There are three days left - until September 1st - in which to vote and comment on the submitted Amex Members Projects to determine the top 25 that will move on to the next stage. The combination of votes and public interest will ultimately determine how American Express awards $2.5 million in philanthropic funding. From the website:

We're inviting you to come together to share ideas for projects that could make a difference in the world. Then it's up to you to support, and ultimately vote on, which projects get $2.5 million in funding from American Express.

As you no doubt know, the Methuselah Foundation volunteers have a well-formed longevity science proposal in the running:

Create a program that utilizes college undergraduates to perform research in a variety of scientific venues surrounding fighting age related diseases such as Alzheimer’s, Parkinson’s, Heart Disease and Cancer and overall extension of healthy human life. Hiring researchers is exceedingly expensive. By outsourcing projects to undergraduate students, laboratory use and labor costs are negligible, and the students receive college credit for their work.

...

People who believe that one day they will peacefully die in their sleep are living in ignorance. The vast majority of age related deaths are a slow, painful, and degrading process over many years of later life. Watching my beloved grandmother die as a result of an age related disease and seeing our adored family friend fall prey to cancer has inspired me to learn more about death and aging pathology, and more importantly, to do something about it.

This is a well-planned project, sized to the funds available. With the backing of the Methuselah Foundation, already very involved in organizing undergraduate and graduate research volunteers, it would do well if victorious. As the vote counts ramp up in the final days of selecting the top 25 projects, it's up to us to help keep longevity science in the spotlight. It is by far the most discussed project, but it needs more votes. Tell your friends!

You don't have to be an Amex cardholder, but you do have to be a US resident in order to register and vote. Some instructions via the Methuselah Foundation blog:

1. Go to this website: http://www.membersproject.com/

2.a. If you are not an Amex Card Member: Click on "Guest Members Log In" in the upper right corner of the screen. Then click on "Guest Members Sign Up Here" at the bottom of the next screen.

2.b. If you are an Amex Card Member: Click on "Cardmembers Log In" on the right side of the screen. If you don't already have an online login click on "Create a Log In" in the next screen.

3. Complete the Registration Form which will give you your Login ID.

4. Once you are logged in on the home page, you can either a) Enter 'Undergrads Fighting Age Related Disease' in the Search box or b) click on 'Health' then 'Diseases and Disorders' at the bottom right of the home page, and scroll down to 'Undergrads Fighting Age Related Disease'. Alternately, here is a direct link to the project page:

http://www.membersproject.com/project/view/BVVE2C

5. Click on the project and then click on the 'Nominate this Project' button. Then click on 'Post Your Comments' at the bottom of the screen to have your say, as discussion board activity counts towards the nomination of the top 25 projects.

Opportunities to take a few minutes to step in and help secure funds for research don't come along every day for most of us. Take advantage here and know that you made a difference!

Posted by Reason at 8:09 PM
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The latest issue of Rejuvenation Research (volume 11, number 4) is available online. As usual, the contributions come from a broad range of fields in the life sciences applicable to extending healthy life span and repairing the damage of aging. Here are a couple of examples that focus on the nuts and bolts of pushing aging cells to perform greater feats of regeneration:

Aging, Stem Cells, and Mammalian Target of Rapamycin: A Prospect of Pharmacologic Rejuvenation of Aging Stem Cells

What is the relationship between stem cell aging and organismal aging? Does stem cell aging cause organismal aging or vice versa? Will stem cell aging aggravate age-related diseases? And what is stem cell aging?

As suggested herein, hyperstimulation of signal transduction pathways can render cells compensatorily irresponsive. And the hallmark of stem cell aging is poor responsiveness to activating stimuli. On the basis of the hypothesis that insensitivity to stimuli is in part due to hyperactivation of the target of rapamycin (TOR), this article suggests a means of pharmacologic rejuvenation of stem cells and wound-healing cells.

This is a useful way of looking at the issue of aging stem cells. I'm not sold on the specific details - the focus on TOR - but the general strategy of exploration and experimentation with stem cell response sounds good. If the cells are still good to go, a great deal of good might be accomplished with some comparatively simple targeted manipulations.

