Sylmar CA Technical and Trade Schools

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Source:
http://www.ilcusa.org/modules/mediablog/rss.php?page_id=43

I view the world of aging and longevity science as divided into three broad classes of research and researchers - something that will already be apparent to regular readers, but which I don't recall having outlined explicitly. This crude model of the research community informs the ways in which I read research and evaluate the state of progress towards meaningful goals: both extension of healthy human life, and - more importantly - forms of medicine capable of repair and reversal of aging.

Class 1: Investigating Aging

By far the largest component of the aging science community is made up of researchers who are not working on ways to alter or repair the aging process. They investigate only, and thus the majority of funds devoted to the science of aging still go towards studies that aim to make no difference to the world beyond gathering data. This group include most of those who run demographic studies of human longevity, for example.

Aging research is unusual in the medically-relevant life sciences by virtue of this preponderance of "look but don't touch." Up until comparatively recently it was extremely hard to find funding or respect for work that aimed to do more than gather data on aging; the scientific community worked to exclude those who had such goals in mind, and funding sources closed their doors to anyone known to harbor heretical thoughts about extending human life through biotechnology.

Class 2: Working to Slow Aging

The larger minority class in aging research is made up of researchers and funding institutions who are working towards ways to slow aging, or working on related areas that will be used in constructing therapies to slow aging. The typical approach here is to reverse engineering the genetic and other low-level biochemical roots of known differences in longevity (such as the effects of calorie restriction, or the differences in life span between similar species), and then try to reproduce some of those differences using drugs, gene therapies, and other similar means. The view of these researchers is largely that we are a long way from any practical results, and those results will only offer incremental gains - a viewpoint I agree with.

Nonetheless, this class is where much of the energy and vigor is in funding and growth for aging research. This may be because this general research strategy is easily understood by traditional sources of funding, and is only an incremental alteration to previous forms of old-school drug development work.

The sea change in the aging research community over the past decade or so has largely manifested as a transformation of researchers from the bulk of class 1 into up and coming enthusiasts of class 2. As it became respectable to talk about doing something about aging - thanks to the hard work of a comparatively small number of advocates and visionary scientists - there has been a steady shifting of research priorities. The investigators still outnumber research groups working on ways to alter the course of aging, but the trend is clearly towards a field that develops clinical applications in medicine rather than only informing the medical profession of what to expect in their patients.

Class 3: Working to Reverse Aging

The smallest and most important cohort of researchers are those who are working on ways to repair, reverse, or work around the root causes of aging - the SENS Foundation research network being the archetype, though not the only set of researchers and laboratories involved in this work. This class are the most important because their approach is the only viable path we can see that has a good chance of producing rejuvenation biotechnology capable of greatly extending healthy life in the elderly - through restoring youthful function and vigor. This is the smallest cohort because we do not live in a particularly rational world.

I have discussed in the past why it is that repair based strategies are so very much better than approaches based on slowing down aging. The short of it is that aging is a matter of damage: slowing down the pace of damage will do little for people who are already old, while repairing damage will be beneficial to everyone. You can only achieve rejuvenation through actual repair, not by slowing down the rust. Given that the cost of producing therapies from the two very different strategic approaches to medicine for aging will likely be in the same ballpark, we should evidently aim for the better outcome.

There is also the matter of time - it will be decades before either side of the house has a mature base of therapies in place, and by the time those therapies are available those of use with the greatest vested interest in using them will be old. So only the strategy of aiming for rejuvenation offers the chance of an outcome that grants additional decades at the end of the day - enough time to push past actuarial escape velocity and thus be able to wait out the advent of even better therapies.

But cogent arguments aside, the greatest growth in aging research is still amongst class 2, those working on the slow road to a poor end result. Now that the research community is essentially persuaded to the view that work on aging is good, interesting, and plausible, the next - and equally important - goal of advocacy is to persuade a great many more researchers to work on the SENS vision for rejuvenation biotechnology or equivalent scientific programs.

Many, many lives depend on it.

