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A Human Interest Naked Mole Rat Story

Posted: December 22, 2010 at 6:12 pm


As you might know, the naked mole rat is of great interest to aging researchers: "For three decades, Old Man selflessly helped scientists unravel the mysteries behind Alzheimer's, osteoporosis, cancer and other age-related diseases. Born in Kenya, he lived an active life - including siring offspring - until early Thanksgiving, when his body was discovered in a lab at the Barshop Institute for Longevity and Aging Studies on the campus of the Texas Research Park. A naked mole rat, Old Man was believed to be 32. ... The Barshop Institute m[aintains] the world's largest mole rat colony. About 2,000 of the tiny, burrowing rodents whose most distinctive feature is their sharp, protruding teeth, live and breed in four basement labs. With their long, hairless bodies and translucent pink skin, they look a bit like Vietnamese spring rolls with legs. ... Because these natives of East Africa live an average 26 years (compared to the 2- to 4-year lifespan of other rodents), they're well-suited for studies of age-related disease. For example, older mole rats develop the same type of brain plaque as that found in Alzheimer's patients. But for reasons unknown, they don't experience similar cognitive decline. Their bones also stay strong and healthy well into their later years. And perhaps most intriguing, mole rats very rarely develop cancer - a common cause of death among other rodents. In fact, when immune-suppressed mice were injected with naked mole rat cells containing tumor-forming genes, they didn't develop cancer. ... Among the many mole rats at the institute, however, Old Man stood out. Because of his advanced age and vigor, he'd claimed a special place in the hearts of many researchers. Laboratory animal attendant Cody Villanueva discovered his body early Thanksgiving morning. 'Oh, it was a sad day,' she recalled. 'I cried. We all did.'"

Link: http://www.mysanantonio.com/news/local_news/article/Old-Man-the-naked-mole-rat-is-no-more-913897.php

Investigating the Details of Regeneration in Lower Animals

Posted: at 6:12 pm


For some years now, researchers have been deciphering the mechanisms of regeneration in lower animals - limbs and organs regrown when lost. Here is an example of the sort of detail work taking place today: "Human regeneration is mainly limited to small portions of liver tissue, bone, or muscle, yet understanding how regeneration occurs in other taxonomic groups may enable scientists to improve human regenerative abilities in the future. ... Lizards can regenerate facial bones, certain areas of the spinal cord, and, as is most commonly known, most lizards can regenerate their tail - including muscles, cartilage, and spinal cord. The regenerated tail does not contain bone, but instead is supported by a tube of hyaline cartilage - the same cartilage humans have lining many of their joints. With widespread medical problems such as arthritis and spinal cord injuries, the application of these regenerative abilities is of extreme interest to medical institutions. .. Many vertebrate and invertebrate species can regenerate tissues, but there are several kinds of regeneration. Lizards most likely use stem-cell mediated regeneration, where new cells involved in regrowth arise from tissue-specific progenitor cells. This type of regeneration is the best bet for a regenerative process compatible with the human system ... the beauty is that now we know enough about development that we can actually have candidates for what cells are making this new tail - we can have guesses as to what might be right. ... Once we understand the nuts and bolts of how this is happening, we can use available technologies to manipulate and change that, then we will try to translate that to the mouse model."

Link: http://www.physorg.com/news/2010-12-tale-told-tails-gained-anoles.html

"Death is an inconvenient obstacle on the road to immortality"

Posted: at 6:12 pm


The title of this post was recently offered up as a pity quote on the Gerontology Research Group mailing list:

"Death is an inconvenient obstacle on the road to immortality."

The spirit in which this is intended is evidently that an army of biogerontologists and supporters should marshal, march, and trample death beneath their sandaled feet - to leave it broken in the dust upon the road that leads to rejuvenation biotechnology and agelessness.

That trampling will undoubtedly happen, albeit far from soon enough. If you stop to think about this for a moment, however, you might conclude that the defeat of death should not in fact be the conceptual focus of efforts to extend the healthy human life span. Let's try an analogy here:

The ground is an inconvenient obstacle on the road to flight.

Fail at flying, and a harsh encounter with the ground is your fate - in much the same way as death by aging is the fate that awaits of of us should we fail to achieve the technologies capable of repairing the biological damage of aging. Yet heavier than air flight wasn't achieved though a focus on the ground: the early aeronauts and their supporters didn't raise funding and convince the public of the viability of heavier than air flight through "defeat the ground!" campaigns. Their eyes looked up, to the skies, to rapid travel across land and ocean, to daring acts and barnstorming.

Returning to physical immortality - meaning the state of agelessness attained through biotechnology and diligent repair - then we might see that the grail here is life achieved, not death denied (or trampled). It is living, being healthy, able to plan ahead for decades without fear, to not be faced with inevitable pain, suffering, and frailty. These points are the focus.

Android Gets Stunted SoundCloud

Posted: at 6:12 pm


more images

Android users have more reasons to cheer as the newly furnished SoundCloud is arriving on the popular SmartPhone platform. However the app actually cuts corners in a few features. We really think that some more polishing should have been done before rolling it out.
The app was very recently named as one of the Top .... Source  : Gaea News Network.

Senescent Cells and Short Term Calorie Restriction

Posted: December 21, 2010 at 6:11 pm


Researchers run short-term studies on calorie restriction because it's cheaper and faster than long-term studies. Fortunately some of the biological changes brought on by calorie restriction take place fairly rapidly, so this is still a way to learn something. Here is one of the results: "Recent evidence supports the contention that cellular senescence is associated with, and may even be a cause of age-related functional impairment. Senescent cells accumulate in multiple tissues with advancing age. Cellular senescence causes a variety of cell types to acquire a pro-inflammatory secretory phenotype that produce a variety of cytokines, chemokines, and extracellular matrix remodeling proteases that are associated with tissue destruction. Chronic presence of senescent cells can accelerate cancer progression, possibly because of this inflammatory secretory phenotype. Engineered deposition of senescent cells in a single organ, skin, can cause functional impairments in multiple organs similar to those occurring with aging. Finally, senescent cell accumulation in progeroid animal models is associated with dysfunction resembling that of aging. Caloric restriction attenuates processes that have been implicated in cellular senescence, including generation of reactive oxygen species (ROS), growth hormone/insulin-like growth factor-1 signaling, and inflammation. Does caloric restriction in fact reduce cellular senescence? [An] important study [found] short term dietary restriction in middle-aged mice is associated with decreased abundance of senescent cells in the liver (centrilobular hepatocytes) and intestine (crypt enterocytes)."

