There will be a SENS Foundation meeting in Los Angeles this coming Wednesday, October 5th. The following is from the Foundation's coordinator Maria Entraigues; if you're in the area an interested then RSVP to the email address provided below.

It's been a long time, since the last occasion that we got together! We at the SENS Foundation have been very busy working harder than ever to take our accomplishments to the next level, and it's been very fruitful. We would like to share this with you in this very special gathering in a most delightful setting.

This will be an exceptional occasion, we will be very lucky to have our CSO, Dr. Aubrey de Grey, presenting some important remarks, as well as our CEO Mike Kope giving an extraordinary presentation. On top of this, we will have special guest Ms. Sonia Arrison, author of the book "100 Plus - How the coming age of longevity will change everything, from Careers and Relationships to Family and Faith." She will engage in a conversation with Aubrey about her new book. Each attendee will get a free copy, and she will be happy to sign it!

Apart from feeding your brain to total satisfaction with interesting and remarkable information, we will also feed you with delicious finger food, beer, and beverages and to make the night "100 Plus" percent perfect, we will have live music by Ancient Lasers closing the event!

Date: Wednesday, October 5, 2011
Time: 6:00 PM

Location: The beautiful house of the Finfers
173 North Anita Avenue
Los Angeles, CA 90049
(Brentwood, near Sunset and Bundy)

6:00 PM -- Reception
7:00 PM -- "100 Plus" Panel, with Author Sonia Arrison and Dr. Aubrey de Grey
7:30 PM -- Q&A
8:00 PM -- Presentation by Mike Kope "The Rise of Rejuvenation Biotechnology"
9:00 PM -- Live music by Ancient Lasers (mingling and networking)

Please RSVP by e-mail. I can't wait to see you all!

Maria Entraigues
maria.entraigues@sens.org
SENS Foundation Global Meeting Coordinator, Volunteer Coordinator
http://www.sens.org
http://sens.org/take-action/volunteer

The SENS Foundation has a growing presence at both ends of California. As you might know, the Foundation's research center is in the Bay Area, and a number of the research institutions in California have both a strong interest in aging research and ties to the Foundation. Some of the folk formerly participating in research at the Foundation are even a part of the biotech side of California start up culture nowadays. Which is not to mention the presence of philanthropist Peter Thiel and his interest and connections in longevity science, and a range of other interested supporters. Connections and relationships are what make the world go round, and one purpose of the ongoing series of Los Angeles meetings is to help enlarge that web of support so to better enable the future growth of the SENS Foundation - and alongside it the new field of rejuvenation biotechnology.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Life science students intern at the SENS Foundation research center in the Bay Area as a part of the Foundation's broader academic initiative, working on the foundations of future rejuvenation therapies. Biotechnology has advanced to the point at which bright graduates can help to meaningfully advance the state of the art, and here is a report from one such: "Sarah Fazal joined our research center team as an intern for the summer. Over the past few months, she worked with our MitoSENS team, primarily verifying the integration of DNA transfected into cells and detecting RNA expression levels. Her efforts contributed greatly to the progress our MitoSENS team has made over recent months, and she presented those results in a poster at our recent SENS5 conference in Cambridge. ... The current project for mitoSENS is allotopic expression, which involves copying the mitochondrial DNA into the nucleus. My project required checking for integration of the DNA transfected into cells, and detecting RNA expression levels. By the end of the summer, I had done this successfully for 4 out of the 13 genes involved in oxidative phosphorylation that are still encoded by mitochondrial DNA. I spent my summer mostly doing PCRs (polymerase chain reaction), DNA and RNA isolations, cell culturing, and gel electrophoresis. I learned to perfect these techniques, to think critically when my results weren't as expected, and to design experiments. My experience at SENS helped shape me into a more confident and better experienced scientist. I would definitely recommend volunteering for this foundation; the experience was educational, the research is open-minded, determined, and bold, and the staff is friendly, welcoming, and helpful."

