Halfway to Our SENS Research Fundraising Goal, and Giving Tuesday is Coming Up on December 1st

This year's Fight Aging! matching fundraiser has a $125,000 fund provided by generous philanthropists, and we are seeking to raise a further $125,000 from the community to fund progress in longevity science. All charitable donations made before the end of 2015 will be matched dollar for dollar, with the funds going to the SENS Research Foundation to support their work on rejuvenation biotechnology. This includes programs aimed the safe removal of senescent cells and glucosepane cross-links, both of which are counted among the root causes of degenerative aging. I'm pleased to note that we're half way to the goal, with a month a half left to go: more than 390 donors have collectively given $67,000 in the last six weeks. There is another $58,000 left to go to hit the target, and if we manage this before the end of the year then we'll have collectively given a cool quarter of a million dollars this year to speed up the best approaches to human rejuvenation therapies.

With this in mind, remember that Giving Tuesday is coming up on December 1st. If you haven't yet donated - or know people who might be persuaded - then that will be a great time to jump in. Medical science doesn't emerge from nothing: it needs your support, and here is a chance for your donations to be matched by other funds as well. From the latest SENS Research Foundation newsletter:

SENS Research Foundation is getting ready to celebrate #GivingTuesday on December 1st. GivingTuesday is now a global event celebrated by supporters of various charities giving to their favorite causes. If you've been planning on contributing to the fight against age-related disease this year, GivingTuesday is a great opportunity to make a difference.

So far, SENS Research Foundation has 3 matching grants set up for GivingTuesday. The first is our FightAging! Challenge which will match every dollar you give us up to $125,000. On GivingTuesday, the first $5,000 we raise will not be doubled or even tripled - it will be quadrupled thanks to the generosity of the Croeni Foundation and Aubrey de Grey. Help us turn $5000 into $20,000 and accelerate the fight against age-related diseases! Donate at http://www.sens.org/donate on December 1st.

If there are any in the audience interested in adding their own $5,000 matching grant to this Giving Tuesday initiative, then by all means contact us with the offer of help, and we'll connect you with the SENS Research Foundation to arrange the details.

It is thanks to philanthropy that SENS research is making progress. Just take a look at the SENS Research Foundation's 2015 annual report: seed funding the US startup Oisin Biotechnology to work on senescent cell clearance; transferring lysosomal aggregate clearance technology to Human Rejuvenation Technologies for development; the French company Gensight is now devoting significant funding to to clinical development of the mitochondrial repair technologies whose early stage research was supported under the SENS banner; progress towards the toolkit needed for glucosepane cross-link clearance was published in the prestigious journal Science. All of these initiatives were funded in part by everyday philanthropists just like you and I, alongside people like Peter Thiel, Jason Hope, and Aubrey de Grey.

The wheel is turning, and meaningful progress towards rejuvenation treatments is taking place. Our donations continue to move SENS research closer to realization, and closer to becoming the mainstream of aging research. The more that we can help to fund the demonstrations of effectiveness at every stage of early research through to early clinical translation, the sooner that therapies to treat and control aging will arrive.


"This includes programs aimed the safe removal of senescent cells and glucosepane cross-links, both of which are counted among the root causes of degenerative aging"

I know it is just pure speculation, but I've got to wonder what the combined effect of fairly comprehensively removing both of these would achieve cosmetically? Would people's skin actually look any younger?

Posted by: Jim at November 17th, 2015 4:11 AM

Jim, a quick Google search suggests that skin age appearance is multifactorial. Removing cross links would help, but driving skin cell division (often induced by peroxide products in acne and "anti-aging" creams), structural protein expression, and restoring subcutaneous fat and skin moisture would probably all contribute to younger-looking skin. I certainly don't have the chops to quantify that :)

I'll ask a dermatologist on my next appointment and get back to you.

Posted by: Seth at November 17th, 2015 8:55 AM

@Jim Crosslinks are a significant contributor to increasing TGF-beta levels which is a big factor in the decline of stem cells due to loss of signalling (Conboys et al). As Michael Rae recently confirmed elsewhere on here, removing the crosslink (glucosepane in particular) would improve signalling and the host of benefits downstream that has and more!

I believe a combination of Senescent cell removal + removing the crosslinks would be a pretty significant boost to lifespan and health. I am hoping the MMTP will shortly be able to test this and prove it. We cannot of course clear crosslinks yet but I am hoping we can test Alk 5 inhibitors to suppress TGF-b levels as the Conboys do and combine it with Dasatinib(Sprycel) & Quercetin which Scripps tested. This should show some of the benefits though it isn't as good as cleaving the crosslinks of course.

We are currently confirming our final test list but I will keep you updated. It is my hope that if we do this it will help highlight how important SENS work to remove crosslinks is and focus more attention on its removal.The relative small price of testing this could really help boost the signal for SENS. I am convinced that dealing with the root damage is really the only sensible proposal.

Interestingly I have seen some papers that also show Metformin has some effect on glucosepane, no surprise people are exploring its use off label.

Posted by: Steve H at November 17th, 2015 10:12 AM

@Jim: You've asked or made suggestions to that effect before, and I thought I'd addressed them — but a Google search of the FA! site suggests I must've been thinking of some other correspondent. I apologize if it seemed like I've been ignoring the question.

As Seth suggests, as with most conditions related to aging, there is no single form of aging damage responsible for the various changes that happen in skin as we age, and it's actually far from clear to me that glucosepane is the most important. The elastin protein that gives skin its elasticity becomes crosslinked and snaps, reducing its youthful ability to snap back into place when pulled, but there's a lot more to the visible and functional aging of the skin than loss of elasticity. The anchored system that supports the collagen-producing fibroblast cells degrades, leading fibroblasts to collapse and stop making new protein; the skin accumulates senescent cells, leading to SASP that spews out a range of inflammatory signaling molecules and proteolytic enzymes that degrade the supportive structures in the skin; the skin accumulates years of oxidative damage, leading to mutations; in many people, the dark pigment melanin that normally darkens our skin to give us an even tan clumps together into concentrated deposits known as "age spots" (often mistakenly attributed to lipofuscin in the anti-aging community, propagating an error first introduced by Pearson and Shaw) (and note that age sposts are both functionally one of the least important kinds of damage in aging skin and yet amongst the most visibly obvious such damage; ongoing rising oxidative stress distorts intracellular signaling, leading to aberrant keratinocyte function; etc. Like Seth, I don't have the chops to quantify all of that — and I doubt his dermatologist has them, either.

@Steve H: I'm not aware of any specific evidence that metformin lowers glucosepane, except in the trivial but theoretical sense that lowering the excess blood glucose in diabetics ought to decelerate its the formation. Do you indeed have more specific evidence, and any at all in nondiabetic mammals?

To really, convincingly rejuvenate the aging skin, therefore, involves tackling a wide range of aging damage — just like tackling other age-related disease and disability.

Posted by: Michael at November 17th, 2015 11:07 AM

Yeah sorry Michael, I'm just asking questions off the cuff. I think I've asked something similar before. I'll try to compile these replies, and read Ending Aging at some point.

Posted by: Jim at November 17th, 2015 5:48 PM

@Michael no not really beyond the extent that you mention. We are sifting a lot of data though at the moment so if I find anything I will let you know.

Posted by: Steve H at November 18th, 2015 10:26 AM

Thanks to Steve and Michael for those explanations; this is a question I've long had myself and I'm glad you could shed some light on it.

Posted by: Nico at November 18th, 2015 12:23 PM

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