t so close, are there?
Aubrey: Well, sure. Absolutely, I mean if you read my book that came out in 2007, you’ll see that there’s a very detailed roadmap. For each of the seven deadly things, there’s a whole chapter talking about where we were at that point in terms of existing results, existing techniques that have been developed, and exactly what needs to be done from there to actually bring these therapies to fruition. Furthermore, if you get the paperback edition of my book which came out twelve months later, it turns out that there was so much progress after that twelve months that in order to keep the book up to date, we had to write an entire new chapter, an afterword, a full length chapter, just to cover one year of advances, so that’s pretty good news!
Adam: Yeah, definitely. So on to Somatic Gene Therapy – getting engineered DNA into specific parts of the genome, editing or altering the DNA whilst in the body as opposed to introduction of the cells or as opposed to before introducing the cells into the body?
Aubrey: Yes, absolutely. Well, we’ve got to distinguish between a number of different approaches to Gene Therapy. So the classical concept with Somatic Gene Therapy is just as you described – one introduces these genes into the body typically packaged in viruses and the viral DNA has the capacity to invade the cells and get into the nucleus of the cell. And by doing so, integrate into the chromosomes so that the cargo, the DNA that we engineered, that we want to introduce, then is transcribed and translated and so on just in the same way that our natural genes are. But there are, as you say, a number of variations on that theme.
One of them is often called Ex Vivo Gene Therapy. It essentially means extracting cells from the body, doing the genetic manipulation outside the body, and then bringing the modified cell back. That has a lot of advantages when you can do it because, well, the biggest advantage of all is safety: we can make sure that the cells we put back are modified in the appropriate way, the way that we intended to and not in any other way. We can do that simply by doing the modification and then by testing the cells in a variety of different ways to make sure that the genetic composition is as we intended.
However there are plenty of cases where that approach – Ex Vivo Gene Therapy simply isn’t available, especially the cases where the cells that we want to fix up are cells that are long-lived and are not dividing and that we don’t want to kill, we just want to alter them while in the body – so we do Somatic Gene Therapy itself some of the time. The safety concerns that I just alluded to are quite severe. There have certainly been cases where people have suffered quite badly from the unintended side effects of Somatic Gene Therapy.
So one big thing that we’d like to be able to do that would alleviate most of those potential risks is to put the DNA not into some random place of the genome, which is what happens typically when you use viruses in this way, but instead to put the DNA into a specific place, a place that has been pre-chosen to be harmless – so nothing would be disrupted. And some very important progress has been made over the past decade especially in doing exactly that. The concept is called Gene Targeting and there’s a number of ways to go about it. The way that currently looks the most promising involves something called Zinc-Finger Nucleases and it would take me a little while to explain what those are.
Adam: Zinc-Finger, where do they come up with these names?
Aubrey: Well, basically there is a zinc atom involved, and the protein formed into a shape that looks like a finger. These particular proteins are very important in nature as what are called ‘transcription factors’ – They are used to determine which genes in a particular cell get expressed and which ones do not. It turns out that Zinc-Finger Nucleases can be made. These are proteins that involve Zinc-Finger proteins fused to a protein that breaks DNA. By doing that, one can have a very strong specificity for exactly where one’s engineered DNA actually enters the chromosome. So we’re making very good progress in that area.
Adam: So Zinc Fingers, have they got the benefits of both the RNA Interference and WILT or are they completely different?
Aubrey: RNA Interference is a family of mechanisms now. It’s a family of potential approaches to suppressing the expression of a particular gene that’s present in the body. There are many reasons why one might want to do that for a particular gene.
But actually in WILT, which is our best approach to combating cancer, what I want to do is more than that. One wants to actually get rid of the gene. One wants to remove the gene completely so that RNAi or doing any other approach simply suppressing the expression of the gene cannot be in any way overcome by mutation of the cell.
So Gene Targeting can be used for that purpose, yes. Gene Targeting achieves what’s called to knock out the genes, to actually create a big deletion in the gene that will stop it from ever being expressed again even if the cell that it is in mutates a great deal.
Adam: WILT is what you put forward as an anti-cancer therapy.
Aubrey: We very much hope that WILT will not be required, because it’s a very elaborate and ambitious therapy. There are many other promising therapies out there which are much simpler to implement, and therefore which would be implemented much more quickly, much sooner. However these therapies are not nearly so certain to work as WILT is. So we just sort of don’t want to be wrong again. We feel that, it’s been forty years and people have been fighting the war on cancer and making much less rapid progress than they were expecting to. I think it’s important not to oversimplify cancer, to remember that cancer really is the hardest aspect of aging to fix, on account of having natural selection on its side and therefore that it may simply outwit us again and again. We really need something that cannot be outwitted in order to be sure that we will eventually hit cancer on the head.
Adam: People have said, look at the ‘war on cancer’ and that’s been really hard. We’re never going to be able to sort of develop any therapies for cancer or much less anything else. But, have there been any interesting and useful fallouts from the research involved in the ‘war in cancer’?
Aubrey: An immense amount! I mean the fact is that we are a lot closer to developing therapies against cancer than we would be if we had not worked on it forty years ago. We have made enormous progress and I would say that we’ve made much more progress than we would have done if it had not been for the decision back in the 1970’s to elevate funding for cancer research.
The fact is, it would be a mistake to call the war on cancer a failure. It was a failure by the standards of the expectations that were put forward back then, but to call it a failure in real terms would be completely wrong.
Adam: Okay. That makes sense. So let’s talk ‘Somatic Protein Therapy’.
Aubrey: Right. So in some cases it is not actually necessary to get genetic changes fixed in the human body. There is a range of diseases called ‘Lysosomal Storage Diseases’ which are diseases of childhood typically and are caused by the genetic absence of a particular protein that’s responsible typically for breaking down a certain class of molecule. They’re called Lysosomal Storage Diseases because the proteins that are missing are typically located in the lysosomes.
About fifty years ago nearly now, people started thinking about doing something about these diseases, not by restoring the genetic composition of the people who were affected but by making a lot of the protein that was missing and just injecting the protein into the circulation.
The idea here was that a small proportion of the injected protein would get into the cells that were affected by the accumulation of molecular garbage that the protein should be destroying and would thereby a cause the destruction of the offending garbage. The first time they tried it didn’t really work. But they figured out a tweak, a way of modifying the protein by basically attaching sugar molecules of a particular type to these proteins and that made it work. Still, if you do this, most of the protein does not get to the required place. It just gets broken down in the liver and excreted. But some of it does – and these therapies actually are effective. There are people hanging around as fully functioning adults today, who would otherwise have died at the age of like five. The only thing that’s unusual about their lives is that they have to inject quite a lot of this protein every so often. So, that’s pretty damn good news!
We realized some years ago that the same sort of approach might work for some types of the garbage that accumulate late in life in normal aging—things that cause some of the most prevalent diseases of old age like Cardiovascular Disease and Macular Degeneration. And so we’ve been working on this for the past several years and it seems pretty promising.
We’ve identified enzymes that can break down the substances that cause those diseases and we’ve certainly made very promising early steps in actually getting those enzymes into mammalian cells in cell culture. Now, the interesting part of this is that whereas for these Lysosomal Storage Diseases we do what’s called Enzyme Replacement Therapy – in other words, we take an enzyme that most of us normally have and the unlucky people don’t have, and we put that in – in the case of what we want to do with the age-related Lysosomal Storage Diseases, we have to identify enzymes from other species, enzymes that we naturally don’t have, none of us have, and put those into the body. There are a whole bunch of problems that could potentially occur as a result of that, but that is not apparently going to cause much of a problem. For example, people are worried about the immune response to that, but the immune response is going to be very mild and perhaps quite transient that we need to overcome.
Adam: Okay. Do you think some of these therapies might be able to be engineered into just everyday food in the future?
Aubrey: Well, I think that we are likely to see over the years a substantial evolution of the delivery modalities for these therapies in general. I think when they first arrive, and of course we still don’t know when that’s going to be, I think we have a 50-50 chance of getting that within the next 20 or 25 years, it could be sooner or later. But, anyway, when they do arrive, like any new experimental first generation therapy it’s going to be quite risky. So I expect what’s going to happen is people will go into hospital for maybe a couple of months even, and will get these therapies with regular monitoring going on to make sure that the therapies are not doing any harm, and such like.
Well, as time goes on and the therapies get more proven and more convenient and cheaper and so on, I wouldn’t be at all surprised to see that they will become outpatients as everything is done by injection and to a certain extent, one might be able to go as far as oral administration, as you suggest. We just can’t tell when and to what extent that’s going to happen.
Adam: Okay. And then lastly there’s Germline Gene Therapy which is adapting the zygote with the sperm or the egg before it actually develops into a human although it’s not going to help anybody who’s still alive.
Aubrey: Right, exactly. And for that reason I expect that Germline Gene Therapy is probably not going to be used for diseases of old age. I think that it is probably going to become an important component of our biomedical arsenal in relation to early onset diseases and particularly in relation to elimination of those diseases from the population.
But when it comes to aging, what we have to look at is the alternatives. We have the option of doing Germline Gene Therapy in ‘year N’ or doing Somatic Gene Therapy in ‘year N+50’ when these diseases that are caused by genetic shortcomings that we might be talking about might be beginning to emerge – and 50 years is a hell of a long time in technology. So I think it’s reasonable to propose, first of all, that we will have a much better idea of what genetic modifications we ought to be making to alleviate a particular problem that we might be looking at. And secondly, of course, that we might actually have Somatic Gene Therapy so much better by that time that it’s good enough to substitute for the Germline Gene Therapy 50 years previous.
Adam: Okay. All right. Well, that’s about all the questions I’ve got for the delivery of therapies. Do you have a bit of time for some different questions?
Aubrey: Just a little bit, yeah. I think my voice is just about up.
Adam: Okay. All right. So, you’ve mentioned in the previous interview about the differences and the similarities between Antagonistic Pleiotropy and accumulated damage. And you’ve said that they shouldn’t be considered as alternatives – that Antagonistic Pleiotropy may be actually a side product or a second order effect of accumulated damage over lifetime. Is that correct or would you like to explain more about it?
Aubrey: Sure, that’s perfectly correct. Antagonistic Pleiotropy is an evolutionary biology concept that basically just says that we may have some aspects of aging occurring as a result of the inappropriate, the maladaptive expression of the genes and genetic pathways later in life that has evolved as a result of the fact that early in life, that same genetic pathway was actually adaptive, was actually good for us.
This is a reasonable concept, but if we relate to the mechanics of aging, if we look at the particular examples, it turns out to be quite complicated. So if we look at the situation around cancer, for example, cancer is probably the most clear-cut example of Antagonistic Pleiotropy in human aging.
What we see here is that early in life it’s important not to die of cancer obviously, and it’s also important, equally obviously, not to die of anything else, like failure of one’s blood stem cells to divide. If one’s blood stem cells stop dividing, then one doesn’t have any blood quite soon after that, so one is going to die before having one’s own offspring and so that’s obviously evolutionarily a bad thing, but if one dies of cancer that’s also a bad thing.
So what evolution has to do is develop a sort of happy medium, a bunch of ways in which to allow certain types of cell to divide as often as the body needs them to do, stem cells in the blood for example. But at the same time, to go about against the possibility that some cells might try to start dividing more often than they’re supposed to, thereby giving rise to cancer and killing us.
And there are a whole bunch of traits and genetic pathways that evolution has created in order to get the best of both worlds. As we look late in life, we may see that the development of those pathways has altered and that in fact the suppression of cell division has developed in order to avoid cancer. It’s largely because there’s more risk of cancer on account of the time that’s gone by and the ability of stem cells to accumulate mutations that may predispose to cancer by that time.
So yes, I think that what you said in the beginning in your question is absolutely correct: that Antagonistic Pleiotropy cannot be regarded in any sense as an alternative to, or opposed to, the concept that aging is driven by the accumulation of various types of damage. That’s rather like comparing apples and oranges. Antagonistic Pleiotropy is the evolutionary theory and the damage accumulation concept is the mechanistic theory.
Adam: Okay. I guess like a strong version of AP, I’m not sure if this is correct, would be some sort of preprogrammed, evolved program of apoptosis of cells after a certain sort of threshold is met within the body which may just be around a certain age for most people.
Aubrey: Right. So that’s actually quite accurate. So Telomere Shortening is an important concept or an important phenomenon that happens in cell culture and which is believed to exist. In other words, the absence of expression of Telomerase, we could come back to their Shortening, is something that has been posed to exist as an anticancer defense. But an anticancer defense may have some drawbacks by virtue of causing cells to get into a state where they don’t behave correctly because they divide too often. It remains to be seen whether that’s really true, but I think it’s fairly likely to be true. However, it also remains to be seen how limited or how widespread the effects of Telomere Shortening are, which is very much a live area of research.
The chances are in my view that the effect of Telomere Shortening is much more restricted than it might have been thought to be forty years ago. But yet there are certain problems in engineering aging especially in the few systems that are predominantly driven by this. So, again, we need a way to try and get the best of both worlds more effectively than what evolution has been able to achieve.
Adam: Excellent. You mentioned Telomerase and Telomeres at the end of cells. I’ve just seen flashes of headlines appear around the place saying they’ve made breakthroughs in certain areas. How do you think the research is going in replacing…?
Aubrey: Well, a lot of the most high profile work on Telomeres and Telomerase that we’ve seen in the media is actually not nearly so dramatic as it is stated to be. But still I would say that we’re now really getting on top of the idea of what Telomere and Telomerase are good for, what they’re bad for, and how to manipulate them. And we’re now definitely also in the stage of doing actual clinical trials of Telomerase stimulators that will have the capacity to, at least to slow down, the shortening of Telomeres in cells that do divide rapidly.