By way of an aside, you might recall that TOR is associated with the biomechanisms of calorie restriction, but then it's one of the pathways associated with everything of importance in the realm of metabolism.

Host Cell Mobilization for In Situ Tissue Regeneration

The goal of the present study was to investigate whether host biologic resources and environmental conditions could be used for in situ tissue regeneration, which may eliminate the need for donor cell procurement and subsequent in vitro cell manipulation. To address this aim, we implanted a common biomaterial into mice and characterized the infiltrating cells to determine their regenerative potential.

...

the infiltrating cells are capable of differentiating into multiple cell lineages, including osteogenic, myogenic, adipogenic, and endothelial lineages, if appropriate conditions are provided. These results suggest that it is possible to recruit a predominance of cells with multilineage potential into a biomaterial scaffold. Therefore, it may be possible to enrich the infiltrate with such cell types and control their fate, provided the proper substrate-mediated signaling can be imparted into the scaffold for in situ tissue regeneration.

Which is a rather long-winded way of saying that suitably designed nanostructures and control over stem cell signaling should be able to replace first generation cell delivery therapies in many situations. In theory, medical science could move the apparatus of programming and activating stem cells entirely inside the body - no need to pull cells out for culturing and manipulation or find transplant sources. It's a promising vision.

Posted by Reason at 6:10 PM
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I consider it to be unfortunate that the bulk of the pro-longevity aging research camp is focused on an inefficient path forward that will in the end lead to lesser benefits. It is their belief that this is the only practical way ahead: a laborious slog towards complete understanding of aging and metabolism, followed by an even more complex navigation through re-engineering that metabolism to age more slowly. The sheer scale and difficulty of that task is why many scientists feel that meaningful engineered longevity - more healthy years through science - is a long way away indeed.

This true in a way: extension of healthy life will be a long time coming if metabolic manipulation is the only path taken by the research community. Fortunately, metabolic re-engineering is not the only way ahead. It's not the most efficient way ahead either. The better path is to refrain from changing the way in which our metabolic processes work. Instead we should indentify the biochemical differences between an old, damaged metabolism and a young, healthy metabolism - and then repair them, thus reversing aging.

It is likely to be easier and less costly to produce rejuvenation therapies than to produce a reliable and significant slowing of aging. A rejuvenation therapy doesn't require a whole new metabolism to be engineered, tested, and understood - it requires that we revert clearly identified changes to return to a metabolic model that we know works, as it's used by a few billion young people already. Those rejuvenation therapies will be far more effective that slowing aging in terms of additional years gained, since you can keep coming back to use them again and again. They will also help the aged, who are not helped at all by a therapy that merely slows aging.

All that said, I noticed that Pure Pedantry is commenting today on an analysis by researchers Jan Vijg and Judith Campisi. It's a view from the metabolic re-engineering camp, dug in for the long, slow haul:

All in all, this a very good review that I recommend reading in its entirety. They strike a note of cautious optimism that I think is right on: we are learning more about this field but there is no justification for irrational exuberance.

Not on that path, in any case. It's hard to be hugely overwhelmed by progress that might, maybe, do a little good for young people fifty years from now. What is needed today is a determined effort to do good for the aged people of twenty to thirty years from now.

Posted by Reason at 8:02 PM
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You might recall that it was back in 2007 I first mentioned research into links between age-related changes in mitochondria, the power plants of the cell, and telomeres, the structures at the end of your chromosomes that form a counter for cell state. Your cell is a complex, unified machine, so in many ways its not surprising to find links between portions of the clockwork that are known to be important in aging. You should wander back into the archives and refresh your memory:

Linking Telomere Shortening and Mitochondrial Damage?

We know that mitochondrial damage is tied to aging via mechanisms such as the production of damaging free radicals such as [reactive oxygen species] - and that some researchers are working on solutions, such as the ability to replace all mitochondrial DNA in the body via protofection. We also know that progessive telomere shortening is tied to aging and age-related disease, and a number of different groups are working on strategies to safely lengthen telomeres.

There is strong evidence to believe that "tied to aging" in this context means "contributes to aging as a cause." Remember that aging is no more than an accumulation of damage in biochemical systems; when we look at these changes that take place with aging, we are looking at damage. This paper offers the possibility that if we repair or prevent the progressive accumulation of mitochondrial degeneration and damage, then the telomeres will take care of themselves - if the results are replicated, of course.

More On Telomere Shortening and Mitochondrial Dysfunction

So, poorly functioning mitochondria lead to telomere shortening, and telomerase somehow improves mitochondrial function to prevent that shortening. This is in place of the more expected path of undoing ongoing telomere shortening by adding extra repeat sequences to the end of the telomeres - that being the better understood function of telomerase.

As I said back then, this cries out for more research - which seems to be taking place. A recent paper pulls the antioxidant catalase into the mix:

Telomerase deficiency promotes oxidative stress by reducing catalase activity:

We used cultured mouse embryonic fibroblasts (MEF) isolated from mice lacking telomerase activity (Terc(-/-)) to analyze the redox balance and the functional consequences promoted by telomerase deficiency.

...

6-month-old Terc(-/-) [mice] showed higher oxidant capacity, lower catalase activity, greater oxidative damage, and higher TGF-beta1 and fibronectin levels ... In summary, telomerase deficiency reduces catalase activity, determining a redox imbalance that promotes overexpression of TGF-beta1 and extracellular matrix proteins.

Back a few years, researchers demonstrated that pouring extra catalase onto the mitochondria - via a genetic mutation to target the chemical to where it was needed - extends healthy life span. Catalase soaks up some fraction of damaging free radicals before they can degrade the mitochondria that produce them, and slowing mitochondrial damage is very beneficial to health and longevity. Is catalase level the mechanism by which telomerase helps out the mitochondria? Stay tuned: the more we know, the easier it will be to develop repair technologies that can set things back to the way they were when we were young.

Posted by Reason at 8:30 PM
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As you might recall, one reason that the immune system declines with age relates to its capacity of cell types. An aged immune system is clogged with useless memory cells, leaving few resources for capable cells to fight new threats. The other reason is the decline of the thymus, source of immune cells:

The immune system undergoes dramatic changes with age - the thymus involutes, particularly from puberty, with the gradual loss of newly produced naive T cells resulting in a restricted T cell receptor repertoire, skewed towards memory cells. Coupled with a similar, though less dramatic age-linked decline in bone marrow function, this translates to a reduction in immune responsiveness

But what if we could regenerate the thymus, restoring it to a vigorous production of new immune cells? That could be one way of pushing out the limits, and making the accumulation of memory cells less harmful at any given age. One of the long-time Fight Aging! readers kindly pointed me to a recent article at Scientist Live on this topic:

Successfully combating illness in elderly individuals can potentially add years to a life. At the centre of this struggle lies an immune system that becomes compromised with age, subsequently leaving the body susceptible to diseases younger bodies would normally keep at bay.

Dr. Claude Perreault and a team of Canadian and Finnish scientists has identified a protein able to stimulate the production of T-cells, the white blood cells involved in the recognition and the elimination of infectious agents.

...

why does the thymus involute early in life so that it leaves older people immunodeficient. For example, thymic atrophy begins as early as one year of age. Progressive thymic involution is responsible for the fact that elderly individuals have very poor thymic function. They produce very little T-Lymphocytes and because of that they are more susceptible to infections, cancer, and autoimmune disease.

We also found that one major characteristic of the thymus found nowhere else in [the] lymphoid organs is the expression of a protein called Wnt4. We hypothesised that Wnt4 had a role in T-Lymphocyte development and that by providing high levels of Wnt4 to hematopoietic progenitor cells we would enhance [production of immune cells]. That is how it began.

We did two series of experiments. In the first set, we induced over-expression of Wnt4 in hematopoietic stem cells and found that compared to mice that received standard cells those that received cells producing high levels of Wnt4 had a bigger thymus and produced 3-4 times more T-Lymphocytes. ... when we knocked out Wnt4 there was thymic atrophy.

Overall, these studies suggest that Wnt4 is necessary for normal T-cell production and that over-expression of Wnt4 is sufficient to improve [production of immune cells]. In the future, we hope to evaluate the best way to give Wnt4 to animals or humans in order to find whether this molecule can be used to treat thymic involution.

An interesting start; I suspect we'll hear more along these lines in the years ahead.

Posted by Reason at 7:34 PM
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As you age, your mitochondria become ever more damaged and dysfunctional, a process that causes further biochemical damage throughout your body, and is in fact an important component of aging.

cells entirely populated with damaged mitochondria start churning out large quantities of free radicals - through another, more forceful mechanism - into the body at large. That's a path to age-related degeneration and fatal conditions like atherosclerosis. The free radical theory of aging is based upon the harm done to tissues, structures and processes by these damaging biochemicals.

Can ongoing mitochondrial degeneration be slowed? Well, yes - calorie restriction appears to slow down every catalogued aspect of aging, and evidence suggests that regular exercise is just about as good for everything except extending maximum species longevity. But can we do better than this for failing mitochondria via new medical technologies?

I stumbled over recent research that suggests there are comparatively simple genetic changes that will slow the rate at which your mitochondria cause the damage that leads to aging:

Mitochondrial DNA (mtDNA) is highly susceptible to injury induced by reactive oxygen species (ROS). During aging, mutations of mtDNA accumulate to induce dysfunction of the respiratory chain, resulting in the enhanced ROS production. Therefore, age-dependent memory impairment may result from oxidative stress derived from the respiratory chain.

...

Mitochondrial transcription factor A (TFAM) is now known to have roles not only in the replication of mtDNA but also its maintenance. TFAM transgenic (TG) mice exhibited a prominent amelioration of an age-dependent accumulation of lipid peroxidation products and a decline in the activities of complexes I and IV in the brain.

In the aged TG mice, deficits of the motor learning memory, the working memory, and the hippocampal long-term potentiation (LTP) were also significantly improved. The expression level of interleukin-1beta (IL-1beta) and mtDNA damages, which were predominantly found in microglia, significantly decreased in the aged TG mice.

...

an overexpression of TFAM is therefore considered to ameliorate age-dependent impairment of the brain functions through the prevention of oxidative stress and mitochondrial dysfunctions in microglia.

Doing something about the decay of mitochondrial function has a number of evident benefits, as demonstrated above. But slowing things down is a second rate strategy at best - especially if it involves genetic engineering, a technology unlikely to be in widespread use for humans for another ten to twenty years. A slowing of damage does little for those who are already damaged and aged. What we really want to be capable of achieving is reversal of existing damage - to be able to restore old and damaged mitochondria to a pristine state.

This goal is unlikely to be any more expensive or time-consuming than engineering a slowing of mitochondrial decay, so it should be the first priority. If you look back in the Fight Aging! and Longevity Meme archives, you'll find mention of a range of potential technologies at varying stages of research:

• Moving Mitochondria
• Can Damaged Mitochondria Repair Their DNA?
• Can We Build a Longevity Therapy Atop Mitoptosis?
• Eating Mitochondria
• Mitochondrial Protofection
• Xenotransplanting New Mitochondria
• MitoSENS Research at the Methuselah Foundation

Posted by Reason at 6:50 PM
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I noticed a rather interesting open access paper the other day: researchers found strong similarities in the gene expression changes with age in several types of mice. On the one hand normally aging mice, on the other hand various long-lived mice (calorie restricted, Ames dwarf mice, etc), and on the third hand progeroid mice suffering from a form of accelerated aging. Changes in gene expression represent, amongst other things, a part of the feedback loop whereby an organism responds to circumstances by changing its own cellular programming. Calorie restriction is a great example of that in action, and demonstrates that this sort of evolved metabolic reprogramming can make a real difference to health and lifespan.

In all the mice examined, the same sorts of gene expression changes were kicking in:

Contrary to expectation, we find significant, genome-wide expression associations between the progeroid and long-lived mice. Subsequent analysis of significantly over-represented biological processes revealed suppression of the endocrine and energy pathways with increased stress responses

...

we subsequently confirmed these findings on an independent aging cohort. The majority of genes showed similar expression changes.

Our tissues react to stress in the same way, whether that stress is accelerated aging, calorie restriction, or the biochemical damage of normal aging. This is a beneficial adaptation - as calorie restriction demonstrates - but it isn't enough to hold back the consequences of either accelerated aging or the accumulated damage of very late stage "normal" aging.

The angle of the researchers here is the search for biomarkers of aging and predictors of longevity. They believe that because so many different biological states cue the same responses, you must look at gene expression of the whole genome to determine whether the state is good or bad:

The correlations we found between certain groups of mice are most likely due to distinct groups of differentially expressed genes, i.e. there might be one large set of genes similarly affected in short-lived and long-lived mice and a separate large group of genes similarly affected in progeroid and naturally aged mice. This appears indeed to be the case. Nonetheless, there are also groups of genes, such as genes of the somatotropic axis that are similarly affected in accelerated, delayed and natural aging.

...

However, the [progeroid] and long-lived animals employed in this study had a biological age of ~50% and 10-15% of their lifespan respectively. Thus, these findings also indicate that a genome-wide correlation analysis may serve as a powerful tool to determine the biological age of animals and might hence allow prognosis of longevity.

Determination of biological age is indispensable for the assessment of anti-aging treatments. Although reliable biomarkers of aging are long sought after, they have yet remained elusive. To this end, single genes or limited sets of genes used as biomarkers of aging may poorly reflect a true biological age; ... In diagnostic terms, a CR treatment might [induce] a similar age-related biomarker [as] treatment with a DNA damaging agent does.

We, therefore, propose the facilitation of comprehensive genome-wide correlation analyses to evaluate pro- and anti-aging effects of treatments aimed at health-span extension.

Posted by Reason at 6:45 PM
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Following on from my last post on the attitudes of pro-longevity bioethicists, here's an open-access piece by Tom Koch. It opens with these questions:

Why has longevity become a source of dismay rather than a cause for celebration? How did we turn the greatest triumph of 20th century public health and medicine into a problem for the 21st century?

This is the view from inside the paradigm of state-regulated, state-controlled medicine. Centralized systems of privilege, cut loose from price signals, inevitably devolve to rationing and crumble beneath increased demand. That increased demand is feared even when it is a great good, such as medical technology. This state of affairs stands in stark opposition to the free market, in which increased demand is a sign of great success - it is the opportunity to create progress through trade, research, and competition. A monolithic system crumbles under growth, while the competitive market thrives. Looking back at the SAGE Crossroads podcasts on (political) economics and engineered longevity, we have this:

Again I say if this were a privatized system, we would all say "gee it’s wonderful. All these people want more health care, this industry is thriving". Let me put one other analogy. Suppose we made cars a government entitlement. Instead of cheering when auto production went up, we’d say, "Oh my God, we can’t afford this!". How you finance it may greatly affect the psychology and actually the freedom of the economy to take advantage of these new opportunities.

Koch concludes in his article:

much of what we think of as geriatric [medicine] is in fact medicine for fragile persons. Geriatric expertise in the maintenance of people with multiple conditions can serve the critically ill of every age.

Blaming people who are over the age of 65 for the rising costs of our publicly funded health care systems permits us to focus on one class of patients. In truth, health care is expensive at every age and not something to be begrudged anyone because of age. The alternative is that we should all die young, at the first hint of illness, or figure out how to live healthily and forever.

If we lived in a world in which government had nothing to do with the provision of medicine, there would be no begrudging, no need for battles over centrally planned resource assignment, no rationing by fiat of the uncaring and distant. There would instead be a ferociously competitive marketplace, responsive to needs, and there would be generous medical charity for the unfortunate; we would do very well by that. It is a great pity that we stand very far indeed from such an ideal.

Posted by Reason at 8:30 PM
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It seems I somehow missed a rather good interview with biomedical gerontologist Aubrey de Grey that was published at Betterhumans earlier this month. There are some good questions in there, touching on areas the average interviewer skips over. For example:

BH: [The Strategies for Engineered Negligible Senescence, or SENS] describes a whole battery of medical treatments that could theoretically defeat the aging process. These treatments range from relatively simple ones like injecting people with enzymes that can break down tough wastes inside of cells, to highly advanced ones like genetically altering trillions of somatic cells in full grown adults. Considering the differential technical challenges, what SENS therapies will most likely become available first, and which will be developed last?

AdG: Some of them are already pretty close: probably the closest is in fact not the enzyme therapy you mention, but the use of vaccines to eliminate extracellular aggregates (especially amyloid). But when we consider the others, actually I wouldn't like to make the call, because the hardest ones are the ones that the Methuselah Foundation and I are prioritising in terms of the early research. In other words, we're hoping that they will start to catch up with the easier ones. I suspect that the challenge of genetically modifying a high proportion of cells by somatic gene therapy will have been largely solved before we complete the development of all the genes that we want to introduce.

...

BH: At one point in your book, you criticize the Food and Drug Administration’s (FDA) drawn-out medical approval process and suggest that drugs should instead be approved after completion of Phase 2 trials. Why do you want such a change, and won’t it lead to more deaths thanks to unsafe drugs and medical procedures becoming available?

AdG: I want this change because it will save more lives than it costs. This question has been carefully analysed by experts and it’s clear that we are vastly over-cautious now in approving drugs. That over-caution is not the fault of the FDA or the government, because it reflects public attitudes: every death from an unsafe medical treatment causes an outcry and a lot of legal action, whereas we turn a blind eye to death from the unavailability of good drugs. But when aging is recognised as defeatable, public opinion will become more rational in this regard, and so will public policy.

It's a long piece - there's much more to read though, so head on over and do just that.

Posted by Reason at 7:31 PM
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The writing of Collin Farrelly is a reasonable median point in the range of views amongst bioethicists in favor of engineering far greater human longevity through medical science. Arthur Caplan might be another good median example.

Personally, I'm not fond of bioethics as a field - its members all too often serve as no more than useful mouthpieces for those who work to suppress freedom of research and development. There will always be demagogues and popular opinion-mongers, but that arena would much more constructive in the absence of empowered bureaucrats and political appointees who delight in shackling a ball and chain to progress. As things stand, modern bioethics all has the air of supplicants to majesties, of begging for scraps and the simple freedom to make progress.

If unelected, unaccountable, uncaring government employees didn't have the power to control the future of your access to medical technology, you could cheerfully ignore bioethicists as another bunch of crazies - men and women busy overthinking the issue of common sense - if you so decided. The world would be a better place for that freedom.

In any case, take a look at this piece that references the Longevity Dividend Initiative:

Given that many people see longevity science itself as unethical, it is not surprising that proposals to invest greater funding into tackling aging, rather than research on specific diseases, will likely be met with strong opposition and protests that this is unfair. For the latter proposal implicates the allocation of scarce resources, and thus it raises complex questions of distributive justice. Is it fair, the critic will ask, to divert resources dedicated to saving lives (e.g. with possible treatments for cancer, AD, etc.) to medical research that seeks to merely extend lives? Let us call this the Fairness Objection to prioritizing aging research.

In this paper I will examine, and critique, this Fairness Objection to making aging research a greater priority than it currently is. The Fairness Objection presumes that support for the Longevity Dividend is limited to a simplistic utilitarian justification. Utilitarians invoke a mode of justification that is, at base, aggregative. Thus the critics of utilitarianism charge that it is a moral theory that maintains that imposing high costs on a few could be justified by the fact that this confers benefits on others, no matter how small these benefits may be as long as the recipients are sufficiently numerous.

On the other hand, given that the course of one's life is a private matter, how about we all just get on with supporting, advocating, fundraising, and conducting longevity research as we see fit? Unfortunately, that delightful thing called government allows naysayers to grab the reins of power and interfere in every private endeavor. Plurity of choice is crushed beneath the battle over control. It is a despicable state of affairs, and I don't see how playing within the system - according any legitimacy to those who would use force to remake your every private choice - will make things better in the long term.

Posted by Reason at 7:12 PM
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Increased understanding and control of the immune system will be just as important to enhanced human health and longevity as advances in stem cell science. The decline of the immune system with age has many detrimental effects, some direct, some indirect. But with greater control our immune systems - even just a little more control than we presently have - many of these age-related problems can be done away with. An immune system that remains efficient and active for many more years will bring increased healthy longevity.

One measure of progress in immune system engineering is the degree to which inroads are made in repairing autoimmune diseases. This is a direct application of new knowledge, run through the existing medical regulatory system. One less subtle approach presently in the works involves destroying and recreating the entire immune system to remove the configuration issue at the root of the disease - it seems to work. A wide variety of other research and development is taking place, such as this recent example:

Hope for arthritis vaccine 'cure':

A single injection of modified cells could halt the advance of rheumatoid arthritis, [one] of a family of "autoimmune" diseases, in which the body's defence systems launch attacks on its own tissues.

...

The precise trigger for these attacks is not known, but the latest technique, so far tested only on cells in the laboratory, aims to "reset" the immune system back to its pre-disease state.

A sample of the body's white blood cells is taken and treated with a cocktail of steroids and vitamins which transforms a particular type of immune cell called a dendritic cell into a "tolerant" state. These cells are then injected back into the joint of the patient.

Professor John Isaacs, who is leading the research, said: "Based on previous laboratory research we would expect that this will specifically suppress or down regulate the auto-immune response."

Just as with stem cell science, a great breadth of work in immunological engineering produces a body of knowledge and research community that can be turned to the repair of aging in years ahead. If today researchers are attempting to repair broken immune systems, tomorrow they will be adding new immune system capabilities - such as a resistance to poor configurations brought on by aging, enhanced cancer and senescent cell destruction, or removing certain damaging biochemicals that build up with age.

The immune systems of the future will be a merging of the natural and the engineered, and will be extremely efficient and long-lasting compared to our present version. Keep an eye on present day immunological research, as it is one of the foundations of tomorrow's enhanced longevity.

Posted by Reason at 8:04 PM
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How do you determine a person's age from a biomedical perspective? Not how many years they have amassed, but to what degree has the body aged relative to some median measure. This is an important question in aging research and longevity engineering - if you have no measurable metric for age, then you can't know whether or not a supposed rejuvenation medicine is working, never mind how well it is working. So a great deal of time and energy has been devoted to establishing biomarkers of aging, and you'll find some discussion on this topic back in the Fight Aging! archives:

How can you rapidly determine that you have successfully developed an anti-aging technology that works in humans if you cannot tell how advanced the aging process is in any given individual, or if you cannot even agree on a working scientific definition for aging? Obviously you can wait around to count years and deaths, but that reliable fallback is not a good approach for those of us who would like to see working healthy life extension medicine in our lifetimes.

As I mentioned back then, I think that damage repair approaches to rejuvenation science - i.e. identify and then revert biochemical changes - sidestep some of these concerns. An array of specific identified biochemical changes (such as the forms of biochemical damage listed in the Strategies for Engineered Negligible Senesence) becomes the metric for aging, and you attempt to fix or revert every change you can identify until you can prove that any specific change is benign.

In any case, we are revisiting this topic today because the most recent batch of podcasts at SAGE Crossroads discuss biomarkers of aging. Head on over and take a look.

#44 - Biomarkers of Aging - Setting the stage: What are biomarkers of aging?

a biomarker is a way to measure a parameter in a biological system or subject. All of us have in our minds how old we are. We use it as we use a clock to count the passage of time. Over a human life, we measure the passage as months, years, decades and so on, but for medical purposes, if we are going to try to develop interventions that modify the rate of aging in individuals, first we have to find a way to validate measuring aging separate from chronological age. We know that not all 50 year olds are the same. The same for all 60 years olds or 80 years olds or any other age. People vary despite their same chronological age, so we have to have measures that get at how old a person really is biologically and how to measure that, and that’s how biomarkers come in.

#45 - Biomarkers of Aging - What came out of the National Institute of Aging's biology of aging program?

it was a 10 year effort to try to find biological markers of aging that are different than chronological markers of aging. ... what we did was to create a very large colony of a variety of mice, inbred mice and inbred rats, as a source for studies looking for biomarkers of aging. ... All together of a 10 year span we had, if I reme