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

A theory that has emerged in recent years points to forms of amyloidosis as the final limiting process for human life span. Extremely long-lived people, who have survived or evaded all the common fatal age-related conditions, appear to die because of amyloid buildup. The evidence is good enough for the SENS Foundation to start funding work on a therapy - like all the mechanisms of aging, this is something that can be fixed through appropriate use of biotechnology. Here's a little more on the topic (and a link to a PDF format research paper): "Supercentenarians are persons who have lived beyond the age of 110. Currently there are only about 80 such known individuals in the world whose age is verified. These people represent the limit of human lifespan. For a variety of reasons not fully understood but including lifestyle choices, genetic variants, and chance, these individuals have escaped the usual causes of death including cancer, heart disease and stroke. However, eventually they too die, with the world record holder being Jeanne Calment who survived until age 122. In a newly published review Drs. Stephen Coles and Thomas Young of the UCLA Gerontology Research Group point out what it may be that is killing supercentenarians: amyloidosis. Amyloidosis is a disease state hallmarked by the deposition of fibers of abnormally clumped masses of transthyretin. The protein transthyretin normally acts to carry thyroid and other hormones. Mutations in the gene make the fibers abnormally sticky and they tend to clump into long fibers which are deposited in multiple organs. Through early onset amyloidosis leads to disease, it is of interests that supercentanarians all seem to have significant amounts of it. Though not proven it is possible the amyloid is killing them. These persons have already escaped the typical causes of death however they have lived for so long, the normally innocuous amounts of amyloid that increase with age may actually become toxic to them because they have lived so many years. Where this line of reasoning gets exciting is that experimental drugs exist which may eliminate amyloid."

Link: http://extremelongevity.net/2012/05/22/is-amyloidosis-the-limiting-factor-for-humans-lifespan/

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

An example of the way in which the machinery of cells is very intertwined, components reused by evolution in many different mechanisms: "This was certainly an unexpected finding. It is rather uncommon for one gene to have two very different and very significant functions that tie together control of aging and inflammation. The two, if not regulated properly, can eventually lead to cancer development. It's an exciting scientific find. ... For decades, the scientific community has known that inflammation, accelerated aging and cancer are somehow intertwined, but the connection between them has remained largely a mystery ... What was known [was] that a gene called AUF1 controls inflammation by turning off the inflammatory response to stop the onset of septic shock. But this finding, while significant, did not explain a connection to accelerated aging and cancer. When the researchers deleted the AUF1 gene, accelerated aging occurred, so they continued to focus their research efforts on the gene. ... The current study reveals that AUF1, a family of four related genes, not only controls the inflammatory response, but also maintains the integrity of chromosomes by activating the enzyme telomerase to repair the ends of chromosomes, thereby simultaneously reducing inflammation, preventing rapid aging and the development of cancer. ... [Researchers are now] examining human populations for specific types of genetic alterations in the AUF1 gene that are associated with the co-development of certain immune diseases, increased rates of aging and higher cancer incidence in individuals to determine exactly how the alterations manifest and present themselves clinically."

Link: http://www.sciencedaily.com/releases/2012/05/120524122851.htm

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

A post at Extreme Longevity touches on an area of interest in aging research, and comes with a link to a PDF versions of the paper in question. It is another study confirming the link between levels of the protein p16INK4A and aging, something that has been known for some years. In particular, it shows up in the senescent cells that accumulate with age, something that researchers have managed to make use of: you might recall last year's study that showed beneficial effects from destroying senescent cells in rats. That research group used p16INK4A as a basis for their method of selective destruction, targeting only those cells that had become senescent and thus removing their contribution to the aging process.

It is worth noting that p16INK4A is a gene with a lot of aliases - which tends to happen when many different researchers have been working on the biochemistry independently. The official name is CDKN2A, or cyclin-dependent kinase inhibitor 2A, but it can be referred to as p16 as well. In any case, here is the Extreme Longevity post, a PubMed reference, and the PDF version of the paper:

In this study the researchers examined skin cells from middle aged people aged 43 to 63. They compared a group who had a strongly family history of extreme longevity to age-matched controls. They found that p16 expression in skin cells was significantly lower in the group that had the strong family history of longevity. They conclude "a younger biological age associates with lower levels of p16INK4a positive cells in human skin."

This study supports the idea that p16 expressing cells are linked to age both from a chronological as well as biological perspective. Work needs to be done to find a way to remove p16 positive cells from all tissues of the body on a regular basis. Such a therapy, if it existed, may act to reduce aging.

This all ties back in to cancer suppression versus tissue proliferation. Increased senescence in cells is one way of biasing the average over time to a lower rate of cancer - because the cells most likely to cause issues have been taken out of circulation and are no longer replicating. They should be destroyed by the immune system, but the immune system has its own age-related issues and falls down on that job, leaving the senescent cells to lurk and emit harmful signaling chemicals that damage surrounding tissue.

