Fight Aging! Newsletter, August 8th 2016

Fight Aging! provides a weekly digest of news and commentary for thousands of subscribers interested in the latest longevity science: progress towards the medical control of aging in order to prevent age-related frailty, suffering, and disease, as well as improvements in the present understanding of what works and what doesn't work when it comes to extending healthy life. Expect to see summaries of recent advances in medical research, news from the scientific community, advocacy and fundraising initiatives to help speed work on the repair and reversal of aging, links to online resources, and much more.

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  • The Next Five Years will be a Critical Time for the Development of Rejuvenation Biotechnology after the SENS Model of Damage Repair
  • An Effort to Obtain More Human Data on Plasma Transfusion from Young to Old
  • The Utility of a Request for Startups in Rejuvenation Research and Development
  • Removing Senescent Cells from the Lungs of Old Mice Improves Pulmonary Function and Reduces Age-Related Loss of Tissue Elasticity
  • The SENS Rejuvenation Research Supporters of the German Party for Health Research to Run in Berlin State Parliament Elections
  • Latest Headlines from Fight Aging!
    • Considering Mitophagy and Cancer
    • In Search of a Foundation for Therapies to Block and Reverse Fibrosis
    • Risk of Heart Attack Continues to Fall
    • One Example Among Many Human Telomere Length Studies
    • Inducing Autophagy as the Basis for an Atherosclerosis Treatment
    • Intestinal Autophagy Important in Calorie Restriction and Longevity in Nematodes
    • Estimating the Cost of Sedentary Lifestyles
    • Quantifying the Positive Effects of Exercise versus the Detrimental Effects of Sitting
    • White Matter in the Brain is Lost More Rapidly in Overweight People
    • Contradictory Results on New Neurons and Old Memories

The Next Five Years will be a Critical Time for the Development of Rejuvenation Biotechnology after the SENS Model of Damage Repair

Tempus fugit. I'm just about old enough to remember a time in which 2020 was the distant future of science fiction novels, too far away to be thinking about in concrete terms, a foreign and fantastical land in which anything might happen. Several anythings did in fact happen, such as the internet, and the ongoing revolution in biotechnology that has transformed the laboratory world but leaks into clinics only all too slowly. Here we are, however, close enough to be making plans and figuring out what we expect to be doing when the the third decade of the 21st century gets underway. The fantastical becomes the mundane. We don't yet have regeneration of organs and limbs, or therapies to greatly extend life, but for these and many other staples of golden age science fiction, the scientific community has come close enough to be able to talk in detail about the roads to achieving these goals.

Of all the things that researchers might achieve with biotechnology in the near future, control over aging is by far the most important. Aging is the greatest cause of death and suffering in the world, and none of us are getting any younger. That may change, however. SENS, the Strategies for Engineered Negligible Senescence, is a synthesis of the scientific view of aging as an accumulation of specific forms of cell and tissue damage, pulling in a century of evidence from many diverse areas of medical science to support this conclusion. Aging happens because the normal operation of our cellular biochemistry produces damage, wear and tear at the level of molecules and molecular structures, and some of that damage accumulates to cause failure of tissues and organs, and ultimately death. That explanation for aging is coupled to the SENS portfolio of research programs that aim to repair this damage: for every type of damage, the appropriate form of repair technology can be described in great detail. The only thing remaining is to build these repair therapies and test them, to see whether or not they produce the expected result of rejuvenation and longer healthy lives.

It has taken a long time, twenty years or so, to make the treatment of aging a mainstream idea in the research community, and for the public to start to catch up. It hasn't helped that the pursuit of rejuvenation has been a realm occupied only by frauds and the delusional for millennia. It has taken many years of hard work for the evidence and the results indicating that rejuvenation can be achieved to circulate and be more widely accepted. Still, the SENS approach to aging, to head straight for damage repair and rejuvenation, and none of this messing around with drugs to try to slightly slow the pace at which damage accumulates, remains a minority vision at this time. Nonetheless, SENS researchers and advocates have made great progress on very little funding, and as a result we now near the point at which the first results will emerge from the labs into the wider world.

The next five years are critical precisely because the first few startup companies to work on the first rejuvenation therapies following the SENS model of damage repair will succeed or fail in this short span of time. The most important of these companies are probably Oisin Biotechnologies and UNITY Biotechnology, both working on senescent cell clearance. They have what looks like the best chance of success given the present state of the science, and are already well underway. Technical success does not necessarily translate to rapid clinical availability in medicine, however. You only have to look at Pentraxin Therapeutics and their work on transthyretin amyloid clearance to see that: they have been locked into a development program with GlaxoSmithKline that took six years to get to a small clinical trial, and there is no sign that this will move any faster following the success of that trial, or that it will be made available for anyone other than late stage amyloidosis patients. Clearance of transthyretin amyloid should be undergone by every human being every few years after the age of 40, given that buildup of this form of amyloid contributes to heart disease and a range of other conditions - but that development group simply isn't heading in that direction. It is one thing to catch the interest of Big Pharma, another thing entirely to make them work rapidly, or to agree with the vision of treating aging as a medical condition.

Thus there is a very large difference between (a) a world in which companies conservatively sell to Big Pharma or raise funds themselves to creep through the regulatory process to gain approval for use with a tiny number of patients in the late stages of aging, and (b) a world in which the first destination is clinical availability via medical tourism in regulatory regions where only safety must be demonstrated, and anyone can walk in and undergo treatment. Stem cell medicine would be nowhere near as far along without the decade of its widespread availability outside the US and Europe. I am very much in favor of a similar progression of availability and development for the range of potentially useful human gene therapies that will be developed in the years ahead, and for the first SENS rejuvenation technologies, such as senescent cell clearance.

