Reminder: Aging 2008 on June 27th at UCLA

By way of a reminder, the Aging 2008 symposium will be held later this month, on June 27th at UCLA, Los Angeles. It's a free event for the public, organized by the Methuselah Foundation, and attended by many of the movers and shakers in aging science and advocacy for longevity research: Applying the new technologies of regenerative and genetic medicine, the engineering approach to aging promises to dramatically extend healthy human life within the next few decades. How do you and your loved ones stand to benefit from the coming biomedical revolution? Are you prepared? Is society prepared? At Aging 2008 you will engage with top scientists and advocates as they present their findings and advice, and learn what you can do to help accelerate progress towards a cure for the disease and suffering of aging. The symposium leads into the Understanding Aging scientific conference, an extension of the Strategies for Engineered Negligible Senescence conference series of past years. These events are a necessary part of establishing a research community sufficiently large and well-organized to make significant progress in longevity science. We'll be seeing more of this sort of thing in the years ahead: connections made, minds changed, notes swapped,...

Friday Science: Aging, Stem Cells and Stem Cell Niches

I notice that two good review papers on the topic of stem cells, stem cell niches and aging are presently freely available in the latest Aging Cell. Journal publishers tend to put out these free full text promotions for a limited time, so take a look while the looking is there. Stem Cell Review Series: Aging of the skeletal muscle stem cell niche Declining stem cell function during aging contributes to impaired tissue function. Muscle-specific stem cells ('satellite cells') are responsible for generating new muscle in response to injury in the adult. However, aged muscle displays a significant reduction in regenerative abilities and an increased susceptibility to age-related pathologies. This review describes components of the satellite cell niche and addresses how age-related changes in these components impinge on satellite cell function. You can find more about satellite cells and the aging stem cell niche back in the Fight Aging! archives as well. Just follow those links. Stem Cell Review Series: Regulating highly potent stem cells in aging: environmental influences on plasticity Significant advances in the past decade have revealed that a large number of highly plastic stem cells are maintained in humans through adulthood and are present even in older...

Legitimacy and Funding for the Fight to End Aging

A timely piece in Wired today: Gandhi once said, describing his critics, "First they ignore you, then they laugh at you, then they fight you, then you win." After declaring, essentially out of nowhere, that he had a program to end the disease of aging, renegade biogerontologist Aubrey de Grey knows how the first three steps of Gandhi's progression feel. Now he's focused on the fourth. "I've been at Gandhi stage three for maybe a couple of years," de Grey said. "If you're trying to make waves, certainly in science, there's a lot of people who are going to have insufficient vision to bother to understand what you're trying to say." This weekend, his organization, The Methuselah Foundation, is sponsoring its first U.S. conference on the emerging interdisciplinary field that de Grey has helped kick start. (Its first day, Friday, will be free and open to the public.) The conference, Aging: The Disease - The Cure - The Implications, held at UCLA, is an indication of how far de Grey has come in mainstreaming his ideas. The Methuselah Foundation's research is beginning to produce results: In research that will first be presented on Friday at the conference, Methuselah-funded scientists will...

Graying Hair and Fading Stem Cells

Hair loses its color with age due to a decline in activity of melanocyte pigment-producing cells, likely another symptom of the general fading of stem cell populations throughout the body. A recent paper adds evidence for that view: Hair graying is one of the prototypical signs of human aging, but its mechanism is largely unknown. To elucidate the mechanism of hair graying, we investigated gene expression related to melanogenesis in human hair. The key molecules in melanogenesis, microphthalmia-associated transcription factor-M (MITF-M), Sox10, Pax3, tyrosine related protein-1 (TRP-1), and tyrosinase, were absent or greatly reduced in the bulbs of white hair compared to black hair. Melanocyte stem cells (MSCs) or melanocytes express markers for neural crest cells, Sox10, Pax3, and MITF-M. Taken together, our data suggest that hair graying is caused by defective migration of MSCs into the bulb area of hair. Setting any given group of aging stem cells back to work by introducing appropriate biochemical signals - or cloning many more stem cells to reintroduce into the body - are very plausible projects for the decade ahead. Either could greatly improve the immediate situation, and the second strategy has already been demonstrated in heart therapies. I can envisage cloning...