The flip side of the coin is that less replication among cells translates to less resilient tissues and organs, and thus faster aging. As mammalian biochemistry is set up by default, you can either be generating lots of fresh cells with a higher cancer risk, or aging faster due to poor tissue maintenance, but with a lower cancer risk. Biotechnology will let us escape from this Hobson's choice in due course - a method for tweaking the system associated with another cancer suppression gene to generate both less cancer and slower aging has been demonstrated in mice, for example. More and better technologies will emerge in human medicine in the fullness of time.

In particular, rather than focusing on metabolic tinkering to incrementally improve matters, the better approaches would be to (a) repair the ability of the immune system to eliminate senescent cells at a youthful level, and (b) develop therapies to regularly completely sweep senescent cells from the body. The effects of reducing senescent cell numbers in rats were sufficiently good that more work will be devoted to that sort of strategy in the future - and a good thing too.

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

The underlying infrastructural methods and technologies for working with stem cells are consistently improving - which lowers cost, thus allowing more research and development to take place. Here is an example: "researchers have proven that a special surface, free of biological contaminants, allows adult-derived stem cells to thrive and transform into multiple cell types. Their success brings stem cell therapies another step closer. An embryo's cells really can be anything they want to be when they grow up: organs, nerves, skin, bone, any type of human cell. Adult-derived 'induced' stem cells can do this and better. Because the source cells can come from the patient, they are perfectly compatible for medical treatments. ... We turn back the clock, in a way. We're taking a specialized adult cell and genetically reprogramming it, so it behaves like a more primitive cell. ... Before stem cells can be used to make repairs in the body, they must be grown and directed into becoming the desired cell type. Researchers typically use surfaces of animal cells and proteins for stem cell habitats, but these gels are expensive to make, and batches vary depending on the individual animal. ... human cells are often grown over mouse cells, but they can go a little native, beginning to produce some mouse proteins that may invite an attack by a patient's immune system. ... [A] polymer gel created by [researchers] in 2010 avoids these problems because researchers are able to control all of the gel's ingredients and how they combine. ... [Researchers] had shown that these surfaces could grow embryonic stem cells, [but] the polymer surface can also support the growth of the more medically promising induced stem cells, keeping them in their high-potential state. To prove that the cells could transform into different types, the team turned them into fat, cartilage and bone cells. They then tested whether these cells could help the body to make repairs. Specifically, they attempted to repair five-millimeter holes in the skulls of mice. The weak immune systems of the mice didn't attack the human bone cells, allowing the cells to help fill in the hole. After eight weeks, the mice that had received the bone cells had 4.2 times as much new bone, as well as the beginnings of marrow cavities. The team could prove that the extra bone growth came from the added cells because it was human bone."

Link: http://www.eurekalert.org/pub_releases/2012-05/uom-sse052312.php

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

Changes in the stem cell niche are a good part of the age-related decline in stem cell activity, which explains why old stem cells can perform like young stem cells if put into a young environment, and vice versa. Here researchers compensate for one of those niche changes: "Stem cells reside within a microenvironment of other cells - the niche - that is known to play a role in stem cell function. For example, after a tissue is injured, the niche signals to stem cells to form new tissue. It is believed that stem cells and their niche send signals to each other to help maintain their potency over a lifetime. But while the loss of tissue and organ function during aging has been attributed to decreases in stem cell function, it has been unclear how this decline occurs. [There are] a number of possible scenarios, such as whether the loss of tissue function is due to a decrease in the number of stem cells, to the inability of stem cells to respond to signals from their niche, or to reduced signaling from the niche. ... researchers discovered that as the stem cell niche [in flies] ages, the cells produce a microRNA (a molecule that plays a negative role in the production of proteins from RNA) known as let-7. This microRNA is known to exist in a number of species, including humans, and helps time events that occur during development. This increase in let-7 leads to a domino effect that flips a switch on aging by influencing a protein known as Imp, whose function is to protect another molecule, Upd, which is secreted from a key area of the niche. In short, Upd promotes the signaling that keeps stem cells active and in contact with the niche so that they can self-renew. And as aging advances, increasing expression of let-7 ultimately leads to lower Upd levels, decreasing the number of active stem cells in the niche. What leads to accumulation of let-7 in the niche of aged flies still remains an open question. The researchers also demonstrated they could reverse this age-related loss of stem cells by increasing expression of Imp."

