FIGHT AGING! NEWSLETTER
October 15th 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!
- Thoughts on Optimizing Health
- Longevity Science and Moral Imperatives
- Where to Find Data on Aging Research?
- Latest Headlines from Fight Aging!
- Comparing Longevity and Damage Resistance in Bivalves
- Considering Longevity in Terms of Damage Versus Damage Repair
- Treating Neurodegeneration by Increasing Neural Plasticity
- Working Thyroid Cells Created From Stem Cells
- Complications in Developing Drugs to Slow Aging
- Commentary on FGF Signaling and Stem Cell Aging
- Converting Supporting Brain Cells into New Neurons
- Lung Health and Brain Function
- An Example of Present Stem Cell Therapy Trials
- The Glenn Foundation Funds Another New Aging Research Lab
THOUGHTS ON OPTIMIZING HEALTH
With regard to personal health, a great deal of time and energy is spent in pursuit of what is probably an unobtainable goal, while ignoring paths that are likely to produce real benefits:
"So the future of medicine is golden, biotechnology is in the throes of a vast expansion of capabilities and free-fall in costs, and we have a good idea as to how to go about reversing aging - if the research community would just stop tinkering with efforts to merely slow down aging and get on with achieving the all-round better goal of rejuvenation. We should all donate money and time to help out, because it's not as though we can take it with us and irreplaceable time is ticking away. A shot at lifespans of centuries and longer is coming, with not so much time left in which to reach for that goal.
Putting all of that to one side for the moment, there is the arguably less important question of how to optimize heath and life span given the present poor tools to hand. Many people spend a great deal of time talking and debating on this topic, immersing themselves in the world of what presently exists, and giving little thought to what might lie ahead. A vast industry caters to people who think they've found the better mousetrap when it comes to personal health and aging. They're all wrong, of course, but that doesn't stop the flow of commerce.
"The sad truth of the matter is that it's simple and easy to achieve the 80/20 result in health and longevity within the bounds of the tools we have available to us today, provided you're starting out as a basically ordinary, healthy individual. Exercise regularly, the 30 minutes daily of aerobic exercise that has been recommended by physicians since way back when, and practice calorie restriction with optimal nutrition - i.e. eat a sane diet, not very much of it, and obtain the necessary levels of micronutrients while doing so. There's also the matter of not harming yourself greatly, but just as I shouldn't have to mention avoidance of knives and falling rocks, I shouldn't have to mention things like giving up smoking.
"These things are not rocket science. They are widely known and most have been advocated for centuries. The supporting statistical data is far better now than at any point in the past, and so you have no excuses: if you're not adopting these practices then it is because you have decided to accept a shorter life expectancy and greater odds of ill health in exchange for the dissipations that you presently enjoy. No-one's perfect, right?
"But here is an interesting thing about trying to reliably forge ahead beyond the 80/20 point in personal health, in search of the optimum level of improvement: it's next to impossible to go further or reliably measure that you have gone further. The research community has expended billions without being able to determine how you can do that - so what makes you think that you can do any better given your far more limited resources? Metabolism and its interactions are so very, very complex. We can list with some confidence what is good for you, but talking about what is optimal is far beyond present capabilities.
"Instead of trying to go further in a presently impossible attempt at optimization, a better use of that time and energy lies in supporting research and development of rejuvenation biotechnology. Even a magically optimized personal health program would not allow most people to live to 100 with today's technology - the only way that the vast majority of us will get to see a three digit birthday cake is through progress in longevity science and its clinical applications. So if you're going to spend any effort on this whole living longer in good health thing, spend it wisely. Don't chase rainbows."
LONGEVITY SCIENCE AND MORAL IMPERATIVES
A range of different arguments and philosophies can be turned to support the idea that we are morally obliged to develop the means to defeat aging through biotechnology. Here you'll find links to the start of a discussion based on social justice and egalitarianism, noteworthy because adherents of those philosophies are usually opposed to the development of life-extending medicine:
"The concepts and ideology relating to egalitarianism and social justice are associated with advocates and a community largely hostile to engineered human longevity. To the lay egalitarian extending healthy life looks like more inequality in the making, so they oppose longevity science for the same reasons they oppose every new idea that they believe might benefit the wealthy first of all: death for everyone before inequality for anyone is, depressingly, pretty much exactly where they stand. You can see manifestations of this line of thought in resource allocations and rationing forced on some regions by centralized planning in medicine - such as the "fair innings" argument in the UK, used to justify moving resources away from medical provision to the old.