Link: http://sens.org/node/2408

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Rapamycin is known to extend life in mice, so researchers are looking into the mechanisms and possible uses as a therapy for age-related diseases. "Previous studies have shown that inducing autophagy ameliorates early cognitive deficits associated with the build-up of soluble amyloid-? (A?). However, the effects of inducing autophagy on plaques and tangles are yet to be determined. While soluble A? and tau represent toxic species in Alzheimer's disease (AD) pathogenesis, there is well documented evidence that plaques and tangles also are detrimental to normal brain function. Thus, it is critical to assess the effects of inducing autophagy in an animal model with established plaques and tangles. Here we show that rapamycin, when given prophylactically to 2-month-old 3xTg-AD mice throughout their life, induces autophagy and significantly reduces plaques, tangles and cognitive deficits. In contrast, inducing autophagy in 15-month-old 3xTg-AD mice, which have established plaques and tangles, has no effects on AD-like pathology and cognitive deficits. In conclusion, we show that autophagy induction via rapamycin may represent a valid therapeutic strategy in AD when administered early in the disease progression." This research is actually fairly indicative of the field as a whole: mechanisms that are potentially modestly useful as ways to slow aging across life are forced into consideration as late-stage therapies only. This happens because regulators will not permit commercialization of ways to treat aging in otherwise healthy people - they only permit treatments for named diseases. So progress is necessarily sub-optimal where it is permitted at all.

http://dx.doi.org/10.1371/journal.pone.0025416

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

I just added to the Fight Aging! Resources page a small number of links to journals and other scientific archives that I graze from time to time. I left out the broad life science journals that sometimes touch on aging in favor of searchable archives and publications dedicated to aging and longevity science. I also tend to favor open-access journals as the resulting material gives me more to read and more to write about. I'd be a pauper if I acquiesced to paywall demands for everything I find interesting enough to want to read, but fortunately paywalls are not the future of scientific publishing. The smaller the hurdle to propagation of scientific knowledge, the more the scientific community will benefit, as the propagation of that knowledge is a very important part of generating support for funding and development of clinical applications.

If you have suggestions for a few other journals or resources that follow the general theme of those already there, let me know.

This minor site update was spurred by my noticing that research blog Ouroboros briefly roused from its slumber to speak about Pathobioliogy of Aging & Age-related Diseases, a new open access journal on aging that launched earlier this year. Its remit looks promising for those of us interested in aging as accumulated molecular damage, and the development of means to repair that damage.

The pursuit of investigations into the science of aging is really designed to understand why cellular processes begin to fail with advancing age, and what molecular events contribute to this failure. In this regard, the distinction between aging and the diseases associated with aging becomes less clear, and they are most likely driven by the same or similar events related to biological decline.

With the launch of Pathobiology of Aging & Age-related Diseases, we hope to enlighten the scientific community by recognizing outstanding pathobiology-based scientific contributions, allowing scientists to communicate data that might be of less interest in other journals more focused on generic aging or specific scientific disciplines. Aging is indeed an 'old' problem and is being studied in a variety of ways that use mammalian model systems to identify mechanistic pathways that can be targeted to maintain healthy living. In this regard, we are providing a 'new' venue for disseminating information that specifically focuses on the pathobiological aspects of aging and the chronic diseases directly associated with aging.

Hopefully this will provide a source of interesting material in the years ahead. A good way for laypeople to learn more about the field of aging and longevity science is to browse the open access journals on a regular basis. If you skip over what is hard and read what isn't, then sooner or later you'll find that less and less of the content is beyond you, and that you understand far more than you used to. I see that process as one of the compelling arguments for destroying the old paywall model of scientific publication: how can laypeople casually increase their knowledge when everything is locked away beyond the impulse decision to spend a little time reading?

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Here is a different way of looking at the material consequences of living a life that allows you to become obese: "The United States has the highest prevalence of obesity and one of the lowest life expectancies among high-income countries. We investigated the relationship between these 2 phenomena. ... We estimated the fraction of deaths attributable to obesity by country, age, and sex and reestimated life tables after removing these deaths. To allow for a possible secular decline in obesity risks, we employed alternative risks from a more recent period. ... In our baseline analysis, obesity reduced US life expectancy at age 50 years in 2006 by 1.54 years for women and by 1.85 years for men. Removing the effects of obesity reduced the US shortfall by 42% for women and 67% for men, relative to countries with higher life expectancies. Using more recently recorded risk data, we estimated that differences in obesity still accounted for a fifth to a third of the shortfall. ... The high prevalence of obesity in the United States contributes substantially to its poor international ranking in longevity."