Calorie Restriction and DNA Damage

We know that calorie restriction slows the accumulation of nuclear DNA damage - possibly by enhancing DNA repair mechanisms - just as it slows more or less every other age-related change of interest that scientists have investigated. The degree to which ongoing random damage to nuclear DNA contributes to degenerative aging is debated, however: A paper by Aubrey de Grey outlines his view of nuclear DNA damage and aging: "Since Szilard's seminal 1959 article, the role of accumulating nuclear DNA (nDNA) damage - whether as mutations, i.e. changes to sequence, or as epimutations, i.e. adventitious but persistent alterations to methylation and other decorations of nDNA and histones - has been widely touted as likely to contribute substantially to the aging process throughout the animal kingdom. Such damage certainly accumulates with age and is central to one of the most prevalent age-related causes of death in mammals, namely cancer. However, its role in contributing to the rates of other aspects of aging is less clear. Here I argue that, in animals prone to cancer, evolutionary pressure to postpone cancer will drive the fidelity of nDNA maintenance and repair to a level greatly exceeding that needed to prevent nDNA damage from reaching...

The Methuselah Gene, Examined

The methuselah gene in fruit flies, which when expressed gives rise to the methuselah cell receptor (or mth), has been known for a decade now. It is one of a small number of single gene manipulations which can meaningfully extend longevity in this species - by 35% in this case. When it comes to figuring out what's going on under the hood, even single gene manipulations in small creatures are terribly, enormously complex. This is one of the many truths that leads those researchers who focus on genetic and metabolic engineering to say that any significant extension of human life span through these methods is far in the future. It's a huge, huge undertaking, from our present position, to consider engineering any form of significant change to the way in which our metabolism works. (Which is why I support far less complex and more certain approaches aimed at repairing the metabolism we have. The mountain of metabolic complexity is there, climb it if you must, but to get to the valley of enhanced longevity on the other side in good time, then use the level road of damage repair strategies that winds around the mountain's base). You should take a...

500 Scientists

The rough estimate of resources required to develop - for mice - the medical capabilities called for by the Strategies for Engineered Negligible Senescence (SENS) is presently $1 billion over ten years, give or take. Each of these [six lines of research] would require total funding in the range of $2m to $15m per year, spread over at least three and sometimes ~15 research teams. These teams will typically be working in a university or other research setting. [The lines of research] span six of the seven types of "damage" that Dr. de Grey has identified as the key intermediates in aging; the one not listed here is cell loss, whose rectification by stem cell and growth factor therapies is the subject of sufficient existing work worldwide. That's for the whole spectrum of longevity therapies: engineering the body to make cancer impossible; replacing lost cells; ensuring mitochondrial DNA damage can no longer cause issues; destroying unwanted cells that cause damage; breaking down crosslinks and amyloid that gum up biochemistry; removing hard-to-degrade biochemicals in old cells. Given all that, you should be able to rejuvenate aged mice, and extend their healthy lives considerably. Then it's onto moving the technology to work...

The Things You Can Change

You have a great deal of control over the course of your future health: how healthy you're likely to be, and how long you're likely to live. The unexpected always happens, but you can greatly influence the odds. Your actions over the years can move your life span across decades, just through simple lifestyle choices and good health practices, and even without the expected advances in medicine that lie ahead. An illustration: A Finnish study of identical twins has found that physical inactivity and acquired obesity can impair expression of the genes which help the cells produce energy. The findings suggest that lifestyle, more than heredity, contributes to insulin resistance in people who are obese. Insulin resistance increases the chance of developing diabetes and heart disease. And more: Here's some very good news: your genes are not your destiny. Earlier this week, my colleagues and I published the first study showing that improved nutrition, stress management techniques, walking, and psychosocial support actually changed the expression of over 500 genes. Taking up exercise and a sane diet rapidly changes the way your body operates at the cellular level, and for the better. The body is a complex machine of regulated processes,...