"To be clear, in that sort of situation it is the centrally planned, command and control Soviet-style institutions of clinical medicine that are the problems - rationing and fierce arguments over who should feed from the trough are only symptoms. These are outgrowths of the other line item that walks hand in hand with egalitarianism: the urge to power. Egalitarian ideals cannot be enacted without the power to force people to do what they would not otherwise have done: along this road lies socialism, fascism, communism. Any flavor of authoritarianism in medicine, as in all other human endeavors, inevitably destroys in the incentives for progress, good service, and quality that exist in a market. It doesn't matter how good the original intentions were, the end result is never in doubt; only how long it takes to destroy the wealth and progress that previously existed.
"In any case, opposition to human life extension based on an assumption that it will create greater inequality is not uncommon. Egalitarians age, suffer, and die just like the rest of us, however, and we are now entering an era in which the research community might develop biotechnologies to reverse aging. Egalitarians thus have a strong incentive to either selectively abandon their convictions or find a way to advocate for work on rejuvenation biotechnology within their philosophies."
WHERE TO FIND DATA ON AGING RESEARCH?
A few pointers can be found in this Fight Aging! post, of interest to those chasing down historical data on the aging research community:
"I was recently asked for pointers on where to look for historical data on aging and longevity research: the number of active biogerontologists, a count of laboratories dedicated to aging research, levels of public and private funding, and other measures that might be taken as proxies for progress (or at least growth in the field). Unfortunately I don't have anything more than the first sketches of a guide to hand: assembling this sort of data for any industry is a fair-sized task. There are plenty of questions without ready answers, especially when it comes to the for-profit side of aging research, where the participants don't tend to publish easily discovered summaries.
"Some obvious starting points exist, however. The International Aging Research Portfolio (IARP), for example, is an initiative that aims to make data on aging research easily available. The present focus there is on funding, but that data can be broken down by laboratory, region, researcher, and date. There are some trend tools to help produce visualizations."
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!
LATEST HEADLINES FROM FIGHT AGING!
COMPARING LONGEVITY AND DAMAGE RESISTANCE IN BIVALVES
Friday, October 12, 2012
Much like mammals, bivalve molluscs exhibit a very wide range of life spans. At the known outer end stands the arctic quahog at more than four centuries, and much studied in recent years so as to understand the roots of its longevity. That research project is still ongoing, as are similar comparative studies of aging and longevity in a range of other species. Here, researchers compare resistance to various forms of physical stress and damage in different bivalve species. As you might expect from the view of aging put forward earlier today, longer-lived species are more resistant to most forms of damage: "Bivalve molluscs are newly discovered models of successful aging. Here, we test the hypothesis that extremely long-lived bivalves are not uniquely resistant to oxidative stressors (eg, tert-butyl hydroperoxide, as demonstrated in previous studies) but exhibit a multistress resistance phenotype. We contrasted resistance (in terms of organismal mortality) to genotoxic stresses (including topoisomerase inhibitors, agents that cross-link DNA or impair genomic integrity through DNA alkylation or methylation) and to mitochondrial oxidative stressors in three bivalve mollusc species with dramatically differing life spans: Arctica islandica (ocean quahog), Mercenaria mercenaria (northern quahog), and the Atlantic bay scallop, Argopecten irradians irradians (maximum species life spans: more than 500, more than 100, and ~2 years, respectively). With all stressors, the short-lived A i irradians were significantly less resistant than the two longer lived species. Arctica islandica were consistently more resistant than M mercenaria to mortality induced by oxidative stressors as well as DNA methylating agent nitrogen mustard and the DNA alkylating agent methyl methanesulfonate. The same trend was not observed for genotoxic agents that act through cross-linking DNA. In contrast, M mercenaria tended to be more resistant to epirubicin and genotoxic stressors, which cause DNA damage by inhibiting topoisomerases. To our knowledge, this is the first study comparing resistance to genotoxic stressors in bivalve mollusc species with disparate longevities. In line with previous studies of comparative stress resistance and longevity, our data extends, at least in part, the evidence for the hypothesis that an association exists between longevity and a general resistance to multiplex stressors, not solely oxidative stress." In mammals, you might look to the naked mole rat as an analogous species: very resistant to all sorts of biological and cellular damage, and extremely long-lived in comparison to similar sized rodent species.
