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The Rise of Oisin Biotechnologies – Interview with Gary Hudson, CEO of Oisin Biotechnologies, by Ariel VA Feinerman

The Rise of Oisin Biotechnologies – Interview with Gary Hudson, CEO of Oisin Biotechnologies, by Ariel VA Feinerman

Ariel VA Feinerman
Gary Hudson


Gary Hudson

Preface

What is ageing? We can define ageing as a process of accumulation of the damage which is just a side-effect of normal metabolism. While researchers still poorly understand how metabolic processes cause damage accumulation, and how accumulated damage cause pathology, the damage itself — the structural difference between old tissue and young tissue — is categorized and understood pretty well. By repairing damage and restoring the previous undamaged — young — state of an organism, we can really rejuvenate it! Sounds very promising, and so it is. And for some types of damage (for example, for senescent cells) it is already proved to work!

Today in our virtual studio somewhere between cold rainy Saint-Petersburg and warm rainy Seattle, we meet Gary Hudson!

He has been involved in private space flight development for over 40 years. Hudson is best known as the founder of Rotary Rocket Company, which in spending ~$30 Million attempted to build a unique single stage to orbit launch vehicle known as the Roton. He helped found Transformational Space T/Space in 2004 and AirLaunch LLC which was awarded the DARPA/USAF FALCON project in 2003.

Previous projects included designs of the Phoenix SSTO, the Percheron, and other rockets, founder of Pacific American Launch Systems, and various consulting projects. Currently, he is the President and CEO of the Space Studies Institute.

Now Hudson brings his excellent engineering skills into rejuvenation biotechnology! He is a founding partner of Oisin Biotechnologies, who are developing a liposomally delivered DNA therapy for the removal of senescent cells from the body. Hudson provided an initial seed donation to help fund the creation of the Methuselah Foundation and SENS Research Foundation.

Interview

Feinerman: Hello, Mr Gary Hudson!

Hudson: Thanks for inviting us to this interview!

Feinerman: You have recently visited an amazing Undoing Aging 2018 conference, which took place in Berlin, 15–17 March, where your colleague, Matthew Scholz, was a speaker. What is your impression?

Hudson: It was a great conference with several important presentations. It put me in mind of the early SENS conferences in Cambridge, UK, which I helped to sponsor. I understand it will now become an annual event. Our CSO Dr. John Lewis also gave an important summary of our work to date.

Feinerman: Will Oisin’s presentations from conference be available for general public?

Hudson: I believe that the SENS Foundation will be posting them but I don’t have details about the timing.

FeinermanYour last interview was in July 2017, more than half a year ago. What has been accomplished?

Hudson: We have conducted many pre-clinical mouse experiments on both cancer and senescent cell removal. All have been successful and produce very remarkable results. We’ve also conducted a pilot toxicity and safety trial on non-human primates. The results of that trial were also successful and encourage us to proceed to human safety trials as soon as regulatory authorities approve them. We have also spun-out a cancer-focused company, Oisin Oncology, and raised a seed round for that venture.

Feinerman: Great to hear! However, when can we see some papers? People usually trust papers more than mere interviews or press releases. Of course, papers need many efforts not related to research but they will allow you attract more attention from general public, researchers, and investors.

Hudson: Papers are being prepared now for submission to major journals, but that process takes time, especially the peer review. For the moment, most of our data is only available to investors and partners in pharma and the biotech industry.

Feinerman: You planned human clinical trials, have you carried them out?

Hudson: It takes quite some time to organize a human trial and to get it approved. Before one can be conducted, we have to set up so-called “GMP (Good Manufacturing Practice) manufacture of our therapeutic, and then we have to conduct “GLP (Good Laboratory Practice) Tox” studies in two different species. Once that is all completed later this year, then we can begin a human safety trial, or a “Phase 1” trial. All this takes time, but we hope that first safety trials in oncology indications might begin this year, or in early 2019.