Link: http://www.ncbi.nlm.nih.gov/pubmed/21940912

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

A piece by Aubrey de Grey at the Huffington Post: "as things stand, no amount of insight into age-related pathology can be sufficient to develop outright cures. Some diseases are the end results of aging, just as starvation is the end result of fasting. The nature of aging is such that many age-related infirmities are certain to afflict anyone who lives long enough. And this will remain the case, until a technology is developed which ameliorates the general decrepitude of old age which underlies these diseases. One can, therefore, identify the future direction of medicine by considering the nature of old age itself. What exactly is being taken from us, year after year, from cradle to grave? As time goes by, your hair goes grey, your face gets coarser, you put on weight, you become weaker, more susceptible to disease, and so on. But what do these things have to do with each other? Fortunately, the answer is not so complex as one might anticipate. Most people think of the science of aging as being very incomplete. It is true that aging as a process is not completely understood (biogerontology, the study of aging, involves many competing theories). But the state of disrepair that aging leaves people in can be observed directly, and in great detail. A comparison between two perfect snapshots of old and young tissue would provide us with a very multi-faceted damage report. The aged tissue is riddled with "junk" molecules (by-products of normal metabolic functions) in and between cells, which do not dissipate, not even as the body heals and replenishes itself day in and day out. It would also show an accumulation of unwanted cells, and a depletion of necessary cells. All this damage reduces our tissue function, then our organ function, and eventually it kills us. How this damage accumulates, and how it leads to our demise, are matters of some dispute. But the bare facts of how our tissues alter over time already provide us with enough of a compass with which to chart the future course of medicine."

Link: http://www.huffingtonpost.com/aubrey-de-grey-phd/age-related-diseases_b_985019.html

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

A piece by Aubrey de Grey at the Huffington Post: "as things stand, no amount of insight into age-related pathology can be sufficient to develop outright cures. Some diseases are the end results of aging, just as starvation is the end result of fasting. The nature of aging is such that many age-related infirmities are certain to afflict anyone who lives long enough. And this will remain the case, until a technology is developed which ameliorates the general decrepitude of old age which underlies these diseases. One can, therefore, identify the future direction of medicine by considering the nature of old age itself. What exactly is being taken from us, year after year, from cradle to grave? As time goes by, your hair goes grey, your face gets coarser, you put on weight, you become weaker, more susceptible to disease, and so on. But what do these things have to do with each other? Fortunately, the answer is not so complex as one might anticipate. Most people think of the science of aging as being very incomplete. It is true that aging as a process is not completely understood (biogerontology, the study of aging, involves many competing theories). But the state of disrepair that aging leaves people in can be observed directly, and in great detail. A comparison between two perfect snapshots of old and young tissue would provide us with a very multi-faceted damage report. The aged tissue is riddled with "junk" molecules (by-products of normal metabolic functions) in and between cells, which do not dissipate, not even as the body heals and replenishes itself day in and day out. It would also show an accumulation of unwanted cells, and a depletion of necessary cells. All this damage reduces our tissue function, then our organ function, and eventually it kills us. How this damage accumulates, and how it leads to our demise, are matters of some dispute. But the bare facts of how our tissues alter over time already provide us with enough of a compass with which to chart the future course of medicine."

Link: http://www.huffingtonpost.com/aubrey-de-grey-phd/age-related-diseases_b_985019.html

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Updates to the Fight Aging! site tend to come in waves, as and when my time frees up sufficiently between the ebb and flow of other projects. The next wave isn't here yet, but will be, so I thought I'd solicit opinions. By all means add yours in the comments to this post.

One thing I hear a lot of is the request for like/share buttons for Facebook, Twitter, and so on - that won't be happening. I've performed this experiment already (you might recall that the previous design included sharing buttons) and the difference between having them and not having them in terms of engagement, new visitors, and overall traffic was minimal. On the other hand, they definitely slowed down page load time and made the site that little bit more ugly into the bargain. More importantly, they tracked visitors, adding to the growing databases that will be used for whatever purposes that the social sites will come up with the future; I'm not of the mindset to help them with the construction of their panopticon foundations at the expense of visitors to my little corner of the web. So on the whole I'm happy to force on you the modest make-work of cutting and pasting the URL you wish to share with your friends - and for a little more make-work you could even arrange matters for your browser to insert a share button regardless of what I do. Ultimately the web page transmitted to you by a server is no more than a suggestion as to what you should actually view: with the proper tools you can rearrange web pages on the fly before they are presented to you.

Another reason to skip the share buttons is that many of them deliver what I would regard as worthless traffic. StumbleUpon is particularly bad in this respect: my logs are full of people turning up from that site, arriving at a long and interesting post, and leaving after a few seconds. Hundreds upon hundreds of them, every day. StumbleUpon is, in some of its incarnations, a channel-surfing engine with infinite channels; people click the button and only stop if something catches their eye in a faction of a second. Next to nothing here will do that, and these are not people likely to be engaged by the Fight Aging! message. I lose nothing by failing to cultivate that traffic.

