SENS Research Foundation Newsletter for June 2014

The latest SENS Research Foundation newsletter arrived in my in-box today, with an update on what is new in the Foundation's programs of research into the foundations of future rejuvenation treatments. There is a conference coming up later this year, a new crop of young scientists interning at various research centers to help advance the state of the art, and recently published research directed at the removal of a form of amyloid implicated in the death of those who live the longest and survive everything else that aging throws at us.

The Foundation staff have set themselves an aggressive mid-year fundraising goal of $250,000 before the end of August. Your home town will burn that much on their next game night, but here this is enough to fund numerous sophisticated projects that advance the state of knowledge in areas of medical science most relevant to treating and reversing the underlying processes that cause aging. There is always a balance between saving for the future and spending now to build better options in the future, but no society in history has ever come close to funding enough work on building better medicine. More is always better. Now we have a golden chance to eliminate the suffering and death caused by age-related disease in just a few short decades of work, and the price to achieve this goal is falling dramatically as biotechnologies improve.

As I mentioned yesterday, we might not be millionaires, but we are the ones with vision enough to band together and help to fund the early work on rejuvenation treatments, the necessary foundations for the proof of concept in mice that will exist in years to come. The big donors always turn up late to the party to pick up the sure thing and carry proven, demonstrated work the last few yard into the clinics. Without us, there would be no party.

At the end of last year the grassroots community raised $100,000 for SENS research, and I'm pleased to have played a modest role in helping that to happen. That was an investment in ensuring that later in our lives we will not be left helpless in the face of age-related disease. I would like to think that we can do just as well this year: more than just money, it is a matter of showing that there are thousands of people who support this work and the goal of an end to the suffering that comes with advancing age. That support attracts attention, and makes it ever more possible for the Foundation to open doors to traditional and more conservative funding sources.

Help Us Meet Our Mid-Year Fundraising Goal

SENS Research Foundation would like to thank all of you for your ongoing support. hanks to your generous donations of time, money, and encouragement, we have been able to continue advancing our work to cure - not just treat, but cure - the diseases of aging. We are accomplishing this goal in 2014 by:

1) Funding promising new research: SRF currently has 3 internal and 15 extramural research projects taking place at universities and research institutes around the world. In March 2014, SENS Research Foundation secured its highest-profile academic publication to date, with the publication by J. Biological Chemistry of a report of SRF-funded work at the University of Texas at Houston. In this study, Dr. Sudhir Paul and colleagues report the isolation of catabodies selective for the type of amyloid that underpins the number one cause of death in the oldest of the old - those who reach the age of 110. A catabody is an unusual type of antibody, on which Dr. Paul is the world leader; rather than just attaching to their target, they actually cut it up. By this means, we can destroy this amyloid and eliminate a major component of aging.

2) Building a strong, collaborative community: We are bringing together leading scientists, regulators, venture capitalists and the general public together at our upcoming Rejuvenation Biotechnology Conference, August 21-23, 2014, in Santa Clara CA.

3) Training the next generation of bright, young scientists: Currently, 17 interns are hard at work contributing to our funded research projects. These students will be presenting in the Poster Session at the Rejuvenation Biotechnology Conference.

However, in order to continue advancing the field of regenerative medicine, we need your help. Simply put, your funding will help us continue our research, support our interns and bring the community together. We've set a funding challenge to raise at least $250,000 between today and August 31, 2014. If you would like to help these programs continue to grow, please show your support by making your tax deductible donation today.

SRF Education: 2014 Summer Scholars Program Is In Session

SENS Research Foundation is pleased to announce the start of the 2014 Summer Scholars Program. Fifteen students were selected to participate this year at the Buck Institute for Research on Aging, the Harvard Stem Cell Institute / Harvard Medical School, University College London, the University of Oxford, the Wake Forest Institute for Regenerative Medicine, and our very own SRF Research Center. Over the next month, SRF will be posting profiles on the SRF Education blog for each of our summer scholars to give you the opportunity to learn more about each scholar and the research he or she will be conducting.

SRF's Thomas Hunt Awarded 2014 Thiel Foundation Fellowship

SENS Research Foundation would like to congratulate Thomas Hunt, who has been awarded one of the 20 Thiel Fellowships granted in 2014. Thomas, 17, began volunteering in our Research Center three years ago and now works alongside our intramural team studying Alternative Lengthening of Telomeres (ALT), a mechanism that may play a key role in the development of cancer. He has a particular interest in automated high-throughput drug screening to find compounds that reduce ALT activity.

As is usually the case, the best part of the newsletter is the question of the month section, in which Michael Rae answers queries from supporters. This month's topic is something I recall discussing once or twice with folk myself, and certainly in past Fight Aging! posts on unusual lower animals such as possibly ageless hydra and rejuvenating microbes. Why can't researchers just investigate the details of the indefatigable regeneration of the hydra and port the underlying mechanisms into our biology? As it turns out there are very good reasons as why we can't do this, much of which stems from the fact that we are more structurally complex. Our lives and our very selves depend on the fine structural details of our tissues, especially the brain and nervous system, remaining intact without being recycled, rebuilt, or otherwise majorly altered.