Nonetheless, whether or not the outcome is much delayed availability of therapies, success in building a company based on SENS therapies is a very important step. It will in some cases, as for Oisin Biotechnologies, bring significant funding for other lines of SENS research as various advocates and the SENS Research Foundation are early investors. More importantly, success in clinical development of a treatment that meaningfully addresses easily measured metrics of aging after one set of treatments - metrics such as the epigenetic clock based on DNA methylation, or inflammation, or skin elasticity, or blood vessel elasticity, and so on - will be widely noted. That will go a long way towards opening many doors to much larger sources of funding. Either this happens soon, for the companies already under way, or they will fail, possibly damaging the view of SENS even should that failure happen for reasons unrelated to the technical aspects of the work. Failure will push back ultimate success in the medical control of aging for years, and that has an enormous cost associated with it: tens of millions of lives lost, and hundreds of millions suffering due to age-related conditions that might otherwise have been turned back. The SENS Research Foundation staff realize this well, and hence their focus on Project|21, launched earlier this year.

In short, this is an important time, and we should all put some thought into how we might best support the work on rejuvenation biotechnology that is presently taking place.

An Effort to Obtain More Human Data on Plasma Transfusion from Young to Old

Here I'll link to a recent press article on Ambrosia, a company currently working to obtain more human data on the effects of transfusing young blood plasma into old individuals. The aim is to see whether or not this can usefully change the balance of signaling molecules to, say, spur greater stem cell activity. There has been a trial in Alzheimer's patients, but some signs in animal studies that transfusions from young to old don't do much. It seems useful to speed up the process of determining whether or not transfusions are an interesting line of research, or something that only looked promising. That means more patients and larger trial populations, which Ambrosia is working on.

These transfusion initiatives are one of a number of outgrowths of parabiosis research in mice. Heterochronic parabiosis is the name given to connecting the circulatory systems of an old and a young individual. The older mouse shows a modest rejuvenation in a number of measures of aging, and the younger mouse shows some greater signs of aging - though most of the focus here has been on the old mouse. In recent years this technique has been used to search for potentially actionable differences in levels of specific signal molecules circulating in the bloodstream. For example, stem cell activity declines with aging, and this is likely governed by signaling processes. If levels of the most relevant molecules could be adjusted in old individuals, it might be possible to produce benefits that look quite similar to those of stem cell therapies: increased regeneration and tissue maintenance. This class of approach puts damaged, aged cells back to work, and does little to address causes of aging based on accumulation of metabolic waste, such as cross-links that stiffen blood vessels, but to the degree that it can improve health it is probably worthy of further investigation in the same way as stem cell therapy was back in the day.

One potential shortcut to the production of therapies is to perform transfusions: deliver young blood or young plasma to old individuals. I call this a potential shortcut because it really is still very uncertain as to (a) whether or not the whole process works in humans anywhere near as well as it works in mice, and (b) whether or not transfusions will recapture the effects of parabiosis to a useful degree. The evidence in mice suggests so far that it may not. It is possible to paint all sorts of scenarios in which the fact that old and young cells are in contact, feeding signals to one another in a feedback loop, is necessary to produce beneficial changes in the old individual. It is also possible to imagine signals with a short half-life, that won't be recaptured in transfusions, or changes in the old environment that are based on an increased level of specific signal molecules. That increased level won't be changed in the slightest by the arrival of some amount of young blood plasma. Only reduced levels are likely to be impacted that way.

In any case, testing and perhaps ruling out the fast path of transfusions seems like a fair plan. If it works, it will draw in more funding to build the better option of manipulating signal molecule levels directly. It if doesn't work, that result will direct scientists to focus on more productive lines of research and development. There is some grumbling from the expected quarters over the structuring of this present initiative by Ambrosia, but getting it done is better than not getting it done. The data will be useful in the sense that only sizable effects are interesting, and thus before and after data for participants will be convincing. Marginal effects, of the sort in which it would have been useful to have a control group to establish whether or not any benefits actually resulted, would mean that this probably isn't worth further exploration. Still, this well demonstrates the fact that many scientists who work within the heavily regulated, slow, and repressive system of medical development really don't like it when people try to get things done more rapidly and more inventively. To the extent that it closes down productive avenues, this is a dangerous attitude.

Young blood antiaging trial raises questions

It was one of most mind-bending scientific reports in 2014: Injecting old mice with the plasma portion of blood from young mice seemed to improve the elderly rodents' memory and ability to learn. Inspired by such findings, a startup company has now launched the first clinical trial in the United States to test the antiaging benefits of young blood in relatively healthy people. But there's a big caveat: It's a pay-to-participate trial, a type that has raised ethical concerns before, most recently in the stem cell field. The firm's co-founder and trial principal investigator is a 31-year-old physician named Jesse Karmazin. His company, Ambrosia in Monterey, California, plans to charge participants 8000 for lab tests and a one-time treatment with young plasma. The volunteers don't have to be sick or even particularly aged - the trial is open to anyone 35 and older. Karmazin notes that the study passed ethical review and argues that it's not that unusual to charge people to participate in clinical trials.

"There's just no clinical evidence [that the treatment will be beneficial], and you're basically abusing people's trust and the public excitement around this," says neuroscientist Tony Wyss-Coray of Stanford University in Palo Alto, California, who led the 2014 young plasma study in mice. Wyss-Coray has since started a company, Alkahest, that, with Stanford, has launched a study of young plasma in 18 people with Alzheimer's disease, evaluating its safety and monitoring whether the treatment relieves any cognitive problems or other symptoms. The company covers the participants' costs. Wyss-Coray expects results by the end of this year.

In Ambrosia's trial, 600 people age 35 and older would receive plasma from a donor under age 25, according to the description registered on, the federal website intended to track human trials and their results. Karmazin says each person will receive roughly 1.5 liters over 2 days. Before the infusions and 1 month after, their blood will be tested for more than 100 biomarkers that may vary with age, from hemoglobin level to inflammation markers. The 8000 cost will cover costs such as plasma from a blood bank, lab tests, the ethics review, insurance, and an administrative fee, Karmazin says. "It adds up fairly quickly."