Feinerman: Does that mean we have a race between Unity Biotechnology and Oisin and you have all chances to win the race?

Hudson: I don’t see it as a race or a competition. I believe that future anti-aging treatment will require multiple complimentary approaches.

Feinerman: When we can expect your therapy available in the clinic?

Hudson: It’s very difficult to predict. I believe that our cancer treatment will make it to the clinic first, and that could happen in less than five years. Since the FDA doesn’t regard ageing as an indication, it may take longer for our SENSOlytic™ treatment to reach the public, since the regulatory environment will need to change.

Feinerman: As Michael Rae has said, we need not to wait when ageing will be recognised as a disease. You can mark your senolytics as a therapy for specific ageing pathology like fibrosis or chronic inflammation in the same way as Unity does.

Hudson: This is certainly true and is part of our strategy, but many of those endpoints are more difficult to ascertain than oncology endpoints. Additionally, going after oncology approvals can be faster and easier to get to clinic. But we will push forward on several fronts as funding permits.

Feinerman: In your previous interview you have said that you make some tweaks to both the promoter side and the effector side of the constructs that will provide even more interesting and useful extensions to the basic capability, but you can’t discuss those for IP reasons. Can you now say about them?

Hudson: I still can’t say too much about them, but we have conducted animal trials on some of these “tweaks” and they work quite well. The downside to the matter is that every “tweak” requires new trials, and our goal is to get something to the clinic as soon as possible, so many of the improvements will have to wait. Progress is limited based on available funds and personnel resources, of course, but we will move as quickly as we can.

Feinerman: Do you use any CAD software to design your constructs? Are you going to make them public so independent engineers will be able to help you identify new useful pairs of promoters and effectors? Your technology is so powerful that Open Source approach would be very helpful!

Hudson: No, the design of the current constructs are very straightforward and simple. As our patents are issued, their design will become public. If people wish to design their own constructs for particular applications they may contact us for collaboration, though we do have several collaborations active at the moment so we may already be working on similar ideas.

Feinerman: What do you think on targeting your machinery on cells with abnormal telomerase activity to kill cancer? Can you use several conditions — like in programming — several promoters to be more specific?

Hudson: If we targeted telomerase we’d also kill stem cells, just like the side effects of much of conventional chemotherapy. That’s probably not a good idea. But multiple promoters, or synthetic promoters, might be used to achieve the aims of killing only cancer cells. Our initial therapeutic will likely just employ p53 promoter targeting, since we have good data that works.

Feinerman: Yeah, the same issue as when we remove or break telomerase gene: there would be nice to do this only in compromised tissue, but as researchers say it is very difficult to make the removal selective. However, it is not a problem with ALT genes, which cause 15–20% of cancers. Are you going to collaborate with the OncoSENS lab? Also killing cells actively expressing telomerase will be very useful in WILT implementation.

Hudson: We’ve had conversations with the SENS Foundation about OncoSENS and cooperated in a preliminary fashion, but I don’t believe it is currently a research priority for them. We already have enough projects to keep us busy for some time, too!

Feinerman: Now you use only suicide gene as an effector, do you plan to use other genes? For example to enhance the cells, give them ability to produce new enzymes, or temporarily shut down telomerase to help anti-cancer therapy to be more effective.

Hudson: We believe we can express any gene under the control of any promoter we wish to use, so the possibilities are almost endless.

Feinerman: Now we know that epigenetic changes (shift) play a huge role in ageing. Even though there is no consensus among researchers whether they are a cause or a consequence of ageing, experiments show that temporal expression of OSKM transcription factors may have some health benefits by restoring “young” epigenetic profiles. You can remember the Belmonte work, for example. However, the problem in their work is that they used transgenic mice and express OSKM in every their cell. If you temporarily express OSKM in an “old” cell, that is OK, you can “rejuvenate” such a cell. While if you express OSKM in a stem cell which is already biologically “young”, you can force the cell into iPSC, which is a way to cancer. Using your machinery we can target only cells which have “old” expression profiles, and involving normal mice! Such a work will be much “cleaner” and safer than Belmonte’s work.