Link: http://www.impactaging.com/papers/v2/n12/full/100247.html

Alzheimer’s and Slow Garbage Removal

Posted: at 6:11 pm


Recent research into the causes of Alzheimer's disease: "Do rising brain levels of a plaque-forming substance mean patients are making more of it or that they can no longer clear it from their brains as effectively? ... Clearance is impaired in Alzheimer's disease. We compared a group of 12 patients with early Alzheimer's disease to 12 age-matched and cognitively normal subjects. Both groups produced amyloid-beta (a-beta) at the same average rate, but there's an average drop of about 30 percent in the clearance rates of the group with Alzheimer's. ... Scientists calculate this week [that] it would take 10 years for this decrease in clearance to cause a build-up of a-beta equal to those seen in the brains of Alzheimer's patients. The results have important implications for both diagnosis and treatment. ... Scientists are now interested in learning how a-beta, a byproduct of normal metabolism, is moved out of the brain for breakdown and disposal. As these details come in, they will be essential for physicians working to diagnose the disease before symptoms develop and for drug developers, who can target the problems with pharmaceuticals. A-beta was recognized long ago as a key component of the brain plaques found during autopsies of Alzheimer's patients. One of the ways the brain clears away the a-beta normally produced by brain cell activity is by moving it to the spinal fluid for disposal. Studies have suggested that a drop in spinal fluid levels of a-beta may be a presymptomatic indicator of Alzheimer's disease, possibly because a-beta is getting stuck in the brain and starting to accumulate there." You might also look back at research into the functional decline of the choroid plexus in connection with Alzheimer's: it is a biological filtration system, and its progressive failure may be the cause of lower rates of clearance.

Link: http://www.eurekalert.org/pub_releases/2010-12/wuso-apc120710.php

Why Has Cryonics So Far Failed to Become a Large and Growing Industry?

Posted: at 6:11 pm


Cryonics, as you no doubt know by now, is the low-temperature storage of the recently deceased. The fine structure of the brain can be very well preserved - well enough that all the data that forms your self remains intact. Future medical technologies, such as applications of molecular nanotechnology, will eventually prove capable of repairing cryopreserved individuals and restoring them to life. A number of people have been cryopreserved and stored over the past few decades, and a modest community of cryobiology researchers, workers, advocates, and funding sources continues this work:

Death is not a topic that people like to think about, and that is just as true of healthy life extension advocates as anyone else. We have to recognise, however, that the future of healthy life extension (regenerative medicine, stem cell therapies, understanding the biochemical processes of aging, and nanomedicine, to name a few fields) will not arrive soon enough to benefit everyone. Many people are too old, or suffer from other conditions that will kill them before cures can be developed. This is an unpleasant reality that we must face.

Do we just write these people off and forge ahead regardless? Of course not. Instead, we turn to the science and business of cryonics, a serious effort to solve this problem that has been underway since the early 1970s.

My attention was recently directed to a series of presentations by Mike Darwin, which are in part an analysis of the failure of the cryonics community of past decades to blossom into a large industry, and in part a personal recollection of that history. If you want to understand more about the history of the cryonics movement, and how it came to be where it is today, you should certainly read this:

These are the URLs for the completed portions of the lectures entitled:
Cryonics: An Historical Failure Analysis. Four parts are completed, two have been fully edited and proofed. The second series of lectures on how to redress the problems discussed in the first lectures will be a limited distribution.

Part I
Part II
Part III

Please note that Part III is still in draft form and I am currently in discussion with the editor about a number of issues. It is possible, and even likely, that there will be significant modifications in the near future.

...

Before I begin the formal, structured part of this presentation, a few words are in order to put it into context. We live in an age where passion and strong emotion have been largely removed from daily discourse and are now considered acceptable only in the realm of fiction; in movies and video games. Characters there are free to speak in extremes and to speak passionately; not so those of us who inhabit the real world. I will be breaking that taboo today because what I am going to talk about is a life or death issue for you, for me, and for the 7 billion or so other human beings on this planet. My life matters to me a great deal, and I'm not ashamed to admit it.

The failure of cryonics to join the ranks of other medical technologies in generating a growth market and worldwide provision of services is a communal failure for all of humanity. Over the decades since cryonics was first seriously proposed and low temperature storage of human tissue became technically viable, perhaps two billion people have died, every one of them an individual of worth, perspective, and unique experience. Every death is a tragedy, and yet deaths occur by the tens of thousands every day, an endless river of horror, pain, and suffering - and in the end, the destruction of oblivion.

This state of nature did not need to continue; cryonics could have spread and succeeded, or plastination in its stead, and many of those lost lives could have been saved. Their bodies and brains, the fine structure and data of memories left intact, would even now be stored, awaiting future technology that could return them to life once more.

Those lost lives are upon our hands and the hands of our parents and grandparents. Saving them was the path not taken.

Intimations of Immortality

Posted: at 6:11 pm


From Daybreak Magazine: "I think immortality is in the same class as Utopia, infinity and perfection: a great destination to travel to, but one that can never be reached. Yet we should try, nevertheless. While immortality is an unreachable ideal, the effort of reaching it will bring huge progress and immense advantages. So let's be a tad more realistic and call it the quest for longevity, or extreme longevity. Problem is, a lot of people think we shouldn't be on this quest anyway, because of several misconceptions. ... Will McIntosh said (I'm paraphrasing here): "the human psyche is not wired for immortality: in almost every thing we do lies the shadow of our oncoming demise." However, this assumes that humans will not change. I think humans will change. Actually, humans are already changing, and have been changing throughout history. ... it will take time to develop much longer lifespans, followed by extreme longevity. Time enough for humans to change, and to adapt successfully to a much longer life. People have been changing all the time - albeit at a much higher rate in the past 100 years - and have been able to cope. Why shouldn't we be able to do so in the future? ... such thinking - [that] humans will remain the same while the world around them changes - is 'a failure of the imagination'. I agree: by the time extreme longevity is possible, we will have developed the right mindset for it."

Link: http://daybreakmagazine.wordpress.com/2010/12/18/intimations-of-immortality-are-we-ready-for-extreme-longevity-or-do-we-even-deserve-it/

Death is a Problem to Be Solved

Posted: at 6:10 pm


From Common Sense Atheism: "Let's imagine that every human who had ever lived awoke in the morning with a terrible migraine just behind the eyes for one hour. Nobody could do any work during this time. We just had to endure for one hour, and when it dissipated, go about our business, and dread the next day's migraine. There was no cure for the morning migraine, and none in sight. It was, unfortunately, fixed into the very nature of being human. I have no doubt we would soon begin to rationalize these morning migraines. We would tell ourselves that they make the rest of each day more wonderful by contrast, and that we would not properly appreciate the rest of each day were it not for the migraines. Someone might even venture to say that it's the morning migraines which makes the rest of life meaningful. But now imagine that thousands of years pass, and very advanced scientists discover that morning migraines can be cured - with methods inconceivable to previous generations. Post-migraine generations look back on past generations and wonder: 'How could they tolerate those awful morning migraines? What a horrible way to live, every day! Thank goodness we found a cure!' I want to say the same about death. We rationalize death because we don't think it can be avoided. But death is horrible, like cancer. Death thwarts an awful lot of desires. I don't think much about death, and I don't worry much about it, but I'm sure that when I lie on my deathbed I will have lots more I wanted to do with my life, and not being able to do those things will suck. But here's the good news. Death can be solved."

Link: http://commonsenseatheism.com/?p=12888

Longevity Meme Newsletter, December 20th 2010

Posted: at 6:10 pm


LONGEVITY MEME NEWSLETTER
December 20th 2010

The Longevity Meme Newsletter is a weekly email containing news, opinions, and happenings for people interested in aging science and engineered longevity: making use of diet, lifestyle choices, technology, and proven medical advances to live healthy, longer lives. This newsletter is published under the Creative Commons Attribution 3.0 license. In short, this means that you are encouraged to republish and rewrite it in any way you see fit, the only requirements being that you provide attribution and a link to the Longevity Meme.

To subscribe or unsubscribe from the Longevity Meme Newsletter, please visit http://www.longevitymeme.org/newsletter/

______________________________

CONTENTS

- Changes Underway at Fight Aging! and the Longevity Meme
- Advancing Biotechnology and the Utility of Savings
- Longevity in the Laboratory
- SENS Foundation is Hiring
- Reports From the 2020 Bay Area Aging Meeting
- Latest Headlines from Fight Aging!

CHANGES UNDERWAY AT FIGHT AGING! AND THE LONGEVITY MEME

As you may have noticed, much of the Longevity Meme has already moved over to Fight Aging! - the introductory articles, topic commentaries, daily news, and so forth. In due course the Longevity Meme will close, and all traffic will be redirected to Fight Aging! Even this newsletter will become the Fight Aging! newsletter, once all of the hundred and one necessary supporting tasks are complete. The hope is that all of this packing up and moving will be seamless for you folk, and so far that seems to be working as planned.

Along the way, I would like to redesign Fight Aging!, as incorporating the main menu and content from the Longevity Meme is making the current design show both its age and lack of sophistication. I am no designer, so if anyone knows of a resource who could volunteer a good site design, please do point them in my direction.

ADVANCING BIOTECHNOLOGY AND THE UTILITY OF SAVINGS

We will soon be entering the era in which money can buy significant amounts of additional healthy life. Saving for later years has never been more beneficial than it is now, and that benefit will grow rapidly.

http://www.fightaging.org/archives/2010/12/advancing-biotechnology-means-that-the-utility-of-savings-is-increasing-rapidly.php

"Not so far down the road are organs grown to match our needs, stem cell transplants that heal our age-damaged tissues from within, artificial cells and engineered bacteria that scour our bodies for the waste products of metabolism that build up to harmful levels in the old. Beyond that even more impressive medical advances await: artificial immune systems, far better than the real thing, the complete implementation of the SENS program for rejuvenation medicine, and the dawn of the age of molecular manufacturing - everything you might need, from drugs to bioimplants, built atom by atom in desktop nanoforge machines. Which brings us to [an important point]: the utility of money is going to rise with advances in biotechnology. Some extra tens or hundreds of thousands of dollars set aside for medical expenses might save your life.

"Whatever resources you have saved up today are growing more and more valuable with time - far more than their present market value would imply - because we are entering the age in which you can use saved resources to buy additional healthy life. With each passing year the amount of additional healthy life you could purchase increases. While that yearly increase is comparatively gentle now, and the amount of extra life very modest, both will become much, much larger ten years or twenty years from now."

LONGEVITY IN THE LABORATORY

It is no longer remarkable that a wide range of animals can be made to live longer in good health through a wide range of methods:

http://www.fightaging.org/archives/2010/12/longevity-in-the-laboratory-the-remarkable-become-unremarkable.php

"When nematode worms were first engineered to live significantly longer in good health, not very many years ago, it was a big deal. Today, few people beyond the life science community take much notice of each new study to result in a way to extend life in lower animals. Today I briefly scanned through the latest aging research papers referenced by PubMed and saw three separate reports of aging slowed in nematodes and flies, all published in just the past week or so. So the world turns: the remarkable becomes unremarkable. This is where we'd like to be with human engineered longevity - for it to be an unexciting topic, well-studied, with the work of commercial development well underway, and everyone taking it for granted that healthy lifespan will be made much longer through medical science. We're not there yet, evidently."

http://www.fightaging.org/archives/2010/12/the-mammals-made-long-lived-in-the-laboratory.php

"A wealth of long-lived mammals can be found in the laboratories of aging researchers. The healthy life spans of these animals are extended by comparatively minor genetic alterations, drugs such as rapamycin, or environmental changes like calorie restriction that are used to identify targets for future genetic engineering. This is the domain of the metabolic engineers, who see no better way forward than to gently slow aging by tweaking the operation of human metabolism. It will be a long and expensive road, and at the end will not produce results that can help people who are already old. Metabolic engineering cannot produce rejuvenation, the reversal of aging - yet it is the dominant body of longevity science in this day and age."

Which is too bad. We would like to see a greater focus on the repair and reversal of aging, such as through realization of SENS, the strategies for engineered negligible senescence. You can learn more about that at Fight Aging!:

http://www.fightaging.org/archives/2004/11/strategies-for-engineered-negligible-senescence.php

SENS FOUNDATION IS HIRING

What more important job could there be than helping to repair the damage of aging, and thereby work towards preventing the more than 100,000 deaths by aging that occur each and every day? In the way of a recent large donation, the SENS Foundation is hiring for a research assistant position in California:

http://www.fightaging.org/archives/2010/12/sens-foundation-is-hiring.php

"They are looking for mitochondrial research experience because the MitoSENS project is forging ahead. The goal of this line of work is to duplicate vulnerable mitochondrial genes in the cell nucleus, while enabling the vital proteins they produce to make their way back to the mitochondria. Thus even if the genes become damaged in the mitochondria, there will be a backup source of proteins to avoid the normal consequences of mitochondrial DNA damage. ... For over 30 years mutations in mitochondrial DNA have been suspected to be important contributors to aging. If we can incorporate working copies of that mtDNA into our nuclear DNA, the mtDNA will be rendered superfluous and any mutations it suffers will be inconsequential."

REPORTS FROM THE 2010 BAY AREA AGING MEETING

Northern California is home to a fair-sized contingent of biogerontologists and several important aging research laboratories, hence the existence of the Bay Area Aging Meetings. Science blog Ouroboros provided coverage of the latest meeting, held earlier this month:

http://www.fightaging.org/archives/2010/12/reports-from-the-december-2010-bay-area-aging-meeting.php

"If aging is an engineering problem, then we should be able to solve the engineering challenges more easily in simple systems. By introducing genes from a long-lived organism into the genome of a short-lived organism, it should be possible to add pro-longevity functions - in effect 'upgrading' the short-lived animal so that it lives longer. Sagi has set out to do just that, by transferring genes from the long-lived zebrafish (4-year lifespan) to the short-lived worm (4-week lifespan). ... The next obvious question: Can 'upgrade' genes be combined to further increase lifespan? Indeed they can: several pairwise combinations of genes combined to extend lifespan longer than either single gene alone. At some point it worked a little too well: the lifespan of the worms started getting long enough that the survival curves became unwieldy."

DISCUSSION

The highlights and headlines from the past week follow below. If you have comments, please do send e-mail to newsletter@longevitymeme.org

Remember - if you like this newsletter, the chances are that your friends will find it useful too. Forward it on, or post a copy to your favorite online communities. Encourage the people you know to pitch in and make a difference to the future of health and longevity!

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LATEST HEADLINES FROM FIGHT AGING!

SUPPRESSING AGING IN OUR LIFETIME
Friday, December 17, 2010
http://www.fightaging.org/archives/2010/12/suppressing-aging-in-our-lifetime.php
Fifteen years ago, this paper or one with similar sentiments wouldn't have been accepted for publication - or if it had, it would have achieved nothing but harming the funding prospects of its author. The aging research community has only recently emerged from an era of self-censorship on the topic of engineering greater human longevity, and a field whose members do not talk about achieving a given goal will certainly make no progress towards that goal. From the abstract: "Although we do not know everything about aging, we now know enough to start its pharmacologic suppression using clinically approved drugs. Aging turns out to be driven by sensing-signaling pathways (such as the mTOR pathway). Given that some inhibitors of the mTOR pathway are already in clinical use, there is a unique opportunity to suppress aging, while treating and preventing diseases. By itself this will answer some burning questions in gerontology. Here I discuss a proposal, starting from retrospective clinical studies to animal and cellular models to drug screens in order to develop non-toxic and effective schedules and drug combinations for extending healthy life span in our lifetime." This is representative of the more eager members of the mainstream of biogerontology, focused on slowing aging through metabolic manipulation.

PRESENT THEMES IN MAINSTREAM AGING RESEARCH
Friday, December 17, 2010
http://www.fightaging.org/archives/2010/12/present-themes-in-mainstream-aging-research.php
From Maria Konovalenko: "Melanie Swan, MBA, is an Affiliate Scholar of the IEET [and] recently summarized some important themes in aging research that were discussed at the second Bay Area Aging Meeting. ... Two interesting talks concerned UCP2 (mitochondrial uncoupling protein 2) an enzyme which reduces the rate of ATP synthesis and regulates bioenergy balance. UCP2 and UCP3 have an important but not yet fully understood role in regulating ROS (reactive oxygen species) and overall metabolic function, possibly by allowing protons to enter the mitochondria without oxidative phosphorylation. The mechanism was explored in results that worm lifespan was extended by inserting zebrafish UCP2 genes (not natively present in the worm) ... Two talks addressed the issue of immune system compromise. One team created a predictive analysis that could be used to assess an individual's immune profile and potential response to vaccines by evaluating demographics, chronic infection status, gene expression data, cytokine levels, and cell subset function. Other work looked into the specific mechanisms that may degrade immune systems in older organisms. ... Aging and other biological processes become more complicated with progression up the chain of model organisms. What works in yeast and worms may not work in mice, and what works in mice and rats may not work in humans. Some interesting research looked at ribosomal proteins, whose deletion is known to extend lifespan in model organisms. The key points were [that] there was fairly little (perhaps less than 20%) overlap in lifespan-extending ribosomal protein deletions conserved between yeast and worms."

THE METHUSELAH FOUNDATION WANTS YOUR OPINION ON THEIR STRATEGIES
Thursday, December 16, 2010
http://www.fightaging.org/archives/2010/12/the-methuselah-foundation-wants-your-opinion-on-their-strategies.php
From the Methuselah Foundation Blog, a message from founder and CEO Dave Gobel: "It has been a while since I sent you an update and there is plenty of good news to share as we work together towards longevity. I also want your input as we make plans for the coming year. ... Methuselah Foundation has successfully promoted the extension of healthy human life - the science of aging has gained acceptance and broad-based support thanks to your ongoing contributions. Now we are strongly supporting science that will lead to tissue engineering and organ regeneration. We will be the catalyst to speed up the development of organ replacement. ... I am continually delving into every area of science, the work being done in universities, labs and biotech companies, to see the latest research and how it might contribute to longer life. I am convinced that there are many viable solutions but we, uniquely, are in a position to move them to a practical place. With this mission in mind we created the NewOrgan Prize. Based on our success with the Mprize, we anticipate this new prize will accelerate the rate of research and bring us closer to practical solutions. ... We must continue to accelerate practical scientific solutions related to aging. You and I - not just our children and grandchildren - should benefit from the advances in tissue engineering that are already on the table. This is why I need your input. We are contemplating a number of initiatives in support of this drive but we want to have the greatest possible impact. I would appreciate your thoughts and suggestions. Please continue reading and I believe you will have a clear understanding of the potential and, hopefully, will have some thoughts to share." Head on over to read the rest of the post: if you have opinions and good ideas, send them to the Foundation."

METHUSELAH FOUNDATION NEWSLETTER FOR NOVEMBER 2010
Thursday, December 16, 2010
http://www.fightaging.org/archives/2010/12/methuselah-foundation-newsletter-for-november-2010.php
I'd neglected to mention that the Methuselah Foundation newsletter for November was posted a couple of weeks ago: "A year ago Methuselah Foundation presented a special Mprize Lifespan Achievement Award to Z. Dave Sharp for his work with rapamycin. By the end of the year Science, Nature and TIME magazines each featured rapamycin - an antibiotic used in transplant patients that extended the life span of aged mice - as one of the most significant and exciting scientific breakthroughs of 2009. At our 2009 presentation at the Friar's Club in New York City, Dave told us a funny (after the fact) story about how the experiment ended up being done on old mice. Basically, by the time they figured out how to sneak the rapamycin into the mice food, the mice had gotten old. But three labs were on stand-by, set to start so they proceeded - making the results all the more remarkable. Rapamycin reversed aging! Now Dave has informed us that a second entire replication of the life span study has been repeated with the same results. This time the mice started taking rapamycin at nine months of age. That makes a total of SIX independent replications of the experiment!" The newsletter also provides updates on several of the Foundation's present projects and investments, such as organ printing startup Organovo.

IF WE CONSIDER PARKINSON'S AN EXAGGERATION OF "NORMAL" AGING...
Wednesday, December 15, 2010
http://www.fightaging.org/archives/2010/12/if-we-consider-parkinsons-an-exaggeration-of-normal-aging.php
Many of the conditions that occur with age might be considered exaggerated forms of "normal" aging - one aspect of damage that has raced ahead in that person for some reason. In Parkinson's disease, this damage takes the form of a decline in dopamine-secreting cells in the brain. That happens to all people to some degree, but Parkinson's sufferers have a much greater loss of these vital cells. Here researchers demonstrate that a treatment for Parkinson's produces benefits for the same symptoms seen to a lesser degree in "normal" aging: "We wished to determine whether L-DOPA, a common treatment for the motor deficits in Parkinson's disease, could also reverse the motor deficits that occur during aging. We assessed motor performance in young (2-3 months) and old (20-21 months) male C57BL/6 mice using the challenge beam and cylinder tests. Prior to testing, mice were treated with L-DOPA or vehicle. Following testing, striatal tissue was analyzed for phenotypic markers of dopamine neurons: dopamine, dopamine transporter, and tyrosine hydroxylase. Although the dopaminergic markers were unchanged with age or L-DOPA treatment, L-DOPA reversed the motor deficits in the old animals such that their motor coordination was that of a young mice. These findings suggest that some of the locomotor deficits that accompany normal aging are responsive to L-DOPA treatment and may be due to subtle alterations in dopaminergic signaling."

REVISITING THE LINK BETWEEN INTELLIGENCE AND LONGEVITY
Wednesday, December 15, 2010
http://www.fightaging.org/archives/2010/12/revisiting-the-link-between-intelligence-and-longevity.php
More intelligent people live longer - and we could propose all sorts of mundane and obvious reasons as to why this is the case, such as a greater and more effective use of health knowledge and medical resources. Here, a researcher proposes that there is in fact a biological reason as well: "Intelligent people live longer - the correlation is as strong as that between smoking and premature death. But the reason is not fully understood. Beyond simply making wiser choices in life, these people also may have biology working in their favor. Now research in honeybees offers evidence that learning ability is indeed linked with a general capacity to withstand one of the rigors of aging - namely, oxidative stress. Ian Deary, a psychologist at the University of Edinburgh, has proposed the term 'system integrity' for the possible biological link between intelligence and long life: in his conception, a well-wired system not only performs better on mental tests but is less susceptible to environmental onslaughts. Gro Amdam of Arizona State University and the Norwegian University of Life Sciences was intrigued by the idea and last year devised a way to test it in bees. ... Amdam hypothesizes that the ability to handle stress could be a component of system integrity; better overall stress resilience may contribute to both higher IQ scores and longer life. And if scientists can unravel what underlies these biological differences, they might be able to alleviate inborn disparities."

CYTOKINE GENE VARIANTS ASSOCIATED WITH HUMAN LONGEVITY
Tuesday, December 14, 2010
http://www.fightaging.org/archives/2010/12/cytokine-gene-variants-associated-with-human-longevity.php
Another set of potential human longevity genes, this time associated with immune system function, and from a Russian study: "The research was aimed at studying molecular genetics basis of human longevity. The genotyping of polymorphisms in genes of interleukins 6, 10, 12, and tumor necrosis factor-alpha from ethnically homogeneous population (Tatars from Bashkortostan Republic) has been carried out. Distributions of allele and genotypes frequencies in different age groups including old men and long-livers have been characterized. Associations have been revealed between age and -627C>A polymorphism of IL-10 gene in men, -572G>C polymorphism of IL-6 gene and -308G>A polymorphism of TNF-alpha gene in women. As a whole the data obtained by us confirm the assumption that polymorphism of cytokine genes can influence on human lifespan." All of these items are associated with the correct functioning of the immune system, and are already targets for drug development in the treatment of autoimmune disorders such rheumatoid arthritis, in which the immune system has become disarrayed and malfunctioning. We should expect to see statistically significant associations between human longevity and gene variants that improve the function and resilience of the most important bodily systems.

