Conference: “New Insights into Healthspan and Diseases of Aging: From Molecular to Functional Senescence”

There’s a Keystone Symposium on this subject Jan 31-Feb 5 2010:

Aging can be defined as the gradual loss of the ability of the organism to maintain homeostasis. Our aim will be to focus on the molecular and cellular mechanisms by which tissue and organ function deteriorate and homeostasis fails rather than on longevity itself, which has been the theme of previous Keystone Symposia meetings on aging. Work from a variety of models is recognizing that organisms, especially humans, are complicated systems in which interventions that extend lifespan might not necessarily block the aging and loss of function in specific organs or tissues and vice versa. Continuing this approach will help us gain an understanding and appreciation of the complexity that underlies aging in humans. The aim of this meeting is to reveal the integration and communication between pathways and systems during functional aging and their relationship with longevity. This meeting will highlight important questions to address in future research. Most importantly, what are the common and disparate causes underlying the cellular and physiological mechanisms responsible for human senescent phenotypes?

It’s at Granlibakken, an adorable Tahoe resort where my old department used to go on retreat every autumn. I’ve never been in the winter, but I hear it’s nice.

Registration information is can be found here. Early registration deadline is November 30, but you can continue to register for full price up until January 31 (or until the conference fills up).

 

Sí se puede

Just to follow up on that last post asking you to help the SENS Foundation win $5000 — it worked! SENS came in first, and won the grand prize. The margins were pretty narrow — well below the number of people who visited the contest page from Ouroboros alone — so it can truly be said that every vote counted.

Thanks to the readers of Ouroboros and everyone else who helped SENS over the top.

The amount of money raised is, in the grand scheme, rather small, but it’s possible that the victory for SENS in what amounts to a popularity contest will help increase awareness of the life extension cause.

“I’m immensely grateful to 3banana for involving us in this great opportunity, and to all the SENSF supporters who took the time to leave comments at the site,” said SENS Foundation CSO, Dr Aubrey de Grey. “These supporters have recognised that a public and eloquent expression of broad-based support for our mission has the potential to raise the profile and perceived legitimacy of our work and thereby greatly amplify the impact of the competition itself.”

 

Help raise $5000 for SENS – by leaving an online comment

The SENS Foundation (which organizes the Strategies for Engineered Negligible Senescence conferences) is in the running for the $5000 grand prize in 3banana’s Share to Win event. The contest seeks to raise money “for causes serving unmet needs in health, education and environment.”

And you can help. It’s pretty simple: All you have to do is leave a comment on this page. (The award goes to the cause with the most comments.) You can sign on using a Google account if you already have one of those, or register for a free one-off account. It’s painless and takes about thirty seconds.

Your comment/vote makes a difference! Right now, SENS is neck-and-neck with the competition — as of this post, they’re 17 votes behind first place. (Well, sixteen, since I just commented.) So don’t just sit there — this is your opportunity to help send real money to a very important cause, at no cost to yourself.

Post your comment now.

There are only four days left in the contest, so time is of the essence.

(For all you social media users, feel free to spread the word via blogs and Twitter. If you’re interested in regular updates from the SENS Foundation, there’s a Facebook page as well.)

UPDATE: The push yesterday put SENS into the lead — thanks to all Ouroboros readers who took the time to comment! But the current lead is tenuous, and it could still be lost. If you haven’t commented yet: it doesn’t take much time, and with margins like these your vote really makes a difference. Would you really want to find out that SENS had lost by a single vote? Please consider taking a minute or so and leaving a comment on the contest page.

 

RIP for MFRTA?

A prominent scholar of the CLK-1 story has called the coroner on the mitochondrial free radical theory of aging (MFRTA). From Lapointe & Hekimi:

When a theory of aging ages badly

According to the widely acknowledged mitochondrial free radical theory of aging (MFRTA), the macromolecular damage that results from the production of toxic reactive oxygen species (ROS) during cellular respiration is the cause of aging. However, although it is clear that oxidative damage increases during aging, the fundamental question regarding whether mitochondrial oxidative stress is in any way causal to the aging process remains unresolved. An increasing number of studies on long-lived vertebrate species, mutants and transgenic animals have seriously challenged the pervasive MFRTA. Here, we describe some of these new results, including those pertaining to the phenotype of the long-lived Mclk1 +/− mice, which appear irreconcilable with the MFRTA. Thus, we believe that it is reasonable to now consider the MFRTA as refuted and that it is time to use the insight gained by many years of testing this theory to develop new views as to the physiological causes of aging.