(The Google Analytics script that still runs on the site will no doubt eventually succumb to the frame of mind outlined in the paragraphs above, but for now it at least somewhat anonymizes your IP address and is fairly easily blocked).

Other suggestions fall into the bucket of fleshing out the functionality: making the site more portal-like at their grandest, such as by adding forums, most popular or most commented lists in the sidebar, more and more varied content, and so on. The less grand suggestions are tweaks to functionality to provide features seen on other tech news and essay sites, or minor additions to content, such as to stop displaying the full text of each post on the home page, enabling visitors to post links to relevant content more easily, adding a list of journals to the resources section, make the comment section more apparent. Thing of that ilk.

Some of these I agree with, some of them I don't. I should explain that Fight Aging! is something of a hybrid of two functions in its present structure. Firstly, it has some pretensions to being a stream of fresh content: a news and opinions site that is relevant to aging research and longevity science. In this it is little different from most blogs and newsletters: we all understand roughly how these things work. They care about the traffic of the now, and comparatively little for their archives, so they tend to become involved in a race for the bottom in gathering attention and being first - quality and correctness come a distant second, and they measure success by page views because that's what drives their revenues. I've never been particularly interested in playing that game. It's useful and, I think, necessary to have a modest flow of new content in order to continue to be relevant as an item of interest in your community, but that's all that's needed: enough to remain relevant so that people will listen when you have something to say.

So much of what you see on revenue-generating news and blog sites is inappropriate or not terribly useful for Fight Aging! The share buttons are a good example: if an item is there for the purposes of accelerating the race to the bottom of the pool of shallow attention, then I don't need it. I'd argue that shallow attention doesn't get you anywhere in the business of advocacy to grow a small community with big, complex ideas, such as the present longevity science community. What you need is engaged, quality attention. It is my belief that shallow attention only becomes useful, or at least convertible into results such as funding or labor, when you have a massive community and you're trying to gain a popular consensus of some sort among the public at large.

The second function of Fight Aging! is to act as a beacon and resource for people who are on the verge: interested enough to look into life extension, aging, and rejuvenation biotechnology, but neither connected nor particularly aware of the community. When they stumble over Fight Aging! in searches, I see that as a chance to inform and educate. So I place a great deal more value on the Fight Aging! archives than I would if this were only a standard issue blog or news site, and the fact that pages in those archives are littered with links to more general and introductory content is important.

So when I think about what should be done in the next wave of alterations to Fight Aging!, I am thinking in terms of advocacy and growth, which may map in some way to the web traffic I see here, but which is definitely not the same as a straight measure of traffic or engagement or any other metric easily chased. In terms of expansion versus focus, I'm presently more in favor of focus: it would be good to narrow down to look at the things that work and see about how to make them more useful, more functional, more widely used, more influential. For example, it's been a while since I've seriously looked at how I might improve the Fight Aging! newsletter or broaden its reach, despite the fact that it has thousands of subscribers. The same goes for the RSS feeds, which have a presently unknown reach and utilization.

On the expansion side, it's not that I'm not in favor of big glittering longevity science web portals, but that I don't think the community is large enough to support such a thing at this point in time. It's my impression that the present longevity science community - people who are interested enough to be a part of the discussion, or who are in the research community, or who are donating funds, and so forth - is at the size sufficient for an active web forum or two and a couple of mailing lists and newsletters. I think that because that number of forums, mailing lists, and newsletters is pretty much what has emerged organically. If there was the interest and the headcount for more than that, then it would already exist; there are any number of people out there whose business is to sniff out new communities and launch websites to serve them news before anyone else does, and they are largely absent - or worse than absent, off servicing the "anti-aging" marketplace instead, as there's real money over there. This is unfortunate, and we'd all like matters to be further along, but it is what it is, or at least until we help it bootstrap into something more.