Calorie Restriction Protects Against Age-Related Muscle Loss

You have to look hard in the scientific literature to find evidence of any age-related changes made worse by the practice of calorie restriction - the only one that springs to mind right now is that progression of ALS is likely to be worsened. The much more common story is that detrimental change is resisted or attenuated: immune system aging, stem cell decline, heart aging, DNA damage, loss of health, loss of vitality, increase in risk of age-related disease ... all slowed by simply eating less while still obtaining optimal levels of nutrients. Almost everything studied by reserchers to date shows strong evidence of being made better through calorie restriction as a lifestyle choice. Now we can add sarcopenia, age-related muscle loss, to this long list. That is counterintuitive - eating more leading to losing more muscle mass over the years - but then what is straightforward and simple in biology? Here's the abstract at PubMed: Sarcopenia, the loss of muscle mass with normal aging, devastates quality of life - and related healthcare expenditures are enormous. The prevention or attenuation of sarcopenia would be an important medical advance. Dietary restriction (DR) is the only dietary intervention that consistently extends median...

Ageless Animals, the Sea Urchin Edition

Many species of animal age very slowly, and some so slowly that researchers have not yet been able to pin down either a rate of aging or a life span absent predation and accident. Some of those species might not age at all, but we'll have to wait for researchers to establish whether or not this is the case. Take the lobster, for example. Despite all the eating and farming that takes place, there's less funding for basic research into lobster biology than you might expect. As a consequence: To date, there is no proven method to determine the exact age of a lobster. ... as best scientists can tell, lobsters age so gracefully they show no measurable signs of aging: no loss of appetite, no change in metabolism, no loss of reproductive urge or ability, no decline in strength or health. Lobsters, when they die, seem to die from external causes. They get fished by humans, eaten by seals, wasted by parasites, but they don't seem to die from within. Of course, no one really knows how the average lobster dies. There are no definitive studies. Turning to another common sea creature, species of sea urchin appear to be...

Aging

There's nothing wrong with becoming old, but everything wrong with aging. Old means experienced, invested, wealthier, time-tested and just all-round better for having been around the block. Aging, on the other hand, is the direct result of biochemical damage you picked up along the way - ongoing deterioration that is a side-effect of being alive. The passage of years brings a constant flow of opportunities for growth and self-improvement, until aging takes away your ability to compete, your ability to take care of yourself, and eventually your life. Someone should look into that. If you're not one to think much about medical research, you might be under the impression that aging is fairly mysterious, a primal and inevitably metered process quite separate from the diseases of old age. In fact that's not the case. Aging is exactly and precisely the root cause of those diseases of old age, and scientists have a good understanding of what aging actually is, once you get under the hood and start looking at cells and the cellular environment: Loss of important cells without replacement over the years Accumulation of damaged, malfunctioning and senescent cells Free radical damage resulting from damaged mitochondrial DNA Accumulation of...

More On Telomere Shortening and Mitochondrial Dysfunction

You might recall that researchers have put forward evidence to suggest that telomere shortening is caused by accumulated damage to mitochondrial DNA - essentially collapsing two areas of intense interest for gerontologists down to one root cause, if confirmed. Back then, I said: We know that mitochondrial damage is tied to aging via mechanisms such as the production of damaging free radicals such as ROS - 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 progressive 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...

Aging as a Challenge For Regenerative Medicine

Regenerative medicine holds great - albeit not unlimited - promise for extending healthy life by replacing age-damaged tissue, and ultimately replacing age-damaged organs. However, as for everything involving our biology, the path forward is not as simple as it might appear. Repairing the damage of aging by simply replacing tissue - even assuming you've repaired any age-related damage in the stem cells taken from the patient to use in therapy - runs into the interconnected nature of the body's systems: Tissue engineering for a new heart, plus the necessary understanding to repair any damage in your stem cells? One problem you quickly run into in this sort of thought experiment is that everything of importance is influenced by everything else. New cells will be damaged by the old intracellular environment, as well as by the actions of old cells next door. An age-damaged immune system can't protect rejuvenated cells in a new heart. And so on; I'm sure you could list many more important connections that will trip you up if you replace only one component of the aging body. This is a challenge for the near future of regenerative medicine - also known as cell therapy in its present...