CONSIDERING LONGEVITY IN TERMS OF DAMAGE VERSUS DAMAGE REPAIR
Friday, October 12, 2012
Here is a framework for thinking about aging and longevity: various forms of low-level biological damage accrue as a result of the operation of metabolism, degrading organs and tissues and ultimately causing death. Where natural selection favors longer-lived individuals, mechanisms will evolve to repair, minimize, or resist the effects of this damage. So aging is driven by damage, but genetic programs interact with that damage, evolved to try to do something about it. Thus we could expect to be able to manipulate life span either by repairing damage or by altering the programs. The former approach should produce far more effective means of healthy life extension, however, including rejuvenation of the old. In comparison, and from what we've seen so far in longevity science, modestly slowing aging is about the best we can expect from the near future of genetic and metabolic alterations. "In spite of exciting new insights into regulatory mechanisms that modulate the aging process, the proximal cause of aging remains one of the unsolved big problems in biology. An evolutionary analysis of aging provides a helpful theoretical framework by establishing boundary conditions on possible mechanisms of aging. The fundamental insight is that the force of natural selection diminishes with age. This does not preclude senescence (age-related decrease in individual fitness) from occurring in natural populations. Senescence can develop because some genes have non-separable, but typically different or opposite, functions in reproductive-age and in old individuals. Such genes, selected according to their "youthful" function, may thus impose a distinct senescent phenotype in old age. In general, however, unless a controversial formulation of group selection is invoked, traits that would become manifest only in old age cannot evolve. This precludes the evolutionary emergence of aging programs, which have been sometimes postulated to exist in analogy to developmental and other biological programs. (By the same token, selective pressure that diminishes with age would also prevent extreme longevity from evolving, if "extreme" denotes a potential life span much longer than that imposed by extrinsic mortality in a given environment.) This and other arguments against the existence of an aging program have been discussed previously. The evolutionary perspective sketched out above does not specify the mechanisms that underlie aging, but it helps to narrow down the possibilities. As already discussed, an evolved deterministic aging program can be ruled out, perhaps with the exception of specific niche situations. In the absence of adaptive life-curtailing processes driven by a putative aging program, we are left with untargeted pro-aging, destabilizing phenomena which, in principle, may range from purely stochastic to side-effects of "legitimate" biochemical pathways. These destabilizing forces are counteracted by evolved, and genetically controlled, longevity assurance (or repair/maintenance) processes. The interplay of these countervailing forces determines the life span. While I have previously presented my detailed interpretation of this model, its central tenets bear repeating: (a) the destabilizing processes that drive aging are neither evolved nor adaptive; (b) in contrast, longevity assurance mechanisms are under genetic control; (c) together, these two opposing forces determine life span; (d) the average life span of a species is set by evolving longevity assurance mechanisms so as to optimize reproductive success under environmental conditions typical for that species."
TREATING NEURODEGENERATION BY INCREASING NEURAL PLASTICITY
Thursday, October 11, 2012
One line of research into treatments for neurodegenerative disorders involves spurring the brain to establish new neural connections to replace those that have been damaged or lost. This seems like an inferior strategy in comparison to trying to identify and remove root causes, one that can only delay the inevitable, but it's nonetheless a fairly entrenched field of work. Here is an example of this sort of research - and note that as for other similar efforts there are hints that an induced increase in neural plasticity would be beneficial for cognitive function in all older individuals: "Researchers have developed a new drug candidate that dramatically improves the cognitive function of rats with Alzheimer's-like mental impairment. Their compound, which is intended to repair brain damage that has already occurred [by] rebuilding connections between nerve cells. [The scientists] have been working on their compound since 1992, when they started looking at the impact of the peptide angiotensin IV on the hippocampus, a brain region involved in spatial learning and short-term memory. ... angiotensin IV, or early drug candidates based on it, were capable of reversing learning deficits seen in many models of dementia. The practical utility of these early drug candidates, however, was severely limited because they were very quickly broken down by the body and couldn't get across the blood-brain barrier. Five years ago, [the scientists] designed a smaller version of the molecule [called] Dihexa. Not only is it stable but it can cross the blood-brain barrier. An added bonus is it can move from the gut into the blood, so it can be taken in pill form. The researchers tested the drug on several dozen rats treated with scopolamine, a chemical that interferes with a neurotransmitter critical to learning and memory. Typically, a rat treated with scopolamine will never learn the location of a submerged platform in a water tank, orienting with cues outside the tank. After receiving the [drug], however, all of the rats did, whether they received the drug directly in the brain, orally, or through an injection. [The researchers] also reported similar but less dramatic results in a smaller group of old rats. In this study the old rats, which often have difficulty with the task, performed like young rats. While the results were statistically valid, additional studies with larger test groups will be necessary to fully confirm the finding."