Question Of The Month #4: Can Medicine Take a Cue from 'Natural' Negligible Senescence?

Q: Amongst the "Strategies for Engineered Negligible Senescence" (SENS), have you considered the original negligibly-senescing organisms as sources for strategies? Organisms like bristlecone pine, lobsters, and the "immortal jellyfish" Turritopsis dohrnii seem to live indefinitely without suffering age-related ill-health or loss of function, so maybe we could learn their tricks and incorporate them into the human genome.

A: As beautifully illustrated in Rachel Sussman's recent book, The Oldest Living Things in the World, the example of these organisms is inspiring and imaginatively appealing. Among other things, they put the lie to the idea that degenerative aging is simply an ineluctable part of being alive, against which nothing can be done. Still, trying to adapt their specific metabolic and structural mechanisms to human use is not likely to help us achieve our goal of preventing and arresting age-related ill health.

While we don't yet know all the metabolic and molecular details, we do have a pretty good idea of why these organisms don't meaningfully age, and unfortunately those reasons aren't compatible with human biology. For instance, bristlecone pines can be said to "live" for thousands of years, but only the outermost layers of the tree are actually still alive: the wood in the middle of a tree is composed of dead 'husks' of cells. The tree is "alive" because the outer layers surrounding the "dead" inner core continues to carry out the business of life, performing photosynthesis and dividing, allowing the composite structure of the tree to keep growing. There is no plausible way to adapt this as a bulwark against the problems of human aging.

The situation is less extreme in the case of most negligibly-senescing animals - but still, it's difficult to see how their tricks could be applied to us without harm. Most such organisms never stop growing, allowing their continuously-dividing cells to literally dilute aging damage away. Rockfish and lobster, for instance, will continue to grow and grow as long as they are fed and not killed by causes unrelated to aging. Aside from the alarming or ridiculous vision of humans that continued to grow and grow year in and year out for centuries, a major problem with adopting this trick is that some of our most of our most important organs are composed of nondividing cells: heart, brain, and skeletal muscle. (That's why major mitochondrial mutations, for instance, build up in these organs and not (for instance) in the skin or liver). We're rather attached to having these cells stay in place and intact, especially when it comes to the way that our neurons arrange themselves; we wouldn't want to tamper with them by triggering them to begin dividing again.

The jellyfish example is even less compatible with the human life cycle (and with our aims biomedically): their "immortality" comes from the fact that they aren't really even single organisms, but colonies of cooperating unicellular organisms that transiently adopt particular functions within the "meta-organism" of the polyp. The individual cells that comprise the polyp potentially divide indefinitely, and can differentiate and re-differentiate to adopt different functions. When a given polyp is irreversibly damaged, this flexibility allows its constituent cells to disperse, regroup, and create a new polyp, with each constituent of the old polyp transforming itself into a different kind of cell to perform a function that is needed by the newly-formed "daughter" polyp. It is not that these abilities allow T. dohrnii cells to indefinitely preserve the healthy function of a single, identifiable organism over time, in other words, but that it allows them to form new polyps when a given polyp-form can no longer be sustained.

These incompatibilities probably mean that the only way to take advantage of these tricks would be to engineer a completely new human-like organism, starting from the embryo and growing it out. Whether or not the life of such an organism is feasible or desirable, it isn't something that we can do to help humans that are alive today to avert a future of age-related disease and disability.

Instead of starting over from scratch and fundamentally reshaping our bodies and brains and way of being alive in the world, the strategy under pursuit by SENS Research Foundation is to repair and renew the bodies that we already have at the cellular and molecular level over time. Organisms that are naturally negligibly-senescent are able to dilute away the cellular and molecular damage that drives degenerative aging. By developing rejuvenation biotechnologies that remove, repair, replace, and render harmless this damage as it accumulates in our own cells and tissues, we can return our bodies to their youthful structural integrity. Through regular applications of this "cellular surgery," we cam restore the structural and functional youth of our bodies to a state of health, vigor, and vitality, keeping the degenerative aging process and its many diseases and disabilities at bay.


I had a look at Dr Sudhir Paul's video on the SENS website. What I found exciting was the idea that catabolic IgM antibodies that break down Alzheimer's disease amyloids themselves may avoid the inflammation problem caused by more 'regular' IgG antibodies which recruit phagocytes to do the job.

I wonder if any Pharmaceutical company or any teams around the world are actively researching this? Or is Dr Paul way ahead of everyone else in the world in the area of catabolic antibodies.

Of course these catabolic IgM antibodies haven't yet been shown to break down an amyloid in vivo yet, which seems to be an important milestone before more people start to take notice.

Posted by: Jim at June 15th, 2014 6:40 AM

I like the drive for money but I feel like they are drawing from the same wells. I wish other people would sign up sooner.

Posted by: Michael at June 17th, 2014 5:49 AM

@Michael: Indeed, broadening the community of donors is pretty important.

As for this fundraising drive, I'm sitting it out in favor of doing something more organized in Q4 of this year, akin to last year but with forethought and planning involved.

Posted by: Reason at June 17th, 2014 6:09 AM

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