SENS Conference, Berlin 2018

Three days in Berlin this spring were perhaps the most exciting three days I have lived in the past few years! I was attending the SENS Conference for 2018 — a conference focused on research aimed at letting us live longer, in fact much longer, lives. If you have hopes of living longer (not just to 80 or 90 or 100 years, but potentially into the hundreds of years) then you really must learn what is going on. The results I heard at this conference were just amazing — I am looking forward to next year’s conference!

To explain what was happening at SENS 2018 it is necessary to give a little background. In 2005, Aubrey de Grey with Michael Rae produced the book “Ending Aging“. The thesis of the book is that we age because of a gradual decay in the microbiological makeup of our bodies. In particular this degradation occurs in seven major areas of our cellular and extra-cellular body structure:

  • cell loss, cell atrophy
  • junk outside the cells
  • crosslinks outside the cells
  • death resistant cells
  • mitochondrial mutation
  • junk inside the cells
  • nuclear mutations– only cancer matters

A more detailed description of the proposed research approach is given on the SENS website.
Ending Aging was published in 2005 and I read it shortly after publication. In 2009, de Grey and others created the SENS foundation to promote research in support of the tenets of the book. A description of the proposed research approach is given on the SENS website. Over the years a number of conferences had been held to review and report progress, firstly in a biannual basis and now, as more activity is occurring, annually. I had been waiting for many years for the sequel to the book and it didn’t come so I thought I would attend the 2018 SENS conference. This year it was held in Berlin.

The scene was electric! The total number of attendees was a little under 400. The mix was interesting. There were the researchers who were presenting or monitoring progress at a technical level. There were investors looking for a chance to invest in a potential gold mine. There were students looking for a field in which to work. And there were a few people like me (hard to believe there weren’t more) who just want to live a long time. We all milled around together and took in a hectic schedule of talks and pauses (where we could network and eat — all meals were supplied). The days lasted from morning until well into the evening. Here is the schedule of talks.

I was one of the attendees who had most TATS (trips around the sun). I am not a cellular biologist, although I have been reading about cellular biology for 60 so TATS. While able to generally follow many of the talks, many were beyond my understanding. So, it is not easy for me to provide a very detailed account of what was presented. Instead, I will summarize my understanding of four talks that I think I understood, and which I thought had very interesting possibilities in terms of longevity, addressing health problems, and/or investment. These are preliminary understandings on my part; I hope to improve my understanding through further research and may have to re-visit and amend these descriptions.

A Treatment for the Symptoms of Alzhiemer’s disease

Doug Ethell, Ph.D., CEO of Leucadia Therapeutics Inc. gave a fascinating presentation titled “Early Alzheimer’s Disease is a Reversible Plumbing Problem”.

Alzheimer’s is a disease which affects over 5 million Americans. The disease results in the buildup of beta-amyloid plaques and neurofibrallatory tangles (called tau tangles) in the brain. The disease begins with mild loss of cognitive abilities and progresses to dementia and complete loss of mental control of the body. The brain shrinks as the disease progresses and permanent irreversible damage occurs.

Dr. Ethell described how the molecules that cause the plaques and tau tangles are normally cleared from the brain by natural processes in a healthy brain and so do not accumulate and create Altzheimer’s disease. The clearing mechanism is through transport from the cranial cavity in the cerebrospinal fluid which drains from cranium through the cribriform plate. The molecules that are so draining are relatively large (too large to pass through the blood/brain barrier). In some individuals the porous channels in the cribriform plate gradually get plugged or sufficiently blocked (perhaps through trauma) to prevent the removal of the larger molecules that are normally purged.

There have been thousands of clinical trials to test drugs which might treat the disease. They have not been successful.

Dr. Ethell presented an approach which does not deal with the cause of the disease (consistent with the SENS approach) but, on the other hand, presents a curative treatment which might arrest the progress of the disease and possibly cause some reversal of the damage caused by Alzheimer’s. It is a surgical procedure, which involves the insertion of a stent into the cribiform plate to allow easy drainage of the spinal fluid. The insertion would involve entering the cranial cavity through a nostril a procedure which he described as likely less intrusive than a tooth root canal treatment. It is an outpatient treatment.

Following on from successful in vivo trials with animals, Dr. Ethell reported that his company hopes to start human trials in early 2019.

A Treatment for Macular Degeneration

As many as 11 million Americans have some form of age-related macular degeneration (AMD), a degradation of vision which can lead to blindness. There are no currently known cures or medications for the disease.

Kelsey Moody of LysoClear gave a presentation where he reported on the results of a SENS type approach to dealing with the problem of AMD. AMD is caused by a gradual buildup of a deposit of lipofuscin in the retinal area. LysoClear investigated a number of enzymes that had the potential to absorb and dispose of the lipofuscin buildup and eventually determined that recombinant manganese perozidase (rMnP) was particularly effective in destroying almost all types of molecules that make up the lipofuscin. They then developed, using techniques which are known in other medical treatments, a method to deliver the rMnP so as to effect the removal — a process that required packaging the rMnP suitably for absorption into the cells and linking with lysosomes so as to degrade and remove the lipofuscin.