In any case, to return to the original point, there will be time for some updates and change ahead - make your preferences known now or forever hold your peace.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Exercise is generally beneficial to long term health in many ways - though it's somewhat cruel that it's so beneficial for the suffers of conditions that make it hard to exercise: "physical activity improves arthritis symptoms even among obese mice that continue to chow down on a high-fat diet. The insight suggests that excess weight alone isn't what causes the aches and pains of osteoarthritis, despite the long-held notion that carrying extra pounds strains the joints and leads to the inflammatory condition. ... Many cases of arthritis are associated with obesity and inactivity, so [the] researchers set out to determine whether a high fat diet induces knee osteoarthritis, and then whether exercise provides a protective effect. Using two sets of male mice - half fed a high-fat diet and the other fed regular chow - the researchers noted significant differences among the two groups. The mice on the high-fat food gained weight rapidly, processed glucose poorly and had much higher blood levels of molecules that trigger the chronic inflammation associated with osteoarthritis. But when these animals got regular running wheel workouts, many of the harmful effects diminished - even though the mice ate the same high-fat food and shed no weight. Glucose tolerance improved, while the inflammatory response was disrupted among key signaling molecules called cytokines, easing the development of arthritis. If the extra weight on the joints had been the cause of the arthritis, the researchers noted, exercise would have exacerbated the problem. Instead, it helped. ... I don't want to say exercise is turning off that inflammatory signal, it just impairs it." The fat tissue accumulated by the obese is a trigger for inflammation via chemical signaling; weight on joints may not be aggravating arthritis, but the increase to levels of chronic inflammation will do just that. Better to be both exercising and shedding the excess fat than just one or the other.

Link: http://www.eurekalert.org/pub_releases/2011-09/dumc-eea092111.php

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

From Popular Science: "Giving cardiac patients a heart of gold nanowires could ensure engineered tissue works like it should, pulsing in unison to make the heart beat. First growing nanowires and then growing heart cells, [engineers] say their new muscle-machine blended heart patch improves on existing cardiac patches, which have trouble reaching a consistent level of conductivity. ... Electrical signals shared among calcium ions dictate when cardiomyocytes contract, making the heart beat. But tissue scaffolds are often made with materials like polylactic acid or alginate, which act as insulators, so the signals are blocked. This makes it difficult to get all the cells in a piece of tissue to coordinate their signals and beat in time, which in turn makes it difficult to build a very big or very effective heart patch. The [rsearch team] gets around this problem by integrating gold, an excellent conductor. They mixed alginate, a gummy substance often used in tissue scaffolds, and grew gold nanowires throughout it. Then they seeded the alginate with cardiomyoctes from rat embryos, and monitored calcium levels to gauge their electrical conductivity. Compared to a typical scaffold system, the gold nanowire cells' conductivity improved by three orders of magnitude."

Link: http://www.popsci.com/technology/article/2011-09/heart-patch-gold-nanowire-helps-rebuild-cardiac-tissue

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

The aging of the human adaptive immune system takes and interesting and distinct form when compared with the aging of other organs and processes. There is accumulating cellular damage, yes, but there is also a very important and ongoing process of misconfiguration: an otherwise largely sound system ceasing to function correctly not because it is damaged per se, but because it becomes poorly organized. That is, potentially, a much easier problem to solve than many of the other challenges presented to us by aging.

The way in which this misconfiguration happens is described back in the Fight Aging! archives. The short version is that the adaptive immune system remembers all threats, but has a limit to the number of cells it can produce; eventually too much of its quota is taken up by memory cells and too little by cells that are actually equipped to destroy things. A small range of persistent but otherwise mostly harmless viruses, such as cytomegalovirus (CMV), greatly speed up this process by hanging around for decades and constantly provoking the immune system into uselessly devoting ever more memory cells to their existence.

There are a range of possible ways to deal with this issue, with varying levels of complexity, cost, and permanence: adding more cells cultured from the patient's own stem cells, destroying the unwanted memory cells using targeted therapies of the sort under development in the cancer research community, and so forth. One of the presentations given at the SENS5 conference discusses the latest research in this area:

Aging is associated with an increased susceptibility of older individuals to new and emerging infections; poor responses to vaccination compound this vulnerability. ... In both mouse and man, repeated interactions between reactivating viruses such as CMV and antiviral T cells leads to memory T-cell inflation (MI) with increasing accumulation of these cells over the lifespan. It was hypothesized that MI may exact a price for the immune system: competition between inflating, CMV-specific memory T-cells and naive T-cells supposed to defend against all other infections may impair the maintenance of a diverse naive T-cell pool, consequently leaving the individual at a disadvantage when exposed to a new pathogen. We have directly tested this hypothesis using a mouse model of lifelong persistent infection.

There is also video of the presentation, which I think you'll find interesting - the research community is clearly within striking distance of a range of novel and effective repair methodologies for immune system aging:

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm