Fight Aging! Newsletter, October 1st 2012

FIGHT AGING! NEWSLETTER
October 1st 2012

The Fight Aging! 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 Fight Aging!

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CONTENT

- A Way to Insert New Mitochondria into Cells
- Future Directions for Fight Aging!
- Progress in Tackling Muscle Aging
- Commentary on the Relevance of Progeria Research
- Discussion
- Latest Headlines from Fight Aging!
    - Shorter People Tend to Live Longer
    - Rate of Increase of Short Telomeres Predicts Longevity in Mammals
    - Overexpressing Fatty-Acid-β-Oxidation-Related Genes Extends Fly Lifespan
    - A Mammal With Superior Regeneration
    - A Few More Longevity-Associated Gene Variants
    - Eunuchs as a Poor Way to Study the Influence of Male Hormones on Aging
    - Nanoparticles to Reliably Target Mitochondria
    - Early Results from a Progeria Therapy Trial
    - An Interesting Comment From a Google Ventures Partner
    - When I'm 164: An Interview With David Ewing Duncan

A WAY TO INSERT NEW MITOCHONDRIA INTO CELLS

The mitochondria swarming in our cells become damaged as a result of performing their biological function, and this damage is a potent contribution to the aging process. Various methodologies are proposed to eliminate this issue, and here is news of progress on one front:

https://www.fightaging.org/archives/2012/09/a-way-to-insert-new-mitochondria-into-cells.php

"Scientists demonstrate that cells will ingest and adopt appropriately engineered mitochondria, adding them to the existing herd without the need for any intervention beyond placing the engineered mitochondria into the same cell culture. The researchers are calling their process peptide-mediated mitochondrial delivery ... As you can imagine, this immediately leads one to think in terms of an infusion-type therapy, where a fluid solution containing hordes of mitochondria can be introduced into tissues and be taken up into cells. The mitochondria themselves can be cultivated like bacteria from a sample from the patient, which is gene engineered to fix issues such as genetic diseases caused by mutations in mitochondrial DNA - or they can be from a donor.

"In a more liberated, free-wheeling future, this sort of approach might be widely used to swap out the mitochondria you are born with for a better set. It is already the case that some mitochondrial lineages have been shown to be better than others in terms of functionality and durability. Looking further ahead, we might see optimal mitochondria: artificially created biological machines that do the same job, but designed to remove the issues that cause harm and aging in the natural version.

"The ability to insert new mitochondria is a viable approach for genetic diseases, where the patient's lineage is damaged. The new fully functional mitochondria will dilute the effects of the established mitochondria, and may largely replace them with time. Thinking on this points out the major issue with wholesale mitochondrial replacement, however: it's not the case that functional mitochondria will necessarily out-compete non-functional mitochondria within a cell over the long haul. Consider that the situation becomes something like competition between bacterial strains in an enclosed environment: whichever strain has the advantage will eventually win out. This picture is complicated by the fact that mitochondria swap components among themselves, but still seems to be a useful model when thinking about results.

"For the genetic disease sufferers, it should be comforting to see that the researchers demonstrated repair of cells with broken mitochondria by inserting working mitochondria. For aging, however, the picture is less certain. After all, the problems caused by damaged mitochondria in aging occur because these damaged cellular components have an advantage to survival - they are damaged in a way that evades the surveillance mechanisms designed to weed out broken, harmful mitochondria. So it isn't clear that throwing in a bunch of working mitochondria will help all that much; one might imagine a short-lived benefit, but then you're right back to where you were before.

"Which is not to say that people shouldn't try this. I say run up some old flies or nematode worms and infuse them with fresh new mitochondria, see what happens. A study in nematodes in particular should proceed fairly straightforwardly from being able to do this in cell cultures."

FUTURE DIRECTIONS FOR FIGHT AGING!

Fight Aging! has been somewhat static in focus and traffic for the past five years at least. Is there anything that can or should be done about changing this state of affairs? Some thoughts on possible strategies and changes of focus can be found in the following post:

https://www.fightaging.org/archives/2012/09/possible-future-directions-for-fight-aging.php

PROGRESS IN TACKLING MUSCLE AGING

Muscles decline with age, and the frailty and weakness that result are a part of the downward spiral of aging. A range of different strategies and mechanisms are emerging as researchers dig into how this process happens. News of progress on two fronts appeared recently:

https://www.fightaging.org/archives/2012/09/inhibiting-fgf2-in-mice-slows-muscle-stem-cell-decline-with-age.php

"Rare muscle stem cells are located inside each skeletal muscle of the body. Also called satellite cells, due to their position on the surface of the muscle fibers they serve and protect, these cells are essential to maintaining the capacity of muscles to regenerate. Satellite cells are able to generate new, differentiated muscle cells while keeping their identity as stem cells, retaining the ability to maintain and repair muscle tissue. Normally in a resting or dormant state, satellite cells respond rapidly to repair injured tissues. The current study finds that aging muscle stem cells lose their ability to maintain a dormant state, so that when called upon to repair injured muscle, they are unable to mount an adequate response. ... Just as it is important for athletes to build recovery time into their training schedules, stem cells also need time to recuperate, but we found that aged stem cells recuperate less often. We were surprised to find that the events prior to muscle regeneration had a major influence on regenerative potential.

"In a series of experiments in mice, the authors found that a developmental protein called fibroblast growth factor-2 (FGF2) is elevated in the aging muscle stem cell microenvironment and drives stem cells out of the dormant state. Satellite cells that are forced to replicate lose the ability to maintain their identity as stem cells, reducing the stem cell population. The authors also found that blocking the age-related increase in FGF signaling both in aged satellite cells or in the cellular microenvironment protected against stem cell loss, maintained stem cell renewal during aging and dramatically improved the ability of aged muscle tissue to repair itself."

https://www.fightaging.org/archives/2012/09/an-update-on-myostatin-research.php

"Blocking myostatin function in normal mice causes them to bulk up by 25 to 50 percent. What is not known is which cells receive and react to the myostatin signal. Current suspects include satellite cells and muscle cells themselves. In this latest study, researchers used three approaches to figure out whether satellite cells are required for myostatin activity. They first looked at specially bred mice with severe defects in either satellite cell function or number. When they used drugs or genetic engineering to block myostatin function in both types of mice, muscle mass still increased significantly compared to that seen in mice with normal satellite cell function, suggesting that myostatin is able to act, at least partially, without full satellite cell function.

"To further confirm their theory that myostatin acts primarily through muscle cells and not satellite cells, the team engineered mice with muscle cells lacking a protein receptor that binds to myostatin. If satellite cells harbor most of the myostatin receptors, removal of receptors in muscle cells should not alter myostatin activity, and should result in muscles of normal girth. Instead, what the researchers saw was a moderate, but statistically significant, increase in muscle mass. The evidence once again, they said, suggested that muscle cells are themselves important receivers of myostatin signals. ... since the results give no evidence that satellite cells are of primary importance to the myostatin pathway, even patients with low muscle mass due to compromised satellite cell function may be able to rebuild some of their muscle tone through drug therapy that blocks myostatin activity.

"Everybody loses muscle mass as they age, and the most popular explanation is that this occurs as a result of satellite cell loss. If you block the myostatin pathway, can you increase muscle mass, mobility and independence for our aging population? [Our] results in mice suggest that, indeed, this strategy may be a way to get around the satellite cell problem."

COMMENTARY ON THE RELEVANCE OF PROGERIA RESEARCH

A therapy for the rare accelerated aging condition progeria is showing some benefits in a trial. Is this relevant to work on normal aging?

https://www.fightaging.org/archives/2012/09/commentary-on-progeria-therapy-trials-at-the-sens-foundation.php

"All of us at SENS Research Foundation are inspired by the rapid progress that was made against this tragic disease ... However, it is also important not to read too much into this apparent advance in regards to its implications for the development of new medicines against the diseases and disabilities of aging. In particular, the common characterization of HGPS 'progeria' as a disease of 'premature aging' leads some to expect that this research has direct implications for the development of rejuvenation biotechnologies, targeting the damage and disabilities of aging.

"It is true that the splicing defect responsible for formation of progerin is sporadically active in wild-type cells, and that number of cells in which progerin is present and the level at which it appears do appear to rise with aging. However, such cells are rare enough, and their progerin levels low enough, as to seem highly unlikely to meaningfully contribute to tissue dysfunction with aging, at least within the bounds of a currently-normal lifespan. Additionally, there is evidence that progerin can be turned over in the nuclear lamina, and the causal relationship between the higher prevalence of progerin in aging cells and cellular senescence or disease are not clear, leaving open the possiblity that repair of well-established forms of aging damage may in turn lead to the reversal or obviation of this phenomenon.

"Notably, the need to remove 'senescent' cells as part of a comprehensive panel of rejuvenation biotechnologies is already clear from first principles, and its potential to ameliorate aspects the frailty and disability of aging has been demonstrated in proof-of-concept rejuvenation research, rendering the specific role of progerin in the process moot. That is, removing 'senescent' cells is essential whether progerin accumulation is a cause or a consequence of cellular senescence, and will be equally effective as a regenerative medical therapy against age-related disability in either case."

DISCUSSION

The highlights and headlines from the past week follow below. 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!

SHORTER PEOPLE TEND TO LIVE LONGER
Friday, September 28, 2012
https://www.fightaging.org/archives/2012/09/shorter-people-tend-to-live-longer.php
It is thought that size in humans relates to life expectancy via aspects of metabolism such as growth hormone - less growth hormone means a smaller size but longer life in mammal species. Ames dwarf mice are an example of this taken to an extreme through genetic engineering, lacking growth hormone but living more than 60% longer than their peers. From an evolutionary perspective, an abundance of food and good health in early life or gestation is thought to trigger a more aggressive front-loading of growth and fertility - which comes at the cost of faster decline once an individual is beyond their reproductive lifespan: "Sardinians have been studied extensively looking for clue to long lifespan. In the current study researchers analyzed the role of a person's height in their eventual lifespan. The researchers analyzed the height of men when they entered the military at age 20 between the years of 1866 and 1915. A total of 685 subjects were analysed. These heights were then related to the persons eventual age at death. It was found that shorter people (shorter than 161.1 cm) lived significantly longer on average than taller people (taller 161.1cm). Furthermore at age 70, taller people lived on average 2 years less than shorter people. At age 70 each quarter inch of height reduced lifespan by one year. The authors write: In conclusion, shorter people and taller people exhibit differences in longevity. Although a tall body generally reflects abundant nutrition and good living conditions during the growth period, this height has negative ramifications as well. Biological mechanisms indicate that a larger body places greater stress on cells, tissues, and organs, which can reduce longevity."

RATE OF INCREASE OF SHORT TELOMERES PREDICTS LONGEVITY IN MAMMALS
Friday, September 28, 2012
https://www.fightaging.org/archives/2012/09/rate-of-increase-of-short-telomeres-predicts-longevity-in-mammals.php
Telomeres are the protective caps at the end of chromosomes. They shorten with cell division, and so are part of the clock which decides when a cell reaches the Hayflick limit and ceases dividing. There is much more to it than this, however: telomere length across all the cells in a piece of living tissue is dynamic, as there are processes that lengthen telomeres as well - such as the activity of telomerase. In general average telomere length erodes with age, reflecting the progressive breakdown of the body's ability to maintain itself - but this proceeds quite differently in different tissues and different species. It can even be reversed in the short term if the health of an individual improves, though in the long term the overall progression is still downhill. Shorter average telomere length has been correlated with measures of health in statistical studies, but data allowing prediction of longevity for an individual has proven elusive to date. Here, however, a more sophisticated measure of telomere dynamics is show to be predictive of life span in individual mice: "Aberrantly short telomeres result in decreased longevity in both humans and mice with defective telomere maintenance. Normal populations of humans and mice present high interindividual variation in telomere length, but it is unknown whether this is associated with their lifespan potential. To address this issue, we performed a longitudinal telomere length study along the lifespan of wild-type and transgenic telomerase reverse transcriptase mice. We found that mouse telomeres shorten ∼100 times faster than human telomeres. Importantly, the rate of increase in the percentage of short telomeres, rather than the rate of telomere shortening per month, was a significant predictor of lifespan in both mouse cohorts, and those individuals who showed a higher rate of increase in the percentage of short telomeres were also the ones with a shorter lifespan. These findings demonstrate that short telomeres have a direct impact on longevity in mammals, and they highlight the importance of performing longitudinal telomere studies to predict longevity."

OVEREXPRESSING FATTY-ACID-β-OXIDATION-RELATED GENES EXTENDS FLY LIFESPAN
Thursday, September 27, 2012
https://www.fightaging.org/archives/2012/09/overexpressing-fatty-acid-β-oxidation-related-genes-extends-fly-lifespan.php
Researchers here investigate another portion of the mechanisms of metabolism that are influenced by calorie restriction and many of the known longevity genes. This sort of discovery helps to fill in a very complicated landscape of intertwining effects and controllers of effects - at some point in the not too distant future the research community will be able to set out a complete map of how all of the longevity genes and known ways to extend life in laboratory animals relate to one another and work through an overlapping set of mechanisms: "In this study, we demonstrated that the overexpression of fatty-acid-β-oxidation-related genes extended median and maximum lifespan [in flies] and increased stress resistance, suggesting that the level of fatty-acid β-oxidation regulates lifespan. Consistent with our results, many investigations have suggested fatty-acid β-oxidation as a lifespan determinant. One of the well-known longevity-candidate genes, AMPK reportedly regulates fatty-acid synthesis and oxidation. Moreover, calorie restriction and [insulin/insulin-like growth factor (IGF) signaling (IIS)] have been reported to promote fatty-acid β-oxidation. In addition, enigma mutant, which exhibits oxidative stress resistance and a longevity phenotype, was found to encode a fatty-acid-β-oxidation related enzyme. ... However, the present study is the first to provide direct evidence that the modulation of fatty-acid-β-oxidation components extends lifespan. Our data showed that lifespan extension by dietary restriction decreased with the overexpression of fatty-acid β-oxidation-related genes, indicating that lifespan extension by fatty-acid-β-oxidation components is associated with dietary restriction. It was previously reported that calorie restriction increased whole-body-fat oxidation. Energy deprivation subsequent to calorie restriction activates AMPK, which subsequently enables the increase of fatty-acid oxidation necessary to utilize the energy resource. These findings suggested that fatty acid oxidation and dietary restriction are related by same underlying mechanisms."

A MAMMAL WITH SUPERIOR REGENERATION
Thursday, September 27, 2012
https://www.fightaging.org/archives/2012/09/a-mammal-with-superior-regeneration.php
We mammals just can't regenerate as well as lower animals - but we all evolved from the same ancestors, so the suspicion is that we might retain at least some of the necessary mechanisms to regrow organs and limbs, just buried and inactive. Some studies have uncovered possible hints of this: you might recall the gene engineered MRL mice that have superior regenerative abilities due to inactivation of p21, for example. Here, researchers note the discovery of superior natural regenerative abilities in a rodent species - which should hopefully lead to some further insight into how we might make humans regenerate more capably: "Two species of African spiny mouse have been caught at something no other mammal is known to do - completely regenerating damaged tissue. ... Acomys kempi and Acomys percivali [have] skin that is brittle and easily torn, which helps them to escape predators by jettisoning patches of their skin when caught or bitten. ... whereas normal laboratory mice (Mus musculus) grow scar tissue when their skin is removed, African spiny mice can regrow complete suites of hair follicles, skin, sweat glands, fur and even cartilage. Tissue regeneration has not been seen in mammals before, but it is common in crustaceans, insects, reptiles and amphibians. Some lizards can regrow only their tails, whereas some salamanders can regenerate entire limbs, complete with bones and muscle. The researchers say that their next step will be to work out the molecular mechanisms and genetic circuits that direct the regeneration process. It's unlikely that these mice have evolved an entirely new method of regrowing tissue ... Rather, the genes that direct regeneration in salamanders are probably switched off in mammals, but have been switched back on in African spiny mice. ... By looking at the common genetic blueprints that exist across vertebrates, we hope to find the ones that we could activate in humans. We just need to figure out how to dial the process in mammals back to do something the entire system already knows how to do."

A FEW MORE LONGEVITY-ASSOCIATED GENE VARIANTS
Wednesday, September 26, 2012
https://www.fightaging.org/archives/2012/09/a-few-more-longevity-associated-gene-variants.php
There are many genes associated with longevity, but one of the present challenges in this research is that few such correlations seem to exist in multiple populations - implying that there is a very large set of individually small contributions from our genes, and that different lineages and lifestyles have significantly different maps of genes to longevity: "Men and women have a different life expectancy. Not unexpectedly, several genes involved in lifespan determination have been found to influence the probability of achieving longevity differently in men and women. This investigation examines the association between longevity and polymorphisms of follicle-stimulating hormone receptor (FSHR, Asn680Ser polymorphism) and peroxisome proliferator-activated receptor gamma (PPARG, Pro12Ala polymorphism), two genes that previous investigations suggested may exert a gender-specific influence on human longevity. A sample of 277 individuals (mean age: 82.9±5.7years) was recruited in 2000. Based on mortality data collected in 2009, the sample was divided into two groups of subjects surviving over 90 years (long-lived) or not (controls). The frequency of FSHR 680 Ser/Ser genotype was significantly higher in the sample of long-lived women compared to controls, indicating that FSHR 680 Ser/Ser genotype may favor survival to more than 90 years of age only in women. In contrast, the frequency of PPARG Pro/Ala genotype was significantly higher in the sample of male subjects who died before 90 years than in the long-lived, suggesting that carrying PPARG Pro/Ala genotype may prevent the attainment of advanced age only in men. We then searched the literature for studies reporting a differential role for the genetic component in male and female longevity; to do this, we selected longevity genes with a gender-specific effect. A review of the studies showed that genetic factors tend to have a greater relevance in determining longevity in men than in women."