The procedure has been proven in vivo with mice and the firm now hopes to go forward in early 2019 with human trials. There are a class of sufferers from macular degeneration who have the condition as a result of inherited genetic defects ( Stargardt and Best diseases) which lead to early blindness. It is hoped that testing on these patients will allow a quicker passage through the FDA approval process for the treatment

You can see Kelsey Moody’s presentation here.

A Treatment for Prostate Cancer and Senescent cells

Dr. John Lewis from the University of Alberta and also Chief Science Officer of Iosin Biotechnology gave a presentation on work that they have been doing to cause senescent cells to commit suicide. The technology is fascinating. In a very abbreviated and simplified description it is as follows: Senescent cells express the P16 protein. Dr. Lewis and his team have created plasmids, encapsuled in lipid nanoparticles (LNPs) which, being so small as to be unnoticed by the immune system, enter cells without generally creating a problem. The plasmids in these LNPs react to the presence of P16 and cause the iCasp9 protein to be generated. This protein in turn causes the cell to ‘commit suicide’. This results in annihilation of the senescent cell. A particular application of this technology is the treatment of prostate cancer which expresses protein p53.

You can see Dr. Lewis’ presentation here (scroll down a bit).

Dr. Lewis reported successful in vivo treatments of prostrate cancer and promising results on longevity with mice. The company plans to proceed with human trials on treating prostate cancer in 2019.

Biomarkers for Aging

Attila Csordas, founder of AgeCurve, gave a fascinating talk on the potential for using biomarkers to measure and monitor the phenomenon of aging.

Attila discussed how, because aging is a multi-faceted form of bodily degradation, biological aging can only be measured by monitoring many different biological factors. While his work in this area is just getting off the ground, he gave a convincing argument for a broad-based measurement of proteins in bodily fluids as a way of creating a database against which individuals could determine where they were in the spectrum of aging and also, from the information, plot strategies to reduce the speed of aging. The method he is using is to take a sample of saliva and then have that sample analyzed, using mass spectrometry, revealing measures on over thousands of proteonic variables (human proteins, bacterial species and bacterial proteins).

The project started in the U.K. and is now available in the U.S. The cost of the package is around $300 US (check the AgeCurve website for current prices).

After hearing his presentation I purchased the service and have been very impressed with the results. The next step is to start using the information to decelerate my personal rate of aging.

An interesting announcement, just recently, indicates that Aubrey de Grey has joined the advisory board of AgeCurve.

Attila’s SENS Berlin 2018 presentation is here.

Topics That Were Missing?

While the conference was incredibly stimulating and full of information that might lead to the target of Undoing Aging, it seemed to me that there were some topics missing — topics that would have been of relevance to the general theme and also of importance to some of those who were attending. Here are my observations:

Planning for Longevity

What should we be doing now? I, like many others, attended the conference looking for guidance on what we should be doing now to improve both our lifespan and our healthspan. There was little or no discussion related to how we take certain actions now to be sure that we were still be alive when ‘longevity escape velocity’ (when we gain at least one year of added life for each year that passes) is achieved.

Nutrition

It appears that the only so far proven method of extending life in humans is through caloric restriction. There was no discussion of this. Is there no further work in this area that is worth reporting?

In addition to caloric restriction there is clear indication that some diets are more beneficial to good health, and hence to increased healthspan, than others. The food at the conference was all catered in a buffet style offering. It was interesting to note that there were many vegan (and after the first day, vegan and gluten-free) options available at each serving. (The food was excellent!). I thought that some focus on nutrition might have been beneficial (especially in the context of actually living long enough and with sufficient good health to achieve significantly extended lifespans).

The Microbiome

We have gradually recognized that perhaps only a quarter of the cells in our bodies are cells with our characteristic DNA. The other cells are bacteria that co-exist with us. What is the relation between these cells and our existence and our longevity? What steps should be taken to nurture our microbiome to enhance longevity?

Does SENS make Sense?

“Ending Aging”, the book published by De Grey with Rae in 2007 described a promising future in which a number of causes of aging (see introduction above) could be overcome by methods of bio-cellular engineering leading to lifespans (and healthspans) into the hundreds of years. de Grey has not written a sequel to let us know of the progress in this direction. It seems relevant, to me, to both examine the model, as presented in the book, and to examine the progress in achieving the goals presented by the authors.

As one not part of the academic, research environment in which progress is occurring, (and since de Grey and Rae have not published a sequel) I would have appreciated some sort of presentation or panel discussion which would have given an balanced assessment of where the model is in the light of current knowledge.

The Future

Where do we go from here?

For me, with 75 TATS, an important issue is will I get to the position of escape velocity?!

And, yes, I do plan to attend SENS 2019.

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