WORKING THYROID CELLS CREATED FROM STEM CELLS
Thursday, October 11, 2012
Nature here notes progress towards tissue engineering of replacement thyroid glands and a demonstration of the ability to repair the thyroid in situ: "The thyroid is the latest in a growing list of body parts that can now be 'fixed' in mice, with the potential to treat diseases from diabetes to Parkinson's ... Progress has been very rapid over the past decade. In recent years we've seen a number of very important studies in which mouse stem cells have been converted to a desired cell type that has then been shown to be functional in vivo, and to confer benefits in mouse models of human diseases. [Researchers] first genetically engineered embryonic stem cells to express two proteins - NKX2-1 and PAX8 - that are expressed together only in the thyroid. When these cells were grown in Petri dishes in the presence of thyroid-stimulating hormone, they turned into thyroid cells. Thyroid cells, however, have to be organized into a particular three-dimensional shape before they can work. They need to form small, spherical follicles containing a cavity in which iodide - a component of some hormones produced in the thyroid gland - can be concentrated before being absorbed and used for hormone synthesis. Remarkably, the stem-cell-derived thyroid cells spontaneously grouped into follicles similar to those in an intact thyroid gland [and] the follicles were able to trap iodide and synthesize thyroid hormones. The next step was to see how these follicles would function in live mice, and to assess their potential to correct hypothyroidism. This condition was induced in mice with an injection of radioactive iodine that accumulated in their thyroid glands, causing the tissue to wither away. Four weeks later, once hypothyroidism had been established, the mice received a graft of stem-cell-derived thyroid follicles. Out of nine mice treated in this way, eight showed complete rescue - their thyroid hormones returned to normal levels."
COMPLICATIONS IN DEVELOPING DRUGS TO SLOW AGING
Wednesday, October 10, 2012
Trying to safely slow down aging, usually by developing drugs to replicate some of the metabolic and epigenetic alterations caused by calorie restriction or exercise, is an immensely complicated undertaking. Success will be slow in coming, and the end result will be of little use for those already old - so other than an increase in the understanding of how metabolism and aging relate to one another, we should not expect this field of research to contribute much to the bottom line of our own longevity. Nonetheless, this is the mainstream of research into longevity science and where most of the money goes. That state of affairs will have to change in favor of a focus on the more practical path of repairing biochemical damage associated with aging, with the aim of creating biotechnologies that can reverse the root causes of aging and thus bring about some degree of rejuvenation. Here is an example of the sort of complications that arise when attempting to adjust metabolism. Interventions that are beneficial at one point in life may be harmful at others, and may further interact poorly with one another to produce a net harmful effect even though they are individually beneficial: "We tested the effects of a Class I histone deacetylase inhibitor (HDAcI) (sodium butyrate, NaBu) on the longevity of normal- and long-lived strains of Drosophila melanogaster. We report that this HDAcI has mixed effects in the normal-lived Ra strain in that it decreases mortality rates and increases longevity when administered in the transition or senescent spans, but decreases longevity when administered over the health span only or over the entire adult lifespan. It has dose-dependent effects when administered over the entire larval+adult life span. Only deleterious effects are noted when administered by either method to the long-lived La strain. This apparently contradictory set of results is, however, what would be expected if the gene regulatory mechanisms affected by NaBu were those intimately involved in inducing gene expression patterns characteristic of a healthy senescence. Thus "mid- to late-life" drugs may have different stage-specific effects on different genomes of a model organism. A different HDAcI (suberoylanilide hydroxamic acid, SAHA) administered to the normal-lived strain showed similar late-life extending effects, suggesting that this is not an isolated effect of one drug."