A STEP TOWARDS TREATING AGE-DAMAGED IMMUNE SYSTEMS
Tuesday, December 14, 2010
http://www.fightaging.org/archives/2010/12/a-step-towards-treating-age-damaged-immune-systems.php
News of research with potentially broad application, given the degree to which immune system damage contributes to age-related frailty: researchers "have discovered that the human body can create its own vaccine, which boosts the immune system and helps prevent chronic inflammatory diseases. ... When administered in the form of a therapeutic vaccine it is able to effectively prevent and treat a number of different inflammatory disease models for multiple sclerosis (MS), rheumatoid arthritis (RA), skin hypersensitivity and allergic asthma (AA). ... The implications of the findings are large as they shed light on an important way that the body combats inflammation and autoimmunity. Moreover, they establish a therapeutic approach for using the newly discovered protein as a treatment for multiple conditions. ... Many inflammatory and autoimmune diseases are chronic and affect a large majority of people. Moreover, there is an inflammatory component to many common diseases, such as Alzheimer's, Parkinson's, RA, AA, MS, type II diabetes and cancers. The vaccine discovered by the researchers boosts special cells of the immune system, called NKT cells. ... NKT cells are a type of T cell that exert profound and diverse regulatory effects in disease, from autoimmunity to responses to pathogens and cancer. For over two decades since their discovery NKT cells have traditionally been considered to be activated by lipid antigens presented by CD1 molecules. However, Professor Issazadeh-Navikas' group was able to show for the first time the ability of a self peptide to activate NKT cells to suppress many tissue-specific inflammatory conditions including experimental autoimmune diseases."

BUILDING NEW INTESTINAL TISSUE FROM STEM CELLS
Monday, December 13, 2010
http://www.fightaging.org/archives/2010/12/building-new-intestinal-tissue-from-stem-cells.php
More progress from the tissue engineers: "For the first time, scientists have created functioning human intestinal tissue in the laboratory from pluripotent stem cells. ... their findings will open the door to unprecedented studies of human intestinal development, function and disease. The process is also a significant step toward generating intestinal tissue for transplantation, researchers say. ... This is the first study to demonstrate that human pluripotent stem cells in a petri dish can be instructed to efficiently form human tissue with three-dimensional architecture and cellular composition remarkably similar to intestinal tissue. The hope is that our ability to turn stem cells into intestinal tissue will eventually be therapeutically beneficial for people with diseases such as necrotizing enterocolitis, inflammatory bowel disease and short bowel syndromes. ... To turn pluripotent stem cells into intestinal tissue, scientists performed a timed series of cell manipulations using chemicals and proteins called growth factors to mimic embryonic intestinal development in the laboratory. The first step turned pluripotent stem cells into an embryonic cell type called definitive endoderm, which gives rise to the lining of the esophagus, stomach and intestines as well as the lungs, pancreas and liver. Next, endoderm cells were instructed to become one those organ cell types, specifically embryonic intestinal cells called a 'hindgut progenitors'. The researchers then subjected the cells to what they describe as a 'pro-intestinal' cell culture system that promoted intestinal growth. Within 28 days, these steps resulted in the formation of three-dimensional tissue resembling fetal intestine that contained all the major intestinal cell types - including enterocytes, goblet, Paneth and enteroendocrine cells. The tissue continued to mature and acquire both the absorptive and secretory functionality of normal human intestinal tissues and also formed intestine-specific stem cells."

DISCOVERY DISCOVERS HORMESIS
Monday, December 13, 2010
http://www.fightaging.org/archives/2010/12/discovery-discovers-hormesis.php
Here is an example from Discovery News of one way in which popular science articles fall down: by focusing too closely on the research immediately to hand and failing to present the wider context. This article looks at the effect of damaging free radicals on life span in laboratory animals, but fails to talk in any detail about the range of research on hormesis effects: "Conventional wisdom has held for decades that free radicals cause aging, and that antioxidants, which squelch the reactivity of these highly reactive molecules, are a way to slow the process. But new work adds to a growing body of research that suggests the story is not so simple. In the new study published in PLoS Biology, worms that made more free radicals or that were treated with a free-radical-producing herbicide actually lived longer than normal worms. What's more, when the longer-lived mutant worms were given antioxidants, the effects were reversed, and the worms had a conventional worm lifespan. The finding flies in the face of the idea that antioxidants battle the effects of aging. ... what is emerging from this and other experiments is a view of free radicals - or, more precisely, reactive oxygen species - as a normal part of the body's stress response, with beneficial effects at certain levels."

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If you have comments, please do email them to newsletter@longevitymeme.org.

Two new initiatives from the CSCC

Posted: at 6:10 pm


The Cancer Stem Cell Consortium (CSCC) has announced the launch of two new initiatives for 2011-2012. Information about these initiatives is available via the websites of the CSCC and Genome Canada.

The two initiatives are:

1. C4Resource: The Canada-California Collaborative Cancer Stem Cell Resource and Technology Platform Network or C4Resource, which would coordinate cancer stem cell research resources and platform technologies more efficiently and effectively to advance research and discovery and accelerate clinical translation of new findings; and,

2. Partnership with CIRM: A second funding partnership with the California Institute for Regenerative Medicine (CIRM) through the CIRM's Disease Team Therapy Development Research Awards.

Information about the CIRM Disease Team Therapy Development Research Award RFA is available at: http://www.cirm.ca.gov/RFA_10-05

Vitamin B6 Cuts Colon Cancer Risk

Posted: at 1:36 pm


By Kathleen Doheny

WEDNESDAY, May 4 (HealthDay News) -- High daily levels of vitamin B6 may reduce the risk of getting colon cancer by 58 percent, claims a new study from Harvard Medical School.

The research, published in the May 4 issue of the Journal of the National Cancer Institute, builds on other studies that have already indicated a strong preventive effect from the vitamin.