MFRTA recently turned 50, and consequently has received a lot of attention lately; q.v. this review and this retrospective by Denham Harman, the originator of the theory. The thesis of most pieces seems to be that the theory hasn’t been demonstrated to explain the bulk of age-related decline, but that there’s still life in the idea. In contrast, the authors of this review argue that the relevant experiments have been performed and that the theory has been falsified — in other words, we’ve done our scientific duty and it’s now time to move on.

I doubt very much that this article will put a permanent end to the controversy. Data reported fairly recently have breathed new life into oxidative theories in general and the MFRTA in particular. While these authors contend that the CLK-1 mouse mutant contradicts the underlying mechanisms of the MFRTA, other recently reported work on this pathway supports the claim that inhibiting mitochondrial respiration delays aging, a key prediction of MFRTA.

Furthermore, if mitochondrially generated oxidative radicals are truly not playing a causative role in aging, it becomes much harder to explain how mitochondrially targeted antioxidants can extend lifespan in mammals.

Lapointe, J., & Hekimi, S. (2009). When a theory of aging ages badly Cellular and Molecular Life Sciences DOI: 10.1007/s00018-009-0138-8

 

Sunday Funnies

(From the Perry Bible Fellowship. For the previous installment of Sunday Funnies, see here.)

 

Conference: Singularity Summit, October 3-4, New York

I attended the inaugural Singularity Summit back in 2006 — it was full of ideas, certainly, but I came away mostly skeptical and disillusioned about the quality of thinking on display there.

The event itself seems to be here to stay, however, and it’s growing: It now lasts two days (up from 1), with 26 speakers (up from 13). The scale of the event seems to be doubling every three years. According to the extrapolative logic so familiar to singularity believers, within 30 years the event will last more than a year, causing each Summit to flow into its successor (the “Calendarity”); within 100 years, everyone in the world will be a speaker (the “Popularity”). Except, of course, that by then we’ll all be hyperintelligent machines, and the event will be a historical re-enactment rather than an exercise in projecting the future.

I mention the summit here because of its small but growing anti-aging and longevity components. Of interests to biologists, biogerontologists and advocates of extending (biological) lifespan:

• DNA: Not merely the secret of life, Ned Seeman
• Artificial biological selection for longevity, Gregory Benford
• The Singularity and the Methuselarity: Similarities & Differences, Aubrey de Grey

There will also be a totally unbiased talk on “Critics of the singularity” by Ray Kurzweil, who doesn’t have a dog in that fight and will be sure to give equal play to both sides.

The cost has more than doubled: It’s up to $498, from $0 – frustrating any attempt to apply logarithmic extrapolation – though there are a number of opportunities to earn discounts.

The 2009 Summit will be held in New York City. You can find out more at the website.

 

SENS4, Session 21: Tissue engineering

Gabor Forgacs gave a very interesting talk about using bioprinting to build entire organs from scratch. He argued that while traditional scaffold-based methods of tissue engineering work for thin tissues, they are not appropriate for thick, complex tissues. They have designed a computer-aided printing system that can put down layers of single cells according to a blueprint, and are applying it to produce vascular and nerve grafts.

Sally Dickinson spoke about the first transplant of a tissue-engineered airway, which took place in June 2008. She played a cool video explaining the whole procedure, which is up on youtube. Using a donor trachea, they first treated it to remove all the donor’s cells; they then took some stem cells from the patient’s bone marrow, turned them into chondrocytes, grew them up and seeded them onto the scaffold; finally, they transplanted the engineered trachea into the patient.

(For an index of coverage of all sessions, see here.)

 

SENS4, Session 18: Recent advances in cell therapies

Daniel Kraft spoke about stem cell transplantation in bone marrow. They developed an alternative method of ‘making room’ in bone marrow for new stem cells that uses antibodies (which is much less toxic than chemotherapy, the usual approach). Also, they developed MarrowMiner, a faster and less painful way to extract bone marrow from a donor using only a single entry site – previous methods require making hundreds of individual needle jabs.

(For an index of coverage of all sessions, see here.)

 

SENS4, Session 16: Delivering genes, proteins and larger structures in vivo

Carlos Barbas talked about altering the activity of individual genes using zinc finger recombinases. They have developed an automated approach for producing enzymes that can accurately target any region of DNA, and made it publicly available – just input your target sequence to ZFTools.

(For an index of coverage of all sessions, see here.)

 

SENS4, Session 15: Rejuvenating the immune system

Justin Rebo spoke about some initial experiments that show it’s feasible to selectively remove anergic T cells from old mice. The basic idea: remove some blood from a mouse; mix it with some selective superparamagnetic antibodies; clean the blood by applying a magnet to separate out tagged cells; put it back into the animal.

(For an index of coverage of all sessions, see here.)