EUNUCHS AS A POOR WAY TO STUDY THE INFLUENCE OF MALE HORMONES ON AGING
Wednesday, September 26, 2012
https://www.fightaging.org/archives/2012/09/eunuchs-as-a-poor-way-to-study-the-influence-of-male-hormones-on-aging.php
A paper that compares genealogical records of Korean eunuchs with their intact peers from past centuries has been doing the rounds, with the data showing a higher life span for the eunuchs. However, there is considerable skepticism from the rest of the research community - there are any number of ways to sneak in a bias towards longer-lived, more robust individuals: how the data came into being; how it is analyzed; how the eunuchs originally came into their position; their life style differences; and so forth. So it is hard to see any good way to discuss the role of male hormones in relation to this data, given all of the potential confounding factors not addressed by the authors. For example, only 81 of 385 recorded eunuchs had enough information present in the genealogy to pin down a life span. This alone could contain a bias towards longer-lived, more active, or more privileged individuals: there is no reason to think that these 81 are representative. But this is the nature of scientific research - individual research results have to be read skeptically and in the broader context of their field: "Historically, eunuchs have been employed as guards and servants in harems across the Middle East and Asia. The Imperial court of the Korean Chosun Dynasty (1392-1910) also had eunuchs. Eunuchs of the Chosun Dynasty lived with privileges: Korean eunuchs were conferred with official ranks and were legally allowed to marry, a practice that was officially banned in the Chinese Empire. In addition, married couples were also entitled to have children by adopting castrated boys or normal girls. The boys lost their reproductive organs in accidents, or they underwent deliberate castration to gain access to the palace before becoming a teenager. ... Several studies have described the long-term consequences of castration in eunuchs, but there have been no data on the lifespan of eunuchs. We examined the lifespan of Korean eunuchs by analyzing the Yang-Se-Gye-Bo - a genealogy record of Korean eunuchs. To our knowledge, this is the only record of eunuch-family histories in the world. ... The Yang-Se-Gye-Bo contains the records of 385 eunuchs. From these records, the lifespans of 81 eunuchs could be identified. The average lifespan of this group was 70.0 ± 1.76 years. As lifespan is affected by genetic and socio-economic factors, we compared the lifespan of eunuchs with the lifespan of men from three non-eunuch families of similar social status, who lived during the same time periods. ... The average lifespan of eunuchs [was] 14.4-19.1 years longer than the lifespan of non-castrated men of similar socio-economic status. Our study supports the idea that male sex hormones decrease the lifespan of men."

NANOPARTICLES TO RELIABLY TARGET MITOCHONDRIA
Tuesday, September 25, 2012
https://www.fightaging.org/archives/2012/09/nanoparticles-to-reliably-target-mitochondria.php
Technology platforms for the delivery of therapies to the mitochondria in our cells are both important and showing signs of progress. There are any number of ways in which we would like to manipulate our mitochondria, most importantly to repair or work around damage to their DNA because that is one of the contributing causes of aging. Given a general method for placing any therapy inside mitochondria we should see more development and experimentation in ways to repair them. Here, researchers "have refined the nanoparticle drug delivery process further by using nanoparticles to deliver drugs to a specific organelle within cells. By targeting mitochondria, 'the powerhouse of cells,' the researchers increased the effectiveness of mitochondria-acting therapeutics used to treat cancer, Alzheimer's disease and obesity in studies conducted with cultured cells. ... The mitochondrion is a complex organelle that is very difficult to reach, but these nanoparticles are engineered so that they do the right job in the right place. [Researchers] used a biodegradable, FDA-approved polymer to fabricate their nanoparticles and then used the particles to encapsulate and test drugs that treat a variety of conditions. ... getting drugs to the mitochondria is no simple feat. Upon entering cells, nanoparticles enter a sorting center known as the endosome. The first thing [researchers] had to demonstrate was that the nanoparticles escape from the endosome and don't end up in the cells' disposal center, the lysosome. The mitochondria itself is protected by two membranes separated by an interstitial space. The outer membrane only permits molecules of a certain size to pass through, while the inner membrane only permits molecules of a given range of charges to pass. The researchers constructed a library of nanoparticles and tested them until they identified the optimum size range - 64 to 80 nanometers, or approximately 1,000 times finer than the width of a human hair - and an optimum surface charge, plus 34 millivolts. ... the components they used to create the nanoparticles are FDA approved and that their methods are highly reproducible and therefore have the potential to be translated into clinical settings. The researchers are currently testing their targeted delivery system in rodents and say that preliminary results are promising."