Hudson: With respect to your comments about reprogramming, Oisin is currently working with a university group on exactly this approach, but I can’t say more at this time. We also believe that first you have to clear existing senescent cells, then you can reprogram successfully.

Feinerman: How many resources, finances, and personnel do you need to move as quickly as possible? Do you have open positions? Maybe, some of our readers have enough finances or experience.

Hudson: We could effectively spend tens of millions or dollar or more, very easily, but it isn’t realistic to assume we could raise that amount — and if we did, we’d lose control of Oisin’s ageing focus, since investors would most likely want us to aim at quick returns. We are always interested in talking with “mission minded” investors, however. As for hiring, we have to do that slowly and judiciously, since labour is one of the biggest costs to a start-up company, and over-hiring can sink a project quickly. We already have more potential hires than we can bring on-board.

Feinerman: Now cryptocurrencies and blockchain technologies allow completely new and efficient ways for investments. We can see this as various no-name companies easily rise tens of millions dollars via ICOs for clearly doubtful projects. Would you like to make an ICO? Oisin shows real progress and can easily rise big sums! People say that they will be glad to buy your tokens if you issue them. You have said that you prefer to work with “mission minded” investors. There are thousands people out there who can invest from $1,000 to $100,000 in cryptocurrencies and who believe that radical extension of healthy life is possible!

If you are worried about legal issues, you can use various cryptocurrency investment funds who act like proxies between holders of cryptocurrencies and companies.

Hudson: We have investigated several of these financing options, but we are not expert in this area, so we have been reluctant to move too quickly. But we continue to have conversations with relevant parties. There is a lot of regulatory uncertainty surrounding ICOs, however, so we must move cautiously.

Feinerman: Now we know enough about ageing to defeat our main enemy. Do you agree that first comprehensive rejuvenation panel is not a scientific problem and even not an engineering problem, but a problem of engineering management?

Hudson: I wouldn’t say that there is no science left to do, but as an engineer myself I naturally agree that proper engineering management and program management skills must be brought to bear on the problem of ageing.

Feinerman: One person has said, we get what we ask for. Can we now aim high and publicly claim that our main goal is not additional five years of life but LEV — Longevity Escape Velocity and finally unlimited healthy life?

Hudson: This is a difficult “public relations” problem. Most investors, the scientific community, and the public are not yet ready to embrace the notion of longevity escape velocity. Thus at Oisin we do pitch health span as a primary goal. But personally I don’t believe that you can obtain health span improvements without making significant progress towards LEV. So in the end, I think we get LEV by targeting health span, and we reduce the controversy by doing so.

Feinerman: Some people ask me how to buy your stocks or invest in Oisin. What can you say?

Hudson: We do have a number of private investors (angel investors) who are “mission minded” or “mission focused” and we welcome discussions with qualified investors and firms who share our vision for dealing with ageing and cancer. Accredited investor candidates may contact us at info@oisinbio.com

Feinerman: David Gobel claims that “By advancing tissue engineering and regenerative medicine, we want to create a world where 90-year olds can be as healthy as 50-year olds by 2030.” And I secretly hope that 40 will become new 30 or even 20 by 2030! Can we achieve that — in principle?

Hudson: I certainly hope so! In 2030 I’ll be 80, so I’m looking forward to feeling like I’m 40…

Feinerman: Thank you very much for your amazing answers! That was a real pleasure to talk with such a great man like you. I hope we all will succeed in our goal and will have hundreds, thousands, and — who knows? — maybe even millions years of healthy life!

Hudson: It is kind of you to say so, but I only consider myself fortunate to be working with the really great men and women in the anti-aging community who are doing the real work. I’m only trying to facilitate their efforts and get treatments to the clinic as fast as possible. I don’t know what will be possible in the long term, but anything will be better than letting nature run its course, producing sickness and declining functional health.