COMMENTARY ON FGF SIGNALING AND STEM CELL AGING
Wednesday, October 10, 2012
You'll recall that researchers recently demonstrated that they could slow or reverse stem cell decline with age by manipulating FGF2 - in the satellite cell population that maintains muscle tissue, at least. Based on their work, the researchers proposed that stem cell aging involves issues with dormancy and recuperation. Because of certain changes in signaling in the supporting stem cell niche, stem cell populations in old muscles are not able to remain dormant sufficiently well to maintain their numbers and functionality. Here is a commentary on this research, placing it into the context of other ongoing investigations into the causes of stem cell decline with aging and consequent loss of tissue integrity: "Gradual declines in tissue homeostasis, function, and regenerative ability are hallmarks of the aging process. Tissue-specific adult stem cells are the primary components of tissue regeneration and homeostasis. Therefore, an attractive theory to explain the age-associated decline in these processes centres around the effects of aging on stem cell function. The current debate focuses on the very nature of how stem cells age. Is the decline in stem cell function with age a cell autonomous change that happens due to the cumulative detrimental effects of DNA damage, epigenetic changes, or metabolic and mechanical stresses over time? Or is it an environmentally induced process whereby a perfectly functional stem cell is instructed to behave in a dysfunction manner by an aging niche or systemic milieu? A recent [study] proposes a unique mechanism whereby a signal from the aged niche causes a cell autonomous and persistent change in the ability of a stem cell to maintain the quiescent state, which, over time, leads into impaired tissue regenerative capacity. ... aged satellite cells display an increased propensity to [leave quiescence, enter] the cell cycle and to undergo apoptotic cell death. ... What is particularly intriguing about environmental theories of stem cell aging is that they imply that the functional changes that occur in stem cells as they age are potentially reversible when the cells are placed in a 'young' environment. This report also touches on another issue that is commonly debated: the role of stem cell number in the effects of aging on tissue function and regeneration. The reported effects of aging on stem cell number vary widely across different stem cell populations but also within the satellite cell literature. [The authors here] report reduced satellite cell numbers in aged animals and attribute that decline to the functional changes they describe: [increases] in cycling and cell death. They propose that functional changes of aged satellite cells, which have previously been shown to impair muscle regeneration, are further exacerbated by declining stem cell numbers. It will be interesting to determine if the maintenance of stem cell number can overcome their functional deficits to prevent an age-related decline in regenerative potential. "
CONVERTING SUPPORTING BRAIN CELLS INTO NEW NEURONS
Tuesday, October 9, 2012
Spurring the brain to produce new neurons more rapidly than it ordinarily does may be a useful form of therapy for a range of conditions - and also quite possibly something you'd want turned on as a matter of course, if it manifests the same sort of benefits to cognitive health as are produced by drugs that induce greater neural plasticity. Here, researchers note an alternative to manipulating stem cell populations into building new neurons - instead work to convert some of the supporting cells in the brain into neurons: ""This work aims at converting cells that are present throughout the brain but themselves are not nerve cells into neurons. The ultimate goal we have in mind is that this may one day enable us to induce such conversion within the brain itself and thus provide a novel strategy for repairing the injured or diseased brain." The cells that made the leap from one identity to another are known as pericytes. Those cells, found in close association with the blood vessels, are important for keeping the blood-brain barrier intact and have been shown to participate in wound healing in other parts of the body. ... Further testing showed that those newly converted neurons could produce electrical signals and reach out to other neurons, providing evidence that the converted cells could integrate into neural networks. "While much needs to be learnt about adapting a direct neuronal reprogramming strategy to meaningful repair in vivo, our data provide strong support for the notion that neuronal reprogramming of cells of pericytic origin within the damaged brain may become a viable approach to replace degenerated neurons.""