Link: http://www.newswise.com/articles/researchers-find-a-way-to-delay-aging-of-stem-cells

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

Exercise already! Regular readers are no doubt sick and tired of hearing about it, but until such time as sensibly directed funding and hard work in the life sciences produce medical technologies that can do better for humans, regular exercise remains one of the two best tools we have to slow our inexorable slide into frailty and disease. It allows us to somewhat shift our life expectancy, and greatly reduce the risk of suffering all of the common chronic conditions of aging.

For those in the middle of life, looking at an ever-uncertain future of technological development, a few years added or subtracted might make all the difference in the world. When it comes down to the wire, will you make far enough to benefit from the first commercial rejuvenation biotechnologies, or will you fall short and be forced to take the second worst end of life option, with an unknown chance of eventual restoration? These are weighty questions, and burying your head in the sand is essentially the same as picking the poorest answer for yourself.

An article on this general theme from the popular press, which goes on to point out a range of data on exercise and specific age-related conditions:

"There's compelling data that older individuals participating in exercise programs show dramatic improvement in function and abilities," says Cedric Bryant, chief science officer for the American Council on Exercise in San Diego. In fact, experts suggest that many ills once attributed to normal aging are now being viewed as a result of chronic inactivity.

Despite this promising message, fewer than 5 percent of seniors follow the recommended guidelines for physical fitness (30 minutes of moderately intense exercise on most days). "Levels of activity in people 65 and older haven't budged in decades," says Miriam Nelson, director of the John Hancock Research Center on Physical Activity, Nutrition, and Obesity Prevention at Tufts University in Medford, Mass.

Even if they've never exercised, the middle-aged and older can still benefit by beginning now. Experts say sedentary people will actually fare better in percentage gains relative to active people, since they're starting from zero. "It doesn't matter how old you are," says Colin Milner, founder and CEO of the International Council on Active Aging in Vancouver, British Columbia. "It's never too late to start exercising."

As a specific example of the sort of low-level mechanisms by which exercise impacts long-term health, you might look at this paper:

A decline in mitochondrial biogenesis and mitochondrial protein quality control in skeletal muscle is a common finding in aging, but exercise training has been suggested as a possible cure. In this report, we tested the hypothesis that moderate intensity exercise training could prevent the age-associated deterioration in mitochondrial biogenesis in the gastrocnemius muscle of Wistar rats.

Exercise training, consisting of treadmill running at 60% of the initial VO2max, reversed or attenuated significant age-associated (detrimental) declines in mitochondrial mass ... Exercise training also decreased the gap between young and old animals in other measured parameters ... We conclude that exercise training can help minimize detrimental skeletal muscle aging deficits by improving mitochondrial protein quality control and biogenesis.

Mitochondrial damage - and thus processes such as autophagy that attempt to reduce levels of mitochondrial damage - seems to be very important in aging. Given that many mechanisms associated with longevity are seen to influence autophagy, it should not be surprising to find exercise on that list.

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

Researchers are working on creating regeneration in mammals where it does not normally happen: "Researchers have long tried to get the optic nerve to regenerate when injured, with some success, but no one has been able to demonstrate recovery of vision. A team [now] reports a three-pronged intervention that not only got optic nerve fibers to grow the full length of the visual pathway (from retina to the visual areas of the brain), but also restored some basic elements of vision in live mice. ... [the mice were able to] regain some depth perception, the ability to detect overall movement of the visual field, and perceive light. ... Previous studies [have] demonstrated that optic nerve fibers can regenerate some distance through the optic nerve, but this is the first study to show that these fibers can be made to grow long enough to go from eye to brain, that they are wrapped in the conducting 'insulation' known as myelin, that they can navigate to the proper visual centers in the brain, and that they make connections (synapses) with other neurons, allowing visual circuits to re-form. ... [Researchers] combined three methods of activating the growth state of neurons in the retina, known as retinal ganglion cells: stimulating a growth-promoting compound called oncomodulin, [elevating] levels of cyclic adenosine monophosphate (cAMP) and deleting the gene that encodes the enzyme PTEN. ... these interventions have a synergistic effect on growth of optic nerve fibers. ... The eye turns out to be a feasible place to do gene therapy. The viruses used to introduce various genes into nerve cells mostly remain in the eye. Retinal ganglion cells are easily targetable."