The scientific design of the trial is drawing concerns as well. "I don't see how it will be in any way informative or convincing," says aging biologist Matt Kaeberlein of the University of Washington, Seattle. The participants won't necessarily be elderly, making it hard to see any effects, and there are no well-accepted biomarkers of aging in blood, he says. "If you're interested in science," Wyss-Coray adds, why doesn't such a large trial include a placebo arm? Karmazin says he can't expect people to pay knowing they may get a placebo. With physiological measurements taken before and after treatment, each person will serve as their own control, he explains. Doubts aside, Ambrosia's trial has already attracted attention from the investment company of billionaire Peter Thiel.

The Utility of a Request for Startups in Rejuvenation Research and Development

The Request for Startups (RFS) is something lately popularized by the venture incubator Y Combinator, a part of their shifting approach to the field. Having achieved sufficient growth and cultural dominance, they now have the ability to play a greater role in shaping the future, insofar as startups and the entrepreneurial community as a whole are tools to create change. To the extent that the Y Combinator principals would like to see specific changes in to world take shape over the decades ahead, they would like to help nudge that along by funding credible startups in some areas presently neglected. So they put out the RFS, a notice they they are willing to listen to pitches and are interested in funding startups in a set of specific fields or with specific focuses. The name is a play on the technical standards practice of putting forward protocol definitions in the form of Request for Comments, RFC. Standards of all sorts become known by their RFC number, and referring to RFC 1234, RFC 3456, and the like in the course of development is very common in software engineering circles.

The few SENS rejuvenation therapy startups launched and underway over the past year or two have adequately demonstrated that there is no real shortage of venture funding for our corner of the medical biotechnology field at the present time. If anything there is far more money on the sidelines waiting for an opportunity than there are SENS-relevant companies to invest in. This is partly a function of the era, in which various self-serving decisions by the powers that be have created a flood of easy money in search of returns, any returns, but more importantly it is a function of the fact that the SENS approach to treating aging is only just starting to emerge from the laboratory. SENS is all about repairing the clearly identified forms of cell and tissue damage that cause aging, which if done well enough should postpone aging indefinitely in younger adults, and at least partially rejuvenate the old. There are numerous types of damage, so while forms of senescent cell clearance are under development in various companies, items like cross-link clearance or mitochondrial DNA repair are still years out, and other problems may still be working their way through the laboratory ten to fifteen years from now.

Given the imbalance between available funding and relevant available startups, I think it would be a good plan for the SENS Research Foundation, or other parts of our community such as the Methuselah Foundation, to publish, maintain, and publicize a Request for Startups - a moderately detailed set of areas that investors in the SENS network are interested in funding. The aging research community is small and highly connected, and it can be argued that the SENS Research Foundation staff are very familiar with a large fraction of all of the research groups who might produce work leading to a startup to develop a possible SENS repair therapy. As matters progress, however, that fraction is going to become smaller. The world is a large place. As new groups focused on aspects of SENS emerge, some form of prominent banner will be useful, influencing unaffiliated researchers in the direction of considering the leap to run a startup. Further, I think that it isn't yet widely known that anyone who turns up with a credible technology and team to start for-profit clinical development of a SENS rejuvenation therapy will have no problems whatsoever in raising funds. In the non-profit laboratory world, aging researchers operate in a very resource poor environment; funding for any type of initiative is hard to come by. It is not always obvious to people immersed that culture that a wealth of funding awaits just on the other side of the conceptual wall that is crossed when moving into for-profit work. How many projects relevant to SENS exist out there, languishing for lack of funding, and where the researchers are not in contact with the SENS Research Foundation? I'd argue that we'll never know the answer to that question unless we aggressively advertise the fact that investors are interested.

It is of course frustrating to see so little interest in funding research while so much money is waiting on the sidelines for that research to reach the point of viable commercial development. It is like watching someone fail to connect the obvious two dots to improve their present situation. Changing this state of affairs is a big challenge, somewhat beyond the scope of this post: I've written on the topic in the recent past. Reforming the investment world to the point at which it is understood that investing in companies is not as effective in many situations as investing in research and then in the resulting companies that emerge from that research ... well, that is the work of a lifetime for some career advocate or leader in the venture community. Sadly all too few investors are in it to change the world, but when it comes to aging research the primary goal is exactly this: to change the world, to eliminate the suffering and death caused by aging. Life trumps money, and money is only useful for what it can do, not what it is. Investing in SENS rejuvenation research and development is one of the growing number of ways in which money can be traded for an expectation of more healthy life in the years ahead.

The recently launched SENS Project|21 is the obvious home for a rejuvenation biotechnology Request for Startups, given the pledge of 5 million in research funding and 5 million in venture investment by Michael Greve earlier this year as a starting point for the initiative. But there are a number of other places such a call to action could usefully reside. This is something for the broader community to think about as we move closer to the advent of the first treatments for the causes of aging.

Removing Senescent Cells from the Lungs of Old Mice Improves Pulmonary Function and Reduces Age-Related Loss of Tissue Elasticity

The open access paper linked below provides another reason to be optimistic about the therapies to clear senescent cells from old tissues that are presently under development. Here, the researchers created genetically engineered mice in which they could selectively trigger senescent cell death in lung tissues. In older mice, the result was improved pulmonary function, and other improvements in the state of lung tissue - turning back the clock on some of the detrimental age-related changes that take place in the lungs.

Cells become senescent in response to damage or environmental toxicity, or at the end of their replicative lifespan, or to assist in wound healing. The vast majority either destroy themselves or are destroyed by the immune system, but a few manage to linger on. Those few grow in numbers over the years, and more so once the immune system begins to decline and falter in its duties. Ever more senescent cells accumulate in tissues with advancing age, and they secrete a mix of signals that can encourage other cells to become senescent, increase inflammation, and destructively remodel nearby tissue structures. In small numbers senescent cells can help to resist cancer or assist healing, but in large numbers they contribute meaningfully to all of the symptoms and conditions of old age. They are one of the root causes of aging.

Building therapies to destroy senescent cells is the best, easiest, and most direct response. If carried out sufficiently well it would remove this contribution to the aging process entirely, and fortunately the cancer research community has been working on targeted cell destruction for many years now: the technologies exist and just need to be hammered into shape. This class of rejuvenation therapy has been advocated as a part of the SENS vision for the medical control of aging for going on fifteen years now, but only in recent years has the research community made useful progress. As for so many promising lines of research related to bringing aging under medical control, it has been next to impossible to raise funds for this work. The most critical studies in senescent cell clearance, those that proved the case beyond any reasonable doubt, were funded through philanthropy, as is often the case for work at the true cutting edge of medical science. The tipping point has come and gone now, however. At present commercial development is underway. Oisin Biotechnologies and UNITY Biotechnology are building various types of therapy to eliminate senescent cells, and I'm sure they'll be joined by other efforts as more evidence rolls in from animal studies.

Of particular interest in the research results linked here is that tissue elasticity improved. Loss of elasticity is of great importance in the aging of many parts of the body, such as skin and blood vessels. In blood vessels, for example, loss of elasticity leads to hypertension which causes cardiovascular disease and then death. It remains an open question as to which of the primary forms of cell and tissue damage are more important in this process of stiffening. If senescent cell clearance helps meaningfully for blood vessels, then we should all be very thankful, as therapies to remove senescent cells will be arriving in the clinic years in advance of rejuvenation treatments that can address other likely causes of loss of elasticity, such as persistent cross-link formation in the extracellular matrix.

The method of senescent cell elimination that the scientists employed in this study is not something that can be turned into a therapy, since it depends on creating a genetically altered lineage of mice, in which cells are primed to accept a self-destruct trigger that operates only on senescent cells. Its utility lies in the ability to remove senescent cells precisely in a given tissue, and at a given time. That precision means that researchers can be more certain that senescent cell clearance is the cause of the observed benefits. Given the growing number of ways to target senescent cells for clearance that can be turned into human therapies, it is fortunately not an issue that the experimental tests are using a more restricted approach. Removal of these cells is the important target, and any safe and effective methodology should do the job just fine.

Elimination of p19ARF-expressing cells enhances pulmonary function in mice

While there is no doubt that cellular senescence prevents cancer, an increasing amount of evidence suggests that cellular senescence is involved in other biological processes and pathologies. Cellular senescence has been shown to contribute to embryonic development, wound healing, and tissue regeneration. Additionally, it has become more evident that cellular senescence contributes to tissue aging. Senescent cells accumulate in many tissues during aging and are considered to underlie aging-associated pathologies. The contribution of senescent cells in aging-associated phenotypes may depend on signaling, such as senescence-associated secretory phenotype (SASP), because the population of senescent cells is very small, even in very old human tissue.

Two major tumor suppressor pathways, namely, the p19ARF (p14ARF in humans)/p53 and p16INK4a/Rb pathways, play critical roles in the induction and maintenance of cell cycle arrest during cellular senescence. In the present study, we established a transgenic model from which it was possible to eliminate p19ARF-expressing cells using a toxin-mediated cell knockout system. Similar to INK4a, the expression of ARF has been shown to increase during aging in the mouse. Using the transgenic model, we successfully eliminated ARF-expressing cells from the lung tissue of 12-month-old animals. The ablation of ARF expression abolished the expression of other senescent markers, including INK4a and p21, suggesting that the expression of ARF reflects the accumulation of senescent cells in tissues. The elimination of p19ARF-expressing cells in lung tissue ameliorates the aging-associated loss of tissue elasticity. Moreover, the expression of a large number of aging-associated genes was reversed after the removal of p19ARF-expressing cells. Taken together, these findings highlight the role of p19ARF in lung tissue aging and indicate that the aging phenotype in lung tissue may be reversed by eliminating p19ARF-expressing cells from tissue.

Senescent cells are known to have an effect on their surrounding "nonsenescent" cells through SASP. Our results suggest that the population of p19ARF-expressing cells was very small, even in adult lung tissue (approximately 1% of the lung mesenchymal population). Nevertheless, our microarray data indicate that these "rare" p19ARF-expressing cells strongly influence gene expression in lung tissue. Hundreds of genes are upregulated and downregulated during aging in the lung, and more than half of these aging-associated genes show p19ARF dependence. Since senescent cells induce senescence-like gene expression in their surrounding cells through SASP, it is reasonable to assume that changes in aging-associated genes in lung tissue do not simply reflect the events within p19ARF-expressing cells, but also include global changes in lung tissue cells that are mostly nonsenescent.

We performed pulmonary function tests on these mice. Static lung compliance (Cst) was significantly higher in older animals than in young animals. The treatment resulted in the marked recovery of lung elasticity (decrease in Cst). Similarly, the treatment reversed aging-associated changes in dynamic compliance, dynamic resistance, tissue elastance, and tissue damping. These results clearly indicated that the p19ARF-expressing cells that accumulated in 12-month-old lung tissue had deleterious effects on pulmonary function and that aging-associated declines in pulmonary function were ameliorated by the elimination of these p19ARF-expressing cells. We also examined the effects of ARF-expressing cell elimination on even older animals. Tumor-free female mice between 20 and 22 months old were treated 1 month. Pulmonary function tests revealed that tissue compliance in older mice was similar to that in 12-month-old mice. The treatment reduced tissue compliance in older animals; however, this effect was less than that observed in 12-month-old mice. Collectively, these results indicated that p19ARF-expressing cells provoked the loss of elastic fibers in lung tissue and were also responsible for the increase in lung compliance in aged animals.