LUNG HEALTH AND BRAIN FUNCTION
Tuesday, October 9, 2012
There is a fair amount of research linking general health with the pace at which brain function declines with age: the less robust you are, the more likely you are to get dementia. We can look at the structural integrity and level of age-related decline in blood vessels in the brain as one possible mechanism to link such things as exercise and fitness to brain health, but there are undoubtedly others. Here researchers look at links between lung health and brain function. Lung health, at least in the way it was measured in this study, may be a good marker for the sort of general robustness that both allows for and is improved by exercise: "Researchers used data from a Swedish study of aging that tracked participants' health measures for almost two decades. An analysis of the data with statistical models designed to show the patterns of change over time determined that reduced pulmonary function can lead to cognitive losses, but problems with cognition do not affect lung health. The study sample consisted of 832 participants between ages 50 and 85 who were assessed in up to seven waves of testing across 19 years as part of the Swedish Adoption/Twin Study of Aging. ... Lung function was measured in two ways: forced expiratory volume, or how much air a person can push out of the lungs in one second, and forced vital capacity, the volume of air that is blown out after a deep inhalation. "The logical conclusion from this is that anything you could do to maintain lung function should be of benefit to fluid cognitive performance as well. Maintaining an exercise routine and stopping smoking would be two primary methods. Nutritional factors and minimizing environmental exposure to pollutants also come into play." Though this study does not explain what a loss of pulmonary function does to the brain, the researchers speculated that reduced lung health could lower the availability of oxygen in the blood that could in turn affect chemicals that transmit signals between brain cells."
AN EXAMPLE OF PRESENT STEM CELL THERAPY TRIALS
Monday, October 8, 2012
The range of stem cell therapies now moving from the lab to the clinic - via the slow, expensive, and largely unnecessary regulatory process of clinical trials - are a long way advanced from the state of the art even as recently as a decade ago. Use of a patient's own cells, engineered and manipulated to improve the chances of a successful outcome, is the new standard. As I've noted in the past, the stem cell research community must solve the issue of age-related decline in stem cell function in order to build effective therapies, as most of the medical conditions that need this sort of regenerative treatment only occur in the old: "Canadian heart-attack survivors will get first crack at an experimental therapy that's moving into clinical trials early next year. The treatment is believed to be the first in the world to test the ability of a patient's own stem cells, genetically engineered to have extra-strong healing powers, to repair damaged tissue caused by a heart attack. To date, more than 2,000 heart-attack survivors, mostly in Europe, have received experimental injections of stem cells, often ones taken from their own bone marrow. However, the overall degree of improvement in the patients' heart function has been disappointingly modest. That has led some researchers to think the stem-cell system itself might age and lose its effectiveness in older people. To solve this problem, [researchers have] come up with a way to turn back the biological clock of aging stem cells by genetically reprogramming them to have stronger healing properties. The theory is that these younger, more potent stem cells could grow enough new blood vessels to improve, if not fully restore, the heart's ability to pump blood. In fact, previous studies have suggested that stem-cell therapy can still improve a patient's quality of life even if the overall improvement to heart function is incremental. "There's less development of heart failure, less hospital readmission, less bypass (surgery) and better survival. The data suggest you don't need to fully normalize. You just need to stabilize to such a degree that you're unlikely to go down that slippery slope.""
THE GLENN FOUNDATION FUNDS ANOTHER NEW AGING RESEARCH LAB
Monday, October 8, 2012
In recent years the Glenn Foundation for Medical Research has established a number of laboratories focused on aging research, building and funding an infrastructure to help grow and sustain this scientific community. The Foundation has donated modestly to SENS research to reverse aging in the past, but these laboratories are firmly in the mainstream of biogerontology. The researchers involved typically investigate mechanisms of aging and ways to slow aging only - this being the slow, hard road ahead that will never lead to methods of rejuvenation. Here is news of the latest: "Under a new $3 million grant from the Glenn Foundation for Medical Research, Princeton University researchers will study the biology of aging and healthspan. The grant will establish the Paul F. Glenn Laboratories for Aging Research at Princeton under the leadership of Coleen Murphy, associate professor of molecular biology and the Lewis-Sigler Institute for Integrative Genomics. The funding will support pioneering collaborative work by faculty members in neuroscience, computer science, computational biology, physics and mathematics on the biological mechanisms that control the aging process. "While great progress has been made in the identification of general longevity regulators, most aging research is focused on late-life physical or biochemical characteristics, such as loss of movement or death," said Murphy, whose cutting-edge research on age-related declines in memory and reproductive ability has received support from several important sources. "Early aging has not been as well studied. I believe that careful quantification of behavioral characteristics will allow us to better analyze these early declines as well as to assess therapeutic improvements.""