Ariel VA Feinerman is a researcher, author, and photographer, who believes that people should not die from diseases and ageing, and whose main goal is to improve human health and achieve immortality.

Message from Ariel VA Feinerman: If you like my work, any help will be appreciated!

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SENS: Progress in the Fight Against Age-Related Diseases – Article by Nicola Bagalà and Steve Hill

SENS: Progress in the Fight Against Age-Related Diseases – Article by Nicola Bagalà and Steve Hill

Nicola Bagalà

Steve Hill


Editor’s Note: In this article, Mr. Nicola Bagalà and Steve Hill discuss the progress that the SENS Research Foundation has made in tackling the aging processes. Below is a brief summary of some of the highlights of their research efforts.  This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                   ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, December 8, 2017

 

 

Today, there are many drugs and therapies that we take for granted. However, we should not forget that what is common and easily accessible today didn’t just magically appear out of thin air; rather, at some point, it used to be an unclear subject of study on which “more research was needed”, and even earlier, it was just a conjecture in some researcher’s head.

Hopefully, one day not too far into the future, rejuvenation biotechnologies will be as normal and widespread as aspirin is today, but right now, we’re in the R&D phase, so we should be patient and remind ourselves that the fact that we can’t rejuvenate people today doesn’t mean that nothing is being done or has been achieved to that end. On the contrary, we are witnessing exciting progress in basic research—the fundamental building blocks without which rejuvenation, or any new technology at all, would stay a conjecture.

In particular, SENS Research Foundation (SRF), a pioneering organization of the field, is sometimes unjustly accused by skeptics for failing to produce results. But produce results it has, and many at that. Skeptics either decide to ignore them or do not have access to reliable sources. For the benefit of the latter, we’ll discuss below what has been achieved by SRF over the past few years, in relation to the infamous “seven deadly things”, the seven categories of damage that aging causes as described in the SENS repair approach.

Mitochondrial mutations

In a nutshell, a mitochondrion is a cell component that is in charge of converting food nutrients into ATP (adenosine triphosphate), a chemical that powers cellular function. Your DNA is contained within the nucleus of each of your cells, but this isn’t the only DNA in your body; mitochondria have their own DNA (known as mtDNA), likely because, at the dawn of life, they were independent organisms that eventually entered a symbiotic relationship with eukaryotic cells, such as those found in our bodies.

Unfortunately, as mitochondria produce ATP, they also produce so-called free radicals as a byproduct—atoms with unpaired electrons that seek to “pair up” with other electrons, and to do so, they’ll gladly snatch them from other molecules nearby, damaging them. As free radicals are created by mitochondria, they’re very close to mtDNA, which is thus very susceptible to being damaged and undergoing mutations.

Mitochondria with damaged DNA may become unable to produce ATP or even produce large amounts of waste that cells cannot get rid of. To add insult to injury, mutant mitochondria have a tendency to outlive normal ones and take over the cells in which they reside, turning them into waste production facilities that increase oxidative stress—one of the driving factors of aging.

MitoSENS: How to solve this problem, and how far we’ve got

Cell nuclei are far less exposed to free-radical bombardment than mitochondria, which makes nuclear DNA less susceptible to mutations. For this reason, the cell nucleus would be a much better place for mitochondrial genes, and in fact, evolution has driven around 1000 of them there. Through a technique called allotopic expression, we could migrate the remaining genes to the nucleus and solve the problem of mitochondrial mutations.

Human-made allotopic expression was a mere theory until late 2016, when, thanks to the successful MitoSENS crowdfunding campaign on Lifespan.io, a proof of concept was finally completed. Dr. Matthew O’Connor and his team managed to achieve stable allotopic expression of two mitochondrial genes in cell culture, as reported in the open-access paper[1] they published in the journal Nucleic Acids Research. As Aubrey de Grey himself explains in this video, of the 13 genes SRF is focusing on, it’s now managed to migrate almost four. This had never been done before and is a huge step towards addressing this aspect of aging in humans. In the past few months, the MitoSENS team has presented its results around the world and worked on some problems encountered in the project.

A list of SRF-funded papers on the topic of mitochondrial mutations can be found here. A more detailed description of its intramural MitoSENS research can be found here.

Lysosomal dysfunction

Lysosomes are digestive organelles within cells that dispose of intracellular garbage—harmful byproducts that would otherwise harm cells. Enzymes within lysosomes can dispose of most of the waste that normally accumulates within cells, but some types of waste, collectively known as lipofuscin, turn out to be impossible to break down. As a result, this waste accumulates within the lysosomes, eventually making it harder for them to degrade even other types of waste; in a worst-case scenario, overloaded lysosomes can burst open and spread their toxic contents around.

This eventuality is especially problematic for cells that replicate little or not at all, such as heart and nerve cells—they’ve got all the time in the world to become swamped in waste, which eventually leads to age-related pathologies, such as heart disease and age-related macular degeneration.

LysoSENS: How to solve this problem, and how far we’ve got

As normal lysosomal enzymes cannot break down lipofuscin, a possible therapy could equip lysosomes with better enzymes that can do the job. The approach suggested by SRF originates with ERT—enzyme replacement therapy—for lysosomal storage diseases. This involves identifying enzymes capable of breaking down different types of intracellular junk, identifying genes that encode for these enzymes, and finally delivering the enzymes in different ways, depending on the tissues and cell types involved.

SRF funded a preliminary research project on lipofuscin clearance therapeutics at Rice University[2] and another project relating to atherosclerosis and the clearance of 7-ketocholesterol[3] (a lipofuscin subtype), which eventually spun into Human Rejuvenation Biotechnologies, an early-stage private startup funded by Jason Hope.

A LysoSENS-based approach is currently being pursued by Dr. Kelsey Moody, who used to work at SRF. Dr. Moody has been working on an ERT treatment for age-related macular degeneration. The treatment consists in providing cells of the macula (a region of the eye’s retina) with an enzyme capable of breaking down a type of intracellular waste known as A2E. The treatment, called LYSOCLEAR, is being worked on by Moody’s company Ichor Therapeutics, which earlier this year has announced a series A offering to start Phase I clinical trials of its product.

If LYSOCLEAR proves successful, it could pave the way for future LysoSENS-based therapies to treat lysosomal dysfunction in different tissues.

A list of SRF-funded papers on the topic can be found here.

Cellular senescence

As cells divide, their telomeres—the end-parts of chromosomes protecting them from damage—shorten. Once a critical length has been reached, cells stop dividing altogether and enter a state known as senescence. Senescent cells are known to secrete a cocktail of chemicals called SASP (Senescence Associated Secretory Phenotype), which promotes inflammation and is associated with several age-related conditions.

However, senescent cells are a bit of a double-edged sword; as explained by Professor Judy Campisi during RB2016, as long as they’re not too numerous, senescent cells carry out an anti-cancer function and may promote wound healing; however, too many of them have the opposite effect, and on top of that, they induce neighboring cells to undergo senescence themselves, starting a dangerous spiral.

Normally, senescent cells destroy themselves via programmed cell death, known as apoptosis, and are then disposed of by the immune system, but some of them manage to escape destruction, and as the immune system declines with age, this gets worse.

The result is that late in life, senescent cells have accumulated to unhealthy amounts and significantly contribute to the development of age-related diseases. Osteoarthritis, cardiovascular diseases, cancer, metabolic disorders such as diabetes, and obesity are all linked to the chronic age-related inflammation to which senescent cells contribute.

ApoptoSENS: How to solve this problem, and how far we’ve got

The proposed SENS solution is straightforward: if senescent cells become too numerous, then they need to be purged. Since they are useful in small amounts, the optimal solution would be periodically removing excess senescent cells without eradicating them entirely—and more importantly, leaving other cells unharmed.

This could potentially be achieved by either senolytic drugs or gene therapies that selectively target senescent cells and trigger programmed cell death. Indeed, a great deal of recent focus by researchers have been on finding ways to remove senescent cells using senolytic therapies.

Another approach that could complement senolytics is to address why the immune system stops clearing senescent cells effectively in the first place. This approach focuses on macrophages and other immune cells involved in clearing senescent cells, aiming to reduce inflammation so that these cells begin to function properly again. The irony is that as inflammation rises with age, the immune system that is supposed to clear senescent cells and keep inflammation levels down actually starts to create more inflammation and becomes part of the problem by not doing its job properly.

SRF has funded a number of studies on the subject of cellular senescence, and it’s recently begun working on a project in collaboration with the Buck Institute for Research on Aging, which is focusing on the immune system and its role in clearing senescent cells. Another extramural project, again with the Buck Institute, is focussed on SASP inhibition.

Senescent cell clearance has been all the rage for the past two years or so; Lifespan.io has hosted the MMTP project, which focused on testing senolytics in mice, and this was later followed by CellAge’s project to design synthetic biology-based senolytics.

There are other companies that have joined the race to add senescent cell clearance to the standard toolkit of doctors, such as Unity Biotechnology and Oisin Biotechnologies.

Unity’s approach uses a drug-based approach to senolytics and is scheduled to enter human clinical trials in 2018. A number of other research teams are also developing drug-based approaches to removing senescent cells, and the competition looks set to be fierce in this area in the coming years.

Oisin’s approach, which we discussed here, makes use of suicide genes and hopefully will be tested in clinical trials not too far into the future, thanks to venture funding presently being collected. If this system can be made to work, it will allow very selective targeting of senescent cells by destroying only those giving off a target gene or genes. Thus, if a unique gene expression profile for senescent cells is determined, it would mean only those cells were destroyed, with less risk of off-target effects.

Oisin owes its existence to the SENS Research Foundation and the Methuselah Foundation, which provided the necessary seed funding. Kizoo Technology Ventures has also invested in Oisin.

Extracellular crosslinks

The so-called extracellular matrix is a collection of proteins that act as scaffolding for the cells in our body. This scaffolding is rarely if ever replaced, and a really bad consequence of this is that its parts eventually end up being improperly linked to each other through a process called glycation—the reaction of (mainly) blood sugar with the proteins that make up the extracellular matrix itself.

The resulting cross-links impair the function and movement of the linked proteins, ultimately stiffening the extracellular matrix, which makes organs and blood vessels more rigid. Eventually, this leads to hypertension, high blood pressure, loss of skin elasticity, and organ damage, among other problems.

While there are different types of cross-links—known as AGEs, short for advanced glycation end-products—glucosepane is arguably the worst, being the most common and long-lasting of all, and the body is very ill-equipped to break it down.

GlycoSENS: How to solve this problem, and how far we’ve got

In order to eliminate unwanted cross-links, the SENS approach proposes to develop AGE-breaking molecules that may indeed sever the linkages and return tissues to their original flexibility. Of course, in order to do so, crosslink molecules need to be available for research to attempt to combat them with drugs, and especially in the case of glucosepane, this has been a problem for years.

Glucosepane is a very complex molecule, and very little of it can be extracted from human bodies, and not even in its pure form. This has been greatly hampering the progress of research against glucosepane, but thankfully, this problem is now solved thanks to a collaboration between the Spiegel Lab at Yale University and the SENS Research Foundation, which financially supported the study. It is now possible to fully synthesize glucosepane, allowing for researchers to create it on demand and at a cost-effective price.

The Spiegel Lab’s scientists are now developing anti-glucosepane monoclonal antibodies to cleave unwanted cross-links. The collaboration between the Spiegel Lab and SRF dates all the way back to 2011, but it was in 2015 that the Lab announced its success and published a related paper [4] in the journal Science.