The SENS Rejuvenation Research Supporters of the German Party for Health Research to Run in Berlin State Parliament Elections

Single issue political parties are near invisible in the US, thanks to the political duopoly that manifests as an outcome of the use of first-past-the-post election rules. In many European countries more representative voting rules allow for the existence of a much larger number of competing parties, and as a result forming a political party to advance a single issue is a entire viable way to run a long-term advocacy campaign. You only have to look at the many environmentalist Green parties, or the more recent growth of the Pirate party, or even the lasting message provided by the Official Monster Raving Loony Party of the UK to see that this can work. Attention can be captured, and a message delivered, even if no governing seats are ever won. A number of advocates for longevity science in Europe have started parties, and have for the past few years put in the hard work to make waves. Most are associated with the International Longevity Alliance, and it is the German Partei für Gesundheitsforschung, the Party for Health Research, that I'll point out today.

The Party for Health Research folk are strong supporters of the SENS rejuvenation research approach to the medical control of aging. Aging is caused by an accumulation of various forms of cell and tissue damage, and repairing that damage is the best way forward to end the frailty and disease that accompanies aging. In the past the Party for Health Research has organized activities including petitions to government to fund this branch of aging research. From the point of view of the continued growth of the movement, it is encouraging to see that these volunteers have now qualified to run in the upcoming elections to the Berlin state parliament. Every long journey consists of a series of small steps. I believe that the Party for Health Research is the first single issue longevity party to make this leap, and congratulations are due to those who put in the work to make it happen.

We reached quorum, and are admitted to the elections in Berlin!

We have collected 2314 signatures, enough to reach the quorum of 2,200 signatures and can thus stand in the election to the Berlin House in September on the ballot! Thanks to all helpers!

Election program in 2016 for election to the Berlin House of Representatives

Most people in Germany fall ill and die of old age diseases like Alzheimer's, cancer, heart attack, stroke and type 2 diabetes. Age-related diseases cause a lot of suffering and immense costs and concern each of us. Today biotechnologies enable us now to finally develop effective therapies against the full range of age-related illnesses and ailments. Age-related illnesses caused by certain developments inside and outside the cells. By repairing these changes at the molecular and cellular level it will be possible in future to cure age-related diseases. The Party for health research advocates for more research against diseases of aging, so that these therapies will be developed faster and they arrive soon enough to benefit people who are already older today. Therefore, the party sets for Health Research committed to build more research institutes in Germany, the work on this issue, and train more researchers in the relevant fields. The party will form a coalition with one or more other parties and even only address health research. In all other political issues, the party does not want to interfere. This can be handled by the coalition partners.

We want to spend an additional one percent of the state budget in the development of therapies against diseases of aging. Since all people are directly or indirectly affected by diseases of aging, all would benefit. To finance this one percent is to be subtracted from each other budgetary item. About half of these additional investments should flow in the construction and operation of new research facilities. With the other half more scientists will be trained in the relevant fields such as biochemistry and molecular biology. For the corresponding departments at the universities of Berlin are to be expanded.

I believe that as research and development of the means to control aging by repairing its causes begins to show signs of concrete progress outside the laboratory, as the first therapies start to emerge, we will see ever more of this sort of political activism in Europe. It will slowly sink in that aging is the greatest cause of death and disease, and that perhaps something can be done, and that will give rise to far greater support for this and other forms of advocacy. The Party for Health Research volunteers are now starting their campaign; there are posters on the website, and posters going up in Berlin. The one pictured below says "Cancer? Alzheimer's? Stroke? NO, THANKS! For more pharma-industry-independent research for better medicine against age-related diseases, vote for the Party For Health Research."

Latest Headlines from Fight Aging!

Considering Mitophagy and Cancer

Mitophagy is the process by which damaged or excess mitochondria in cells are destroyed, their parts recycled. Mitochondria, and in particular the level of damage in mitochondria, are important in aging. For most things that are important in aging, there is also a fair amount of evidence suggesting relevance to cancer, and mitochondria are no exception. Researchers here consider some of the known links between the modulation of mitophagy and the development of cancer, and taken as a whole the evidence suggests anything but a simple relationship. Depending on the particular context, when it comes to cancer it can be argued that either less mitophagy or more mitophagy is a bad thing. This is not the case for aging, in which greater mitophagy should always be beneficial, to the extent that it maintains lower levels of mitochondrial damage and the harms that result from that damage.

Macroautophagy, hereafter referred to as autophagy, is a highly conserved degradation process targeting large and possibly toxic structures in the cell. Mitochondria-selective autophagy (mitophagy) plays a pivotal role in the maintenance of mitochondrial homeostasis, regulating the size and quality of the mitochondrial population. In addition, mitophagy eliminates damaged mitochondria under diverse stress conditions. Healthy mitochondria are also removed when attenuation of mitochondrial function is required upon hypoxia, caloric restriction, or during certain developmental processes. Mitochondrial surveillance and quality control mechanisms, including mitophagy, decline with age and in several pathologies, causing progressive deterioration of mitochondrial function. Deregulation of mitophagy is closely linked to cancer development and progression. Thus, elucidation of the mechanisms governing mitophagy holds promise for novel anticancer interventions.

In C. elegans, inhibition of mitophagy increases mitochondrial mass, uncouples respiration from ATP production, enhances mitochondrial ROS production, and increases cytoplasmic calcium levels. These phenotypes are commonly observed in aged animals, and across large evolutionary distance. Increased ROS contribute to carcinogenesis by causing DNA damage and triggering aberrant alterations in gene expression. Therefore, in addition to the manifestation of pro-aging phenotypes, impairment of mitophagy potentially facilitates tumorigenesis. Yet cancer cells within several types of solid tumors induce autophagy and mitophagy to adjust to their microenvironment of limited nutrient and oxygen availability. In the largely hypoxic solid tumor environment, energy production shifts from oxidative phosphorylation to glycolysis, leading to increased glucose uptake and reduced oxygen consumption, a phenomenon known as the Warburg effect. Mitophagy induction has thus been proposed to be part of a hypoxia adaptation response that promotes cancer cell survival.