"There are several smaller studies that have found a protective effect from dietary intakes of B6," said lead researcher Esther K. Wei, an instructor in medicine at Harvard Medical School and Brigham and Women's Hospital. However, "this is the first large study of women to look at blood levels of B6" and find a protective effect, she added.

Wei and her colleagues evaluated nearly 33,000 women who were participants in the Nurses' Health study, a long-running study that began in 1976. Since then, researchers have focused on subsets of the original 121,700 participants, all nurses between 30 and 55 years of age when they enrolled, to study various health issues. Read more...

Ayurstate for Prostate Care

Adverse Events in Hospitals- United States Department of Health Report slams current measures in US hospitals

Posted: at 9:34 am


OFFICE OF , INSPECTOR GENERAL of US Department of Health and Human Services, released a report on the national incidence of adverse events for hospitalized Medicare beneficiaries, the preventability of such events, and associated costs to Medicare.

The report released last month month found that one in seven of the patients experienced an adverse event such as excessive bleeding, a hospital-acquired infection or aspiration pneumonia. Those events, both preventable and not preventable, led to about 180,000 deaths a year.

The complete report available at

http://oig.hhs.gov/oei/reports/oei-06-09-00090.pdf


 

Reports From the December 2010 Bay Area Aging Meeting

Posted: December 19, 2010 at 6:12 pm


Aging science blog Ouroboros recently roused from its slumber for an excellent series of posts covering the Bay Area Aging Meeting held earlier this month. This is a well attended gathering of biogerontologists, who are fairly numerous in that part of the world. There are a number of important laboratories in California, such as the Kenyon Lab at UCSF and the Buck Institute for Age Research, which leads to a fair turnout at most local life science events.

Here is the coverage by session, one post for each set of presentations, with some of the highlights singled out and quoted below:

Bay Area Aging Meeting: Session I

Cognitive decline occurs with age: speed of processing, working memory, and long-term memory all decline. Presumably cell loss is partially to blame - not only loss of neurons, but also other types of cells (e.g., oligodendrocytes). Neural stem cells (NSC) can regenerate lost cells to some extent, but their ability to do so diminishes with age.

The Brunet lab is looking at the idea that pathways that control lifespan in "lower" organisms (worms; yeast) may be involved in regenerative capacity in "higher" organisms (us; mice). Rafalski's work is focusing on the now-famous SIRT1. SIRT1 is downregulated over the course of differentiation, so there's a smoking gun - but is there a causative relationship between SIRT1 downregulation and loss of regenerative capacity in NSCs?

Bay Area Aging Meeting: Session II

Furman looked at the response of 85 individual human subjects to vaccination, making a wide range of measurements (antibody titer, cytokine levels, gene expression), with the goal of creating a classifier system that can be used to predict the efficacy of the immune response. Young people tend to respond to antigens very similarly to one another (i.e., efficiently), whereas elderly subjects were split into two categories: cytokine responders and non-responders. These categories correlated with expression of genes associated with longevity, suggesting that immunosenescence and longevity represent two sides of the same coin.

Bay Area Aging Meeting: Session III

Regulatory T cells (Treg) maintain immune tolerance, i.e., they stop the rest of the immune system from attacking the body. They accomplish this by suppressing differentiation of naive cells and the activation of effector cells. This, in turn, helps to prevent autoimmune disease and graft rejection. However, Treg cells increase their activity during aging, which might make elderly people more susceptible to infection.

Treg activity is regulated by FoxP3, which is in turn modified by acetylation that is regulated by SIRT1. ... In questions, I asked whether SIRT1 inhibition could therefore be used to prevent autoimmune disease - the short answer is "yes"

Bay Area Aging Meeting: Session IV

If aging is an engineering problem, then we should be able to solve the engineering challenges more easily in simple systems. By introducing genes from a long-lived organism into the genome of a short-lived organism, it should be possible to add pro-longevity functions - in effect "upgrading" the short-lived animal so that it lives longer. Sagi has set out to do just that, by transferring genes from the long-lived zebrafish (4-year lifespan) to the short-lived worm (4-week lifespan).

...

The next obvious question: Can "upgrade" genes be combined to further increase lifespan? Indeed they can: several pairwise combinations of genes combined to extend lifespan longer than either single gene alone. At some point it worked a little too well: the lifespan of the worms started getting long enough that the survival curves became unwieldy.

Evolution doesn't select for longevity - a fact amply demonstrated by how many different minor changes in metabolism can make worms, flies, and mice live longer in good health.

Suppressing Aging in Our Lifetime

Posted: at 6:11 pm


Fifteen years ago, this paper or one with similar sentiments wouldn't have been accepted for publication - or if it had, it would have achieved nothing but harming the funding prospects of its author. The aging research community has only recently emerged from an era of self-censorship on the topic of engineering greater human longevity, and a field whose members do not talk about achieving a given goal will certainly make no progress towards that goal. From the abstract: "Although we do not know everything about aging, we now know enough to start its pharmacologic suppression using clinically approved drugs. Aging turns out to be driven by sensing-signaling pathways (such as the mTOR pathway). Given that some inhibitors of the mTOR pathway are already in clinical use, there is a unique opportunity to suppress aging, while treating and preventing diseases. By itself this will answer some burning questions in gerontology. Here I discuss a proposal, starting from retrospective clinical studies to animal and cellular models to drug screens in order to develop non-toxic and effective schedules and drug combinations for extending healthy life span in our lifetime." This is representative of the more eager members of the mainstream of biogerontology, focused on slowing aging through metabolic manipulation.