So, it may be an approach that’s dangerous because it can cause cancer, but equally may not and this is exactly what needs to be looked at really closely. A lot of people are actually now considering the possibility within a certain limited way, a limited context, increasing Telomerase expression thereby suppressing the shortening of Telomeres may actually be a good defense against cancer because it’s stopping cells from getting into a nasty state called crisis which is what happens when a Telomere gets exceptionally short, and which is actually something that can accelerate the development of cancer.
Adam: Okay. Interesting. So is there some sort of a Gene Therapy they can knock out a gene that produces too many Telomeres and causes cancer. Is that right?
Aubrey: Well, that’s essentially what we’re proposing with WILT. It’s to knock out the genes responsible for creating Telomerase. It remains to be seen whether the side effects caused by that will be addressable adequately by using Stem Cell Therapy and Cell Replacement.
Adam: Okay. There’s also another thing that I mentioned. I remember you mentioned in a video about replacing some bone marrow stem cells, for instance, a special form of White Blood Cells can help sort of go out and replenish the existing cells. Does that sound anyway close to correct?
Aubrey: In a way, in some ways. One part of WILT that is an anticancer approach is to replace the cells that make blood. So the hematopoietic stem cells which are of course located in the bone marrow, as you say. Now it not only creates White Blood Cells, they also create Red Blood Cells. And actually cells that go out and fix up the rest of the body are different type of bone marrow cells called Mesenchymal Stem Cell, and in fact there is a third cell called the Endothelial Progenitor Cell which again is located in the bone marrow.
Now, there are established approaches, established chemicals, that are known that can be administered to people to help elevate what’s called mobilization of these cells, the tendency of these cells to vacate their niches in the bone marrow and to go out into the circulation where they then have a tendency to home in on damaged tissue and replace it. So that could end up being a significant string to our bow in this whole area. What’s not yet clear is whether that sort of approach, circulating Mesenchymal Stem Cell or Endothelial Progenitor Cell, is able to target the very low level distributed, diffuse type of damage that tends to accumulate during aging. That’s reason to believe that it may not be so good at that just because it doesn’t do so naturally without the application of any of these chemicals.
Adam: Okay. All right. Well, just to finish off the science-y questions, what do you think are the major bottlenecks that you see in the development of SENS at the moment and how do you think we’ll overcome those bottlenecks?
Aubrey: There’s really only one bottleneck which is money at the moment. No, I’m serious. We have at the moment a very good, very sophisticated and detailed idea about what in SENS needs to be done, needs to be developed, in order to actually bring SENS to reality. We also have an equal essential ingredient. We have the right scientists, all the real world leaders in all of the various areas that are relevant to the SENS. They are very enthusiastic about the applying their expertise to the problems of aging and to the application of regenerative medicine to diseases and disabilities of old age.
This is essentially what SENS is. So that’s what’s in place. What is not in place is the resources to allow those people to actually get on and do that experiment. So that’s why I spend humongous amounts of my time going around the world, getting additional funding to be allocated to this work.
Adam: Okay. So what do you think what people can do in order to help fund this up, like obviously donate into the SENS foundation?
Aubrey: But there is plenty more involved in this. Basically everyone, however wealthy you are, you can do something. So if you’re a journalist, you can interview me. If you are a conference organizer, you can get me or one of my colleagues to come speak. You know, getting the word out is an enormous part of this. What anyone can do, whoever they are, is advocacy. You can always talk to your family, your friends, your colleagues.
You can get them to understand that this is both feasible and desirable and to be realistic about this to understand that ultimately this is no different than any other type of medicine except for the fact that it doesn’t yet exist. It is no different than any type of medical research.
I use the phrase “Preventive Geriatrics” a lot, In other words, to emphasize that what we’re talking about here is simply preventative medicine for the diseases and disabilities of old age that all of us already know that we don’t want to get. So it’s perfectly legitimate, perfectly regular, normal medical research and it just needs to be thought about in that way. The more the word gets out, the more public enthusiasm there is for this, the more public policy will respond to that public enthusiasm and the more public money will be available and it won’t be reliant any longer on the largesse of private individuals.
Adam: There is or there used to be like a volunteer section on the website, I did some work with Kelsey Moody quite a while ago, did some web development trying to make sort of an online application to sort of make banners and buttons for people. This was before SENS Foundation was created. Is that student research program still going?
Aubrey: Absolutely. So the Academic Initiative as we now call it, is absolutely very much alive and kicking, and is now headed by another of our people Daniel Kimbel. You can have a look on the website now SENS.org to find it. Actually we’re about to have a big re-vamp of the website. But yes, we’re definitely very much still active.
Adam: Sure. Okay. That’s fantastic. Thank you, that’s been really good interview. Have you got any concluding remarks you’d like to add?
Aubrey: Well, thank you for doing the interview. I’d like everyone to go to SENS.org and have a look at what we’re doing and what we would like to do. And generally get out there and get involved.