Notably, we found that DCT-1 upregulation under mitophagy-inducing conditions is mediated by SKN-1, the nematode homolog of mammalian Nrf2, a transcription factor that becomes activated upon oxidative stress to preserve mitochondrial homeostasis. SKN-1 also stimulates the expression of core mitochondrial components, promoting the assembly of fresh mitochondria. Our findings reveal a new layer of mitophagy regulation, which interfaces with mitochondrial biogenesis resulting in rejuvenation of the cell's mitochondrial pool. These observations highlight SKN-1/NRF2 as a new anticancer target whose activation could induce both mitophagy and mitochondrial biogenesis. This dual coordinating role may shield mitochondrial metabolism from oncogenic transformation by opposing the Warburg effect to increase healthspan. Decreased insulin signaling is an evolutionarily conserved molecular pathway that promotes longevity. We have shown that mitophagy is a significant contributor to lifespan extension under low insulin conditions. Indeed, inhibition of mitophagy shortens the lifespan of long-lived animals carrying lesions in daf-2, the gene encoding the sole insulin/IGF-1 receptor homolog in C. elegans. SKN-1 and DAF-16 underlie mitophagy induction under low insulin signaling conditions.

In summary, mitophagy is emerging as a nexus of cellular and organismal physiology. Several mitophagy promoting conditions engage distinct transcription factors that impinge on cancer-associated processes. The extent of mitophagy induction is critical for the onset and progression of carcinogenesis. Impairment of mitophagy in healthy tissues can promote tumor formation and mobility of cancer cells, whereas mitophagy induction in hypoxic solid tumors promotes adaptation and tumor cell survival. Coordination of mitochondrial biogenesis and removal could provide a new pathway to circumvent the adverse effects of mitophagy in this context. Further dissection of this pathway could unravel new potential anticancer interventions targeting tumorigenesis by promoting mitochondrial rejuvenation.

In Search of a Foundation for Therapies to Block and Reverse Fibrosis

Fibrosis is a form of inappropriate scarring, connective tissue forming where it should not inside organs, destroying the structures necessary for correct function. Fibrosis is involved in many age-related diseases, notably in liver conditions, for example. Researchers have in the last couple of years made a few initial inroads in targeting cell behavior to reduce fibrosis in some organs, but there is still comparatively little that can be done for patients suffering fibrotic conditions. Better and more universal approaches to block the mechanisms of fibrosis are needed, but as the publicity materials here indicate, the process of discovery is still in comparatively early stages.

Researchers have utilized the new software tool to evaluate the perturbation status of many signaling pathways. This new system aimed to identify robust biomarkers of fibrotic disease and develop effective targeted therapy. Fibrosis, a progressive accumulation of extracellular matrix, can occur in a wide range of organs and potentially distort their structure and function; most commonly it affects lung and hepatic tissues, causing idiopathic pulmonary fibrosis (IPF) and liver fibrosis respectively. Fibrosis accounts for up to 45% of deaths in the developed world, yet to date no effective therapeutic treatment has been developed. "Currently, there are no approved anti-fibrotic remedies and no reliable fibrotic biomarker. Our system can detect hidden fibrotic molecular signatures based on a pathway network analysis, and identify specific fibrogenic molecular changes regardless of detecting platform and tissue of origin. Despite many efforts, fibrosis is often misdiagnosed. Our system is supposed to help with proper and timely diagnostic."

With broad screening across multiple fibrotic organs, the platform identified pathogenic pathways that served as potential targets for the anti-fibrotic therapy. This approach led to a selection of the list of small molecules and natural compounds by their ability to minimize the signaling pathway difference between a fibrotic and a healthy state of the tissue. Further work with provides promising opportunities to identify conserved biological pathways that play a critical role in fibrosis development. "We have discovered previously-undetected pro-fibrotic signatures in glaucoma, based on pathway analysis. This new knowledge will allow us to cooperatively select and develop anti-fibrotic small molecule interventions to minimize or reverse this fibrotic state, and restore the tissue to normal function."

Risk of Heart Attack Continues to Fall

Among the many noteworthy achievements in modern medicine over the past few decades is the reduction in heart attack risk, alongside reduced rates of many other aspects of cardiovascular disease. The data I'll point out here is but one example in a much broader trend. This is the higher end of what can be achieved through compensatory medicine for age-related disease, a set of increasingly sophisticated efforts to patch over the consequences of dysfunctional tissues, but without actually repairing the molecular damage that causes that dysfunction. Keeping a damaged machine functioning without repairing it is expensive and challenging. To go beyond the incremental improvements produced by medical science in the recent past, it will be necessary to change the high level strategy, and start to address the root causes of aging and age-related disease rather than merely papering over the problem.

Heart attack rates among an ethnically diverse population of more than 3.8 million Kaiser Permanente members in Northern California fell 23 percent from 2008 to 2014. Researchers studied rates of heart attacks by severity, age, gender, and diabetes status. While the incidence of heart attacks was highest in men, older age groups, and people with diabetes, similar declines in heart attack rates were seen across all subgroups - including those most at risk and with the highest rates, as well as among lower-risk patients, such as younger patients and women. The findings of this latest study build on research published in 2010 that demonstrated a 24 percent decline in heart attacks between 1999 and 2008.

A key difference in the two time periods studied was the type of heart attack that accounted for the majority of the declines. More severe but less common heart attacks, known as ST-elevation myocardial infarction or STEMI, which typically require an immediate procedure to open a blocked artery, fell by 62 percent from 1999 to 2008. The number of these heart attacks fell by an additional 10 percent from 2008 to 2014, resulting in a total reduction of 72 percent in these severe heart attacks from 1999 to 2014. The more common but less severe heart attacks, known as non-ST-elevation myocardial infarction or NSTEMI, showed the greatest decline from 2008 to 2014. These types of heart attacks peaked in 2004 and have fallen 33 percent through 2014. When taken together, there was a 40 percent reduction in all types of heart attacks across Kaiser Permanente in Northern California from the peak in 2000 through 2014, the most recently studied year. "While the decline in severe heart attacks across our population has been astonishing, we now see consistent declines in all types of heart attacks. Reductions in less severe heart attacks, which are nearly four times as common as the severe heart attacks, drove the bulk of the recent decline. But what is most heartening is that these reductions were consistent across every demographic and risk group we examined."

