The SENS Research Foundation is one of the few scientific organizations energetically working on realistic approaches to human rejuvenation treatments, based on repair of the known cellular and molecular damage that causes aging. This is very much a departure from the current mainstream of medicine where researchers largely ignore aging as a cause of disease in favor of trying to patch over age-related conditions in their late stages. As a strategy this is doomed to be an expensive and poor path forward, which is precisely why we need disruptive initiatives like the SENS Research Foundation to shake things up and illustrate the better path ahead. The Foundation funds research where there are roadblocks or a lack of progress, but is as much involved in advocacy, both within the scientific community to convince more researchers to work in this important field, and outside the community in order to sway funding sources and the public at large.
The latest SENS Research Foundation newsletter arrived in my in-box today, along with an announcement that registration is open for a new rejuvenation biotechnology conference that will be held in California later this year.
Registration Now Open For Rejuvenation Biotechnology 2014
Where: Hyatt Regency Santa Clara, Santa Clara, CA
When: August 21 - 23, 2014
To Register: http://sens.org/rb2014
SENS Research Foundation is pleased to announce that registration is now open for the Rejuvenation Biotechnology 2014 Conference. The conference theme is Emerging Regenerative Medicine Solutions for the Diseases of Aging. The Rejuvenation Biotechnology Conference builds upon novel strategies being pioneered by the Alzheimer's and cancer communities. By convening the foremost leaders from academia, industry, investment, policy, and disease advocacy, SRF seeks to inspire consideration of the wider potential of these strategies and evaluate the feasibility of preventative and combinatorial medicine applications to treat all aging-related diseases.
Confirmed speakers include:
* Richard Barker, CASMI
* Maria Blasco, Spanish National Cancer Research Centre
* George Church, Harvard Medical School
* Aubrey de Grey, SENS Research Foundation
* Caleb Finch, USC Davis School of Gerontology
* Jeanne Loring, Scripps Research Institute
* Stephen Minger, GE Healthcare Life Sciences, UK
* Brock Reeve, Harvard Stem Cell Institute
* Matthias Steger, Hoffmann-La Roche
* Michael West, Biotime, Inc.
Students and researchers are invited to submit poster abstracts for the Rejuvenation Biotechnology Conference Poster Session. Poster submissions will be evaluated by members of the SENS Research Foundation Team. The deadline for poster submissions is July 15, 2014.
We invite everyone in our community to register and participate in this new conference, our first in the US in over 6 years.
As is usually the case, the scientific section of the newsletter is also well worth reading. This time it is an examination of mitochondria and their role in aging:
Question Of The Month #2: Aging and the Limits of Mitochondrial Restoration
Q: Why can't fixing mitochondrial mutations and restoring peak ATP levels in the majority of cells in older people fix everything? I understand there are several classes of accumulated age-related damage like plaque build-up and glycation, which is why it seems like we'd need more than one approach to reverse aging, but if we give cells enough energy, could it be possible that all of it will just take care of itself? In other words, if cells once again have enough energy to perform their jobs to full capacity, couldn't they then carry out functions/mechanisms crucial to getting rid of all the age-related damage? I mean it sounds odd if you think of it using the car analogy: if you give an old car a new battery it's not going to fix other things like rust accumulation or leaky pipes... but because cells all work as a system, I think it's more likely that they'd be able to help control age-related accumulations.
A: While mitochondrial DNA mutations are indeed important to address in the context of a comprehensive rejuvenation strategy like SENS, there are several reasons to think this alone would not be enough to deal with most other forms of aging damage.
First, it's actually not all that clear that the mitochondria in the great majority of an aging person's cells actually suffer much decline in capacity to produce ATP. Certainly many older cells do suffer energy deficits, related to insulin resistance and/or secondary to other age-related metabolic (mal)adaptations - but those are causes unrelated to mitochondrial mutations.
True, the cells whose mitochondria we're most concerned about suffer a pretty drastic reduction in energy production: those are cells that have been taken over by mitochondria harboring large deletions. But remember that such cells constitute a tiny percentage of the cells in the body. If the goal is simply to restore the capacity of the mitochondria in the majority of aging people's cells to produce ATP to levels similar to young people, we're already there.
Also, while individual cells overtaken by mutant mitochondria certainly lack energy, such energy deficits don't do anything to hold back the great majority of the body's cells (since individual cells have their own mitochondrial power supply). Yet they still suffer aging damage. Furthermore, much aging damage accumulates because we lack the means to deal with it, meaning no amount of energy alone can prevent its accumulation.
Third, a lot of aging damage is extracellular, and such damage can't really be addressed in most cases by cells. This is especially true in the case of damage to extracellular matrix (glycation crosslinks and mechanical fatigue of arterial and other elastin lamellae, for instance), where typically there isn't even any ATP available, irrespective of a person's age.
Fourth: remember, we were all young once. At that point, few or none of our cells had been taken over by mutant mitochondrial DNA, and yet even at that point in our lives we were aging. Indeed, this is true of the two examples you cite in your question: we are all born with at least some aging damage, such as fraying of arterial elastin and early atherosclerotic lesions. If youthful mitochondrial energetics were enough to abrogate the accumulation of aging damage, the degenerative process wouldn't get going until a substantial number of our cells were occupied by mutant mitochondria (which, again, arguably doesn't even happen when people reach what are today rather advanced ages).
Most importantly: while it may one day be possible to begin administering rejuvenation therapies to people who are still in their youthful prime, at present we do not have the luxury to do this. Early recipients of rejuvenation biotechnologies will, by and large, be people whose bodies are already riddled with multiple kinds of cellular and molecular aging damage. Even if mitochondria capable of churning out ATP with the alacrity of Usain Bolt in his prime were enough to prevent other forms of aging damage from getting started (and again, the normal course of aging argues strongly otherwise), it seems far less plausible that it would be able to reverse the accumulation of aging lesions in people who have already been suffering such damage for six decades or more of life.
In short: if we are to save the greatest possible number of people from the age-related slide into disease, disability, dependence, dementia, and eventual death, we are going to have to tackle the full spectrum of aging damage that has already riddled their bodies, and obviating mitochondrial mutations seems highly unlikely to achieve this key goal on its own.