EARLY RESULTS FROM A PROGERIA THERAPY TRIAL
Tuesday, September 25, 2012
https://www.fightaging.org/archives/2012/09/early-results-from-a-progeria-therapy-trial.php
Researchers here show data resulting from a therapy targeting the underlying cause of progeria. Accelerated aging conditions are extremely rare, but this is interesting to the rest of us because the same mechanisms that run wild in progeria sufferers apparently occur in a minor way during normal aging - so a cure for progeria might have some utility for the rest of us as well: "Results of the first-ever clinical drug trial for children with Progeria, a rare, fatal 'rapid-aging' disease, demonstrate the efficacy of a farnesyltransferase inhibitor (FTI), a drug originally developed to treat cancer. The clinical trial results, completed only six years after scientists identified the cause of Progeria, included significant improvements in weight gain, bone structure and, most importantly, the cardiovascular system ... Twenty-eight children from sixteen countries participated in the two-and-a-half year drug trial, representing 75 percent of known Progeria cases worldwide at the time the trial began. Of those, 26 are children with the classic form of Progeria. ... One in three children demonstrated a greater than 50 percent increase in annual rate of weight gain or switched from weight loss to weight gain, due to increased muscle and bone mass. ... On average, skeletal rigidity (which was highly abnormal at trial initiation) improved to normal levels after FTI treatment. ... Arterial stiffness, strongly associated with atherosclerosis in the general aging population, decreased by 35 percent. Vessel wall density also improved with treatment."

AN INTERESTING COMMENT FROM A GOOGLE VENTURES PARTNER
Monday, September 24, 2012
https://www.fightaging.org/archives/2012/09/an-interesting-comment-from-a-google-ventures-partner.php
Via CNBC: "Google's Venture fund is planning to invest $1 billion in a wide-range of start-ups over the next five years, but the firm isn't necessarily looking for the next Facebook, Twitter or other media related business. ... 'There's a whole world of innovation out there outside of social media. It's a huge growth area, but we're investing a lot of money in life sciences,' said William Maris, Google Ventures managing partner. ... Maris said the fund seeks entrepreneurs that 'have a healthy disregard for the impossible' with forward-thinking ideas, especially in biotech. Maris said some of the areas he is interested in include businesses that are focused on radical life extension, cryogenics and nanotechnology. ... 'Part of my job is to discern the fine line between crazy and genius,' Maris said. 'We're looking for entrepreneurs that want to change the world for the better and that's important. So I do think our values are a little bit different than the typical sort of venture capitalist you might meet.'" This is just a comment, of course, and at present the fund isn't invested in anything that works directly towards the defeat of aging: one partner's views don't necessarily have anything to do with how the fund moves in aggregate. One of the real challenges in longevity science today is that there's little to effectively commercialize, even if you want to be really aggressive and pull results right out of research into an unregulated region of the world for development as a therapy. Things don't get interesting until SENS programs or similar start to deliver results that can be turned into an early product, or the tissue engineers and stem cell researchers make more of an inroad into reversing the changes in stem cell populations that occur with age. The leading edge of all this is still a few years away at the very earliest, and more like at least a decade for much of it, so far as I can see.

WHEN I'M 164: AN INTERVIEW WITH DAVID EWING DUNCAN
Monday, September 24, 2012
https://www.fightaging.org/archives/2012/09/when-im-164-an-interview-with-david-ewing-duncan.php
Author David Ewing Duncan is presently touting a new book on aging and aging research entitled "When I'm 164". Here is an audio interview: "With a new understanding of the biology of aging, we may be on the cusp of pushing life expectancy to ages once considered unimaginable. Journalist and author David Ewing Duncan in his book When I'm 164, examines the potential technologies that could lead us to radical life extension and some of the consequences should science bring about a dramatic demographic shift. We spoke to Duncan about his book, how close we are to scientific advancements in the area, and why not everyone wants to live forever. ... While riffing on the Beatle's song 'When I'm 64,' the book surveys the increasingly legitimate science of radical life extension - from Healthy Living and Genetics to Regeneration and Machine Solutions - and considers the pluses and minuses of living to age 164, or beyond; everything from the impact on population and the cost of living to what happens to love, curiosity, and health. He shares classic stories and myths of people determined to defeat aging and death, and offers real-life tales of the techno-heroes and optimists who believe that technology can solve the 'problem' of aging. Concluding that anti-aging technologies will probably succeed in the next 30-50 years despite his earlier skepticism, he brings us back to the age-old question: 'will you still need me, will you still feed me, when I'm...'"

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