One Example Among Many Human Telomere Length Studies

Average telomere length decreases with aging, and is commonly measured in immune cells taken from a blood sample. Telomeres are a part of the mechanism that limits the number of times most cells can divide. Tissues are made up almost entirely of such limited cells, each losing a little telomere length during each division. When telomeres become short, the cell self-destructs or becomes senescent and ceases to divide. An associated stem cell population supports the tissue by delivering a continual supply of new daughter cells with long telomeres to replace the losses. Thus average telomere length is a function of cell division rates and cell replacement rates. Since stem cell activity declines with aging, it shouldn't be surprising to see that average telomere length does as well. In fact average telomere length in immune cells is highly variable between individuals, and even with circumstances for the same individual, and the rate of decline is small. It thus makes a pretty terrible measure of aging, a point reinforced by the numbers in this open access paper.

In the current study, we first examined the cross-sectional associations between leukocyte telomere length (LTL) and age, and, like previous reports, we found an inverse relationship with increasing age. Second, using up to five measurements across 20 years, we found that LTL decreases with age in a two-slope model with a small acceleration of decline after 69.3 years of age. Men have shorter telomere lengths than women, and genetic variation has an additional influence on overall LTL.

Several earlier studies have reported an inverse association between age and telomere length, as did we, and we further demonstrated that women have longer LTL, which is in line with earlier research. Taking our results and prior literature together, shorter telomeres in men could result from very small but consistent attrition throughout adulthood rather than a steeper decline compared to women in old age. Moreover, previous literature from cross-sectional and longitudinal studies has suggested a linear relationship between telomere length and age. We found both the one-slope and the two-slope models to be significant, with a substantially better fit of the latter. While the overall average trend was linear, there was systematic variability around the average trend, better described in a two-slope model accounting for more individual differences. The magnitude of this age-related decline was small overall, and with slight acceleration in the old-old. This observation is in line with earlier research in the field where faster decline in LTL is believed to take place in childhood and old age.

The two-slope trajectory analyses supported both familial and non-familial influences on LTL, with equal contributions to average LTL level (at age 69) and non-familial sources featuring more prominently in the change before age 69 than after age 69. This suggests that in young-old age, individual-specific lifestyle factors may prove more relevant to accelerated LTL shortening above and beyond familial and environmental contributions to overall LTL; however, in old-old age, familial factors may become increasingly salient to accelerated LTL shortening. Moreover, we note that the variation in rate of change was larger in young-old age; hence, evaluating variation in trajectories beyond the assumption of simple linearity and average trends is important for understanding etiological underpinnings.

Inducing Autophagy as the Basis for an Atherosclerosis Treatment

More of the cellular housekeeping process of autophagy appears to be an unalloyed good: more repair means less damage. It shows up in a range of interventions that modestly slow aging in mice and other species, such as calorie restriction. In fact it may even be essential to the ability of calorie restriction to extend healthy life spans in these studies. One place in which greater levels of autophagy might do some good is in the development of atherosclerosis, a pervasive age-related condition in which an overreaction to minor molecular damage in blood vessel walls snowballs into zones of inflammation and growing plaques made up of fats and dead cells. Eventually these plaques cause ruptures or blockages of major blood vessels that are frequently fatal. Higher levels of autophagy should slow the pace of progression of this problem through increased clearance of plaque materials, though it seems clear from the data here that much more aggressive interventions to clean up the waste and damage will be needed to solve it completely. The effects are small.

Spermidine is an endogenous biological polyamine that exhibits broad longevity-extending activities via the induction of autophagy. Because basal autophagy is atheroprotective during early atherosclerosis but dysfunctional in advanced plaques, the aim of the present study was to assess the potential beneficial effects of autophagy induction by spermidine on atherosclerotic plaque progression and composition. Apolipoprotein E-deficient (ApoE-/-) mice prone to development of atherosclerosis were fed a Western-type diet for 20 weeks with or without 5 mM spermidine in the drinking water.

Analysis of plaques in the aortic root, proximal ascending aorta and brachiocephalic artery showed that spermidine changed neither the size of the plaque nor its cellular composition. However, spermidine treatment significantly reduced necrotic core formation (6.6 ± 0.5% vs. 3.7 ± 0.5% in aortic root) and lipid accumulation inside the plaque (27 ± 3% vs. 17 ± 1% oil red O positivity in thoracic aorta). In vitro experiments showed that macrophages, unlike vascular smooth muscle cells (VSMCs), were relatively insensitive to autophagy induction by spermidine. Along these lines, spermidine triggered cholesterol efflux in autophagy-competent VSMCs (5.7 ± 1.2% vs. 8.7 ± 0.2%), but not in autophagy-deficient VSMCs or macrophages. Analogous to the experiments in vitro, spermidine affected neither necrosis nor lipid load in plaques of autophagy-deficient ApoE-/- mice.

In conclusion, spermidine inhibits lipid accumulation and necrotic core formation through stimulation of cholesterol efflux, albeit without changing plaque size or cellular composition. These effects, which are driven by autophagy in VSMCs, support the general idea that autophagy induction is potentially useful to prevent vascular disease.

Intestinal Autophagy Important in Calorie Restriction and Longevity in Nematodes

Based on the evidence accumulated from many years of studies of flies and nematodes, intestinal function is fairly central in aging and longevity. This is one of those things that probably doesn't translate so well to higher, more complex, and larger species, but the general principle of better organ function correlating to better health and a longer life expectancy is something to hold on to. In this open access paper the the increased activity of the cellular housekeeping mechanisms of autophagy, produced alongside greater longevity by the practice of calorie restriction, is investigated in the context of intestinal function in nematodes:

Dietary restriction (DR) without inducing malnutrition has robust beneficial effects on lifespan in many species, including humans. The cellular recycling process of autophagy contributes to DR-mediated longevity. Autophagy is triggered by nutrient scarcity and increases the degradation of cytosolic molecules and organelles in the lysosomes. Using the nematode Caenorhabditis elegans as a model organism, we previously showed that genes involved in autophagy are required for lifespan extension through DR; however, it is not clear whether autophagy in individual tissues plays critical roles in DR-mediated longevity.