Horizons For Immunotherapy

I'm given to note that progress in targeted therapies - in particular those that use nanoparticles like dendrimers to string together homing mechanisms with cell destruction payloads - is very important. All sorts of cells need killing as we get older, to prevent the damage they cause: cancer cells, senescent cells, and so forth. Targeted nanoparticle therapies will soon provide a broad and extensible technology platform to get that job done, for any cell whose biochemistry we know how to distinguish, thus lightening the load of age-related damage in our bodies. When you stop to think about it, we already have a flexible, targeted cell destruction therapy roaming our bodies from day one: it's called the immune system. Immune cells are very much more sophisticated than the dendrimers being built in laboratories today, and are capable of destroying much more than just errant cells. Any biochemical that can be broken down within a cell is fair game, not just those biochemicals that make up our cells. Looking ahead, we can see three paths: The path of nanoparticles, nanoscale targeting devices and payloads to destroy the specific cells The path of manipulating our immune system into destroying targeted cells and cleaning...

Complicating WILT

Whole-body Interdiction of Lengthening of Telomeres (WILT) is the Strategies for Engineered Negligible Senescence (SENS) answer to cancer, filed under the OncoSENS project category. Get to the root of it all, and yank that root out: This is a very ambitious but potentially far more comprehensive and long-term approach to combating cancer than anything currently available or in development. It is based on the one inescapable vulnerability that all cancer cells share in common: their absolute need to renew their telomeres, the long stretches of gibberish DNA that cap their chromosomes. Telomeres fulfil a role that is similar to that of the nibs on the tips of your shoelaces, keeping the DNA from becoming frayed and unravelled. Each time a cell reproduces, the telomeres become a little worn down, and when a cell runs out of telomeres it quickly self-destructs. Because cancer cells reproduce at a furious pace, they quickly reach the ends of their telomeric "ropes," and need to find a way to exploit the cell’s natural machinery for renewing telomeres (telomerase and [alternative lengthening of telomeres, or ALT]) to restore normal telomere length, or their growth will come to an end. The thorough elimination of these genes from...

What are the best anti aging products?

When it comes to the best anti aging products, the key is to understand what helps reverse the aging process in the first place. There are several factors, and by combining them in your daily life you will get the most out of your body and experiences. The Best Anti Aging Products - What you Need to Reverse TimeAntioxidants - Antioxidants are really important, but also really over-marketed. You don't need goji juice for $30 per bottle. You need to eat lots of raw fruits and vegetables every day (about 8-12 servings). I like to make a green shake with a bunch of different things like kale, spinach, red pepper, and so on to get a big chunk of that. Enzymes - Enzymes are the catalysts for building and repairing. They only come from raw food, or enzyme supplements. I suggest the former as it is cheaper to eat raw food. Minerals - Minerals restore tissues and help you repair damage lost from work, exercise or infections. There are many great mineral supplements out there, but I would suggest going to swansonvitamins.com and looking for the Albion brand. So there you have it - the best best anti aging products out there!

Is Lifecell Face Cream Worth the Money?

The manufacturers of Lifecell face cream claim that it eliminates the need for Botox or other extreme cosmetic procedures. Lifecell face cream is also alleged to prevent future ageing. If these claims are accurate, then the price of $189 is justified. However, does Lifecell face cream do everything the manufacturers say it does? There are many Lifecell reviews on the Internet. The most honest review I found was on a site called beautyproductscompared.com. This review pointed out the good and bad aspects of Lifecell face cream, which contains the active ingredients Nitric Oxide and Idebenone. What is good about Lifecell face cream? The active ingredients will expand the capillaries and augment healthy blood circulation to the skin as well as protecting it from the damaging effects of free radicals. Lifecell has a legitimate website and the manufacturers offer a thirty-day money back guarantee. What is bad about Lifecell face cream? Beauty Products Compared could not find any standardized control tests. Nor could they discover a comprehensive list of ingredients. Lifecell face cream is very expensive and no free trial sample is available. None of the celebrity endorsements for this product have been proven and the active ingredients can be found in other face creams. The folks at Beauty Products Compared conclude that more solid data is required to justify the steep price of Lifecell face cream.