Link: http://medicalxpress.com/news/2012-05-scientists-regenerate-optic-nerve-components.html

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

Ongoing work in regenerative medicine: "scientists have succeeded in taking skin cells from heart failure patients and reprogramming them to transform into healthy, new heart muscle cells that are capable of integrating with existing heart tissue. The research [opens] up the prospect of treating heart failure patients with their own, human-induced pluripotent stem cells (hiPSCs) to repair their damaged hearts. As the reprogrammed cells would be derived from the patients themselves, this could avoid the problem of the patients' immune systems rejecting the cells as 'foreign'. ... Recent advances in stem cell biology and tissue engineering have enabled researchers to consider ways of restoring and repairing damaged heart muscle with new cells, but a major problem has been the lack of good sources of human heart muscle cells and the problem of rejection by the immune system. Recent studies have shown that it is possible to derive hiPSCs from young and healthy people and that these are capable of transforming into heart cells. However, it has not been shown that hiPSCs could be obtained from elderly and diseased patients. In addition, until now researchers have not been able to show that heart cells created from hiPSCs could integrate with existing heart tissue. [Researchers] took skin cells from two male heart failure patients (aged 51 and 61) and reprogrammed them by delivering three genes or 'transcription factors' ... Crucially, this reprogramming cocktail did not include a transcription factor called c-Myc, which has been used for creating stem cells but which is a known cancer-causing gene. ... The resulting hiPSCs were able to differentiate to become heart muscle cells (cardiomyocytes) just as effectively as hiPSCs that had been developed from healthy, young volunteers who acted as controls for this study. Then the researchers were able to make the cardiomyocytes develop into heart muscle tissue, which they cultured together with pre-existing cardiac tissue. Within 24-48 hours the tissues were beating together. ... The tissue was behaving like a tiny microscopic cardiac tissue comprised of approximately 1000 cells in each beating area. ... Finally, the new tissue was transplanted into healthy rat hearts and the researchers found that the grafted tissue started to establish connections with the cells in the host tissue."

Link: http://www.eurekalert.org/pub_releases/2012-05/esoc-stp052112.php

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

Michael Rae has written a long post at the SENS Foundation on the topic of the recently published Spanish study that produced life extension in mice through a telomerase gene therapy. He has been following this line of research closely for some years, and has been critical of the results reported in the past. The post is well worth reading for a better view of both the chronology and the limitations of the work that led to this latest result.

Tale of Telomerase: Lessons and Limits in a Late-Life Launch

The connection between telomeres, telomerase, and cellular and organismal "aging" was a matter of significant scientific interest but little public awareness until the early 1990s, when Dr. Michael West founded Geron Corporation. In the process of launching that venture, and in the following years, West succeeded in embedding a controversial thesis deeply into the public imagination: that the (re)activation of telomerase in somatic cells could retard or even reverse the degenerative aging process. There were always problems with this thesis, and with public (mis)understandings of it, but its sheer simplicity and public prominence has in direct and indirect ways advanced scientific research that has answered many of the questions that thesis forced upon the scientific community, and opened up important new avenues for research in telomre biology and in biomedical gerontology.

The most direct and important fruits of that expansion of research into telomerase have been studies on the pharmacological and transgenic activation of telomerase in the tissues of aging mice. Several such reports have appeared over the years, each hailed prematurely as evidence of the life- and health-extending power of the enzyme. The most important of these studies have been a series of experiments by María Blasco, PhD, SENS Foundation Research Advisory Board member and Director of the Molecular Oncology Programme at Spain's National Cancer Research Centre (CNIO). A tantalizing new report in this series has just appeared -- but to understand it in context, we will first review those that led up to it.

You should read the whole thing; it is very educational, and a good illustration of the way in which there are no sudden breakthroughs in science - just sudden attention paid to steadily ongoing progress. Each new advance rests upon decades of past work and the efforts of a range of other research groups. It also illustrates the need to look past the headlines to pick at the details of heralded research. For example:

several caveats must be noted about the results themselves, and their implications for medical therapies against the degenerative aging process in humans. As in the previous studies, the apparent increases in survival in this new report were, in fact, ambiguous. The study was substantially underpowered to detect a true increase in maximal lifespan; and even taking the results at face value, the reported survival data - even for treated animals - were, once again, well within the range typical for well-husbanded, untreated control mice reported in other studies.

...

Additionally, there was relatively little effort invested in ruling out a possible effect of Calorie restriction (CR) in this study.

...

Presuming, however, that the life- and healthspan benefits reported in this study should be taken at face value, the ultimate question is their human translatability - and there are reasons to be skeptical that a similar therapy could be safely used to retard the degenerative aging process in humans. Some would note first that safe and effective gene therapy is not yet available for our species - but that, like many other matters in biomedical gerontology, is only a matter of time and investment. Of greater concern is the safety of telomerase therapy, granted the very different body plans of humans as compared to mice.

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