Link: http://www.ncbi.nlm.nih.gov/pubmed/21150328

Present Themes in Mainstream Aging Research

Posted: at 6:11 pm


From Maria Konovalenko: "Melanie Swan, MBA, is an Affiliate Scholar of the IEET [and] recently summarized some important themes in aging research that were discussed at the second Bay Area Aging Meeting. ... Two interesting talks concerned UCP2 (mitochondrial uncoupling protein 2) an enzyme which reduces the rate of ATP synthesis and regulates bioenergy balance. UCP2 and UCP3 have an important but not yet fully understood role in regulating ROS (reactive oxygen species) and overall metabolic function, possibly by allowing protons to enter the mitochondria without oxidative phosphorylation. The mechanism was explored in results that worm lifespan was extended by inserting zebrafish UCP2 genes (not natively present in the worm) ... Two talks addressed the issue of immune system compromise. One team created a predictive analysis that could be used to assess an individual's immune profile and potential response to vaccines by evaluating demographics, chronic infection status, gene expression data, cytokine levels, and cell subset function. Other work looked into the specific mechanisms that may degrade immune systems in older organisms. ... Aging and other biological processes become more complicated with progression up the chain of model organisms. What works in yeast and worms may not work in mice, and what works in mice and rats may not work in humans. Some interesting research looked at ribosomal proteins, whose deletion is known to extend lifespan in model organisms. The key points were [that] there was fairly little (perhaps less than 20%) overlap in lifespan-extending ribosomal protein deletions conserved between yeast and worms."

Link: http://mariakonovalenko.wordpress.com/2010/12/16/melanie-swan-a-summary-of-important-themes-in-aging-research/

SENS Foundation is Hiring

Posted: at 6:11 pm


The SENS Foundation, freshly infused with money from a recent half-million dollar donation, is hiring a new research assistant for their California research center. As you'll all know by now, the Foundation works on developing rejuvenation biotechnologies to repair and reverse the damage of aging. Do you want to be a part of that grand and noble effort? Then read on.

SENS Foundation seeking to hire Research Assistant

SENS Foundation is hiring a Research Assistant for our research center located in Mountain View, CA. Qualified candidates will a BS or MS in the chemical/biological sciences and two years of work experience. Experience should be in using standard equipment, including but not limited to standard bench cell biology/biochem/molecular biology techniques. Good fundamental laboratory skills to include safety, excellent pipetting skill, and mammalian cell culture.

Duties will include cell culture, transfection, microscopy, and protein work (western blot, IP, etc.). Subcloning / PCR cloning a plus. Experience working with mitochondria a strong plus. Research assistants will work under the supervision of the facility's senior researcher to carry out experiments directed towards establishing the viability of the SENS mission and chosen therapeutic goals. Research Assistants will receive general instruction on routine work and detailed instruction on new assignments. Other duties include providing support in areas such as lab maintenance, maintaining lab notes, procuring supplies, organizing research materials, and editing and filing documentation.

They are looking for mitochondrial research experience because the MitoSENS project is forging ahead. The goal of this line of work is to duplicate vulnerable mitochondrial genes in the cell nucleus, while enabling the vital proteins they produce to make their way back to the mitochondria. Thus even if the genes become damaged in the mitochondria, there will be a backup source of proteins to avoid the normal consequences of mitochondrial DNA damage.

For over 30 years mutations in mitochondrial DNA have been suspected to be important contributors to aging. If we can incorporate working copies of that mtDNA into our nuclear DNA, the mtDNA will be rendered superfluous and any mutations it suffers will be inconsequential.

Do you have laboratory experience? Then apply. After all, there is no more important task than helping to eliminate degenerative aging and age-related disease. No other area of present human endeavor has the potential to save as many lives and relieve as much suffering.

The Methuselah Foundation Wants Your Opinion on Their Strategies

Posted: at 6:11 pm


From the Methuselah Foundation Blog, a message from founder and CEO Dave Gobel: "It has been a while since I sent you an update and there is plenty of good news to share as we work together towards longevity. I also want your input as we make plans for the coming year. ... Methuselah Foundation has successfully promoted the extension of healthy human life - the science of aging has gained acceptance and broad-based support thanks to your ongoing contributions. Now we are strongly supporting science that will lead to tissue engineering and organ regeneration. We will be the catalyst to speed up the development of organ replacement. ... I am continually delving into every area of science, the work being done in universities, labs and biotech companies, to see the latest research and how it might contribute to longer life. I am convinced that there are many viable solutions but we, uniquely, are in a position to move them to a practical place. With this mission in mind we created the NewOrgan Prize. Based on our success with the Mprize, we anticipate this new prize will accelerate the rate of research and bring us closer to practical solutions. ... We must continue to accelerate practical scientific solutions related to aging. You and I - not just our children and grandchildren - should benefit from the advances in tissue engineering that are already on the table. This is why I need your input. We are contemplating a number of initiatives in support of this drive but we want to have the greatest possible impact. I would appreciate your thoughts and suggestions. Please continue reading and I believe you will have a clear understanding of the potential and, hopefully, will have some thoughts to share." Head on over to read the rest of the post: if you have opinions and good ideas, send them to the Foundation."

Link: http://blog.methuselahfoundation.org/2010/12/id_like_your_opinion_as_we_plan_for_the_future.html

PharmaNet unveils touch screen capable data capture platform for Phase I Clinical Trials

Posted: at 6:11 pm


The implementation of this platform enables rapid study set-up, automated CRF generation and better study recruitment and communication tools for general and special populations. Mobile workstations allow for rapid data entry and data is captured directly using bar codes and interfaces to medical equipment, such as blood pressure monitors. The Initiator platform also interfaces with the Company’s LIMS, as well as its diagnostic laboratory software and investigational drug management system.

Detailed PR available at PharmNet website

http://phx.corporate-ir.net/phoenix.zhtml?c=234619&p=irol-newsArticle&ID=1506686&highlight=

 

Sanofi-Aventis ties up with Oxford Univ for oncology research in India

Posted: at 6:11 pm


Sanofi-Aventis and Oxford University have entered into an agreement with INDOX, an academic oncology network to conduct oncology clinical and translation research in India.

The company said that through this partnership, Sanofi-Aventis will have access to experience and expertise of India’s top oncologists which will help the company in conducting clinical research. “The collaboration between sanofi-aventis, Oxford University and the Indian Cancer Centers fosters a model for academic researchers and industry to work together for the benefit of patients,” said Debasish Roychowdhury, MD, Senior Vice President, Head of Oncology, sanofi-aventis.

Sanofi-Aventis said that the company will provide financial assistance to Oxford University to manage INDOX’s eigh cancer reseach centres in India. The university, on its part, will provide training and support to investigators and reseach coordinators to help in carrying out the research.

INDOX is a partnership between Oxford University and India’s top eight cancer research centres in India.

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