Further information on glucosepane cross-link breakers can be found in this interview with Dr. David Spiegel from Yale University on Fight Aging!; a list of studies on the subject funded or otherwise supported by the SRF is available here.

SRF also worked with the Babraham Institute on a cross-link quantification project.

Let’s help SRF move forward

Readers who wish to donate to SRF to help the organization in its crusade against the ill health of old age can do so by contributing to its winter fundraiser or even becoming SRF patrons. Have a look at SRF’s donation page to find out more.

NB: Dr. Aubrey de Grey (Chief Science Officer and Co-founder of SENS Research Foundation) himself held an AMA (“ask me anything”) on Reddit on December 7, at 14:00 PST (22:00 UTC, 17:00 EST). The questions and Dr. de Grey’s responses can be found here.

Literature

[1] Boominathan, A., Vanhoozer, S., Basisty, N., Powers, K., Crampton, A. L., Wang, X., … & O’Connor, M. S. (2016). Stable nuclear expression of ATP8 and ATP6 genes rescues a mtDNA Complex V null mutant. Nucleic acids research, 44(19), 9342-9357.

[2] Gaspar, J., Mathieu, J., & Alvarez, P. (2016). A rapid platform to generate lipofuscin and screen therapeutic drugs for efficacy in lipofuscin removal. Materials, Methods and Technologies, 10, 1-9.

[3] Mathieu, J. M., Wang, F., Segatori, L., & Alvarez, P. J. (2012). Increased resistance to oxysterol cytotoxicity in fibroblasts transfected with a lysosomally targeted Chromobacterium oxidase. Biotechnology and bioengineering, 109(9), 2409-2415.

[4] Draghici, C., Wang, T., & Spiegel, D. A. (2015). Concise total synthesis of glucosepane. Science, 350(6258), 294-298.

 

About Steve Hill

As a scientific writer and a devoted advocate of healthy longevity technologies, Steve has provided the community with multiple educational articles, interviews, and podcasts, helping the general public to better understand aging and the means to modify its dynamics. His materials can be found at H+ Magazine, Longevity Reporter, Psychology Today, and Singularity Weblog. He is a co-author of the book Aging Prevention for All – a guide for the general public exploring evidence-based means to extend healthy life (in press).

About Nicola Bagalà

Nicola Bagalà has been an enthusiastic supporter and advocate of rejuvenation science since 2011. Although his preferred approach to treating age related diseases is Aubrey de Grey’s suggested SENS platform, he is very interested in any other potential approach as well. In 2015, he launched the blog Rejuvenaction to advocate for rejuvenation and to answer common concerns that generally come with the prospect of vastly extended healthy lifespans. Originally a mathematician graduated from Helsinki University, his scientific interests range from cosmology to AI, from drawing and writing to music, and he always complains he doesn’t have enough time to dedicate to all of them which is one of the reasons he’s into life extension. He’s also a computer programmer and web developer. All the years spent learning about the science of rejuvenation have sparked his interest in biology, in which he’s planning to get a university degree.

About LIFE EXTENSION ADVOCACY FOUNDATION (LEAF)

In 2014, the Life Extension Advocacy Foundation was established as a 501(c)(3) non-profit organization dedicated to promoting increased healthy human lifespan through fiscally sponsoring longevity research projects and raising awareness regarding the societal benefits of life extension. In 2015 they launched Lifespan.io, the first nonprofit crowdfunding platform focused on the biomedical research of aging.

They believe that this will enable the general public to influence the pace of research directly. To date they have successfully supported four research projects aimed at investigating different processes of aging and developing therapies to treat age-related diseases.

The LEAF team organizes educational events, takes part in different public and scientific conferences, and actively engages with the public on social media in order to help disseminate this crucial information. They initiate public dialogue aimed at regulatory improvement in the fields related to rejuvenation biotechnology.