Here, we investigated the contribution of autophagy in genetically dietary-restricted eat-2 mutants. Our major findings include: (i) Inhibition of autophagy in the intestine prevents the long lifespan observed in eat-2 mutants; (ii) the intestine of eat-2 mutants contains an expanded lysosomal compartment and flux assays indicate increased autophagosome turnover, consistent with elevated autophagy in this tissue; (iii) intestinal autophagy is required for the improved intestinal integrity observed in eat-2 mutants; (iv) autophagy inhibition impairs motility in older animals; and (v) inhibition of autophagy in the intestine accelerates the motility decline in eat-2 mutants. Collectively, these studies suggest a critical role for intestinal autophagy in dietary-restricted animals, and highlight the importance of this process in maintaining fitness and longevity.

Estimating the Cost of Sedentary Lifestyles

It is known that leading an inactive life, one lacking in physical exercise, has a fairly large negative effect on health and life expectancy. In a similar way to past studies that assessed the overall cost of obesity across populations, researchers here investigate one methodology by which it is possible to estimate the global cost of sedentary lifestyles:

A study has revealed that in 2013, physical inactivity cost 67.5 billion globally in healthcare expenditure and lost productivity, revealing the enormous economic burden of an increasingly sedentary world. Based on data from 142 countries, representing 93.2 per cent of the world's population, this study provides the first-ever global estimate of the financial cost of physical inactivity by examining the direct health-care cost, productivity losses, and disability-adjusted life years (DALYs) for five major non-communicable diseases attributable to inactivity: coronary heart disease, stroke, type 2 diabetes, breast cancer and colon cancer.

"Physical inactivity is recognised as a global pandemic that not only leads to diseases and early deaths, but imposes a major burden to the economy. Based on our data, physical inactivity costs the global economy 67.5 billion in 2013, with Australia footing a bill of more than AUD 805 million. At a global and individual country level these figures are likely to be an underestimate of the real cost, because of the conservative methodologies used by the team and lack of data in many countries. Increasing physical activity levels in communities is an important investment that governments should consider which could lead to savings in healthcare costs and more productivity in the labour market."

The 67.5bn in total costs, including 53.8bn in direct cost (healthcare expenditure) and 13.7bn in indirect costs (productivity losses), breaks down as follows. 31.2bn for total loss in tax revenue through public healthcare expenditure; 12.9bn as the total amount in private sector pays for physical inactivity-related diseases (e.g. health insurance companies); 9.7bn as the total amount households paid out-of-pocket for physical inactivity-related diseases. Type 2 diabetes was the costliest disease, accounting for 37.6bn (70 percent) of direct costs.

Quantifying the Positive Effects of Exercise versus the Detrimental Effects of Sitting

One of the themes that has emerged from the past few years of studies on the epidemiology of activity versus inactivity is the suggestion that time spent sitting is harmful regardless of whether or not an individual exercises. This relationship is extracted from statistical studies across populations, and as is usual in these matters the conclusion is disputed. In general, it is a good idea to give little weight to any one such epidemiological study and look instead for the consensus across many studies. That a sedentary lifestyle is bad for health and that regular moderate exercise is good for health is not in dispute, but arguments take place over the interpretation of population data for more subtle aspects of the relationship between these two things. This latest research should be added to the existing stack and considered in that context:

Ever since a study back in 1953 discovered that London bus drivers were at greater risk of heart disease compared to bus conductors, scientists have found increasing evidence that lack of physical activity is a major risk factor for several diseases and for risk of early death. Recent estimates suggest that more than 5 million people die globally each year as a result of failing to meet recommended daily activity levels. Studies in high-income countries have suggested that adults spend the majority of their waking hours sitting down. Current physical activity guidelines recommend that adults undertake at least 150 minutes of moderate intensity exercise per week.

In a recent analysis that draws together a number of existing studies, an international team of researchers asked the question: if an individual is active enough, can this reduce, or even eliminate, the increased risk of early death associated with sitting down? In total the researchers analysed 16 studies, which included data from more than one million men and women. The team grouped individuals into four quartiles depending on their level of moderate intensity physical activity, ranging from less than 5 minutes per day in the bottom group to over 60 minutes in the top. Moderate intensity exercise was defined as equating to walking at 3.5 miles/hour or cycling at 10 miles/hour, for example. The researchers found that 60 to 75 minutes of moderate intensity exercise per day were sufficient to eliminate the increased risk of early death associated with sitting for over eight hours per day. However, as many as three out of four people in the study failed to reach this level of daily activity.

The greatest risk of early death was for those individuals who were physically inactive, regardless of the amount of time sitting - they were between 28% and 59% more likely to die early compared with those who were in the most active quartile - a similar risk to that associated with smoking and obesity. In other words, lack of physical activity is a greater health risk than prolonged sitting. "There has been a lot of concern about the health risks associated with today's more sedentary lifestyles. Our message is a positive one: it is possible to reduce - or even eliminate - these risks if we are active enough, even without having to take up sports or go to the gym."

White Matter in the Brain is Lost More Rapidly in Overweight People

Researchers here find yet another reason to avoid becoming overweight, in that the brains of people who are overweight tend to lose white matter at an accelerated rate. The mechanism involved remains to be determined, but based on past research, the greater levels of chronic inflammation produced by larger amounts of visceral fat tissue would seem to be a good place to start looking.

Our brains naturally shrink with age, but scientists are increasingly recognising that obesity - already linked to conditions such as diabetes, cancer and heart disease - may also affect the onset and progression of brain ageing; however, direct studies to support this link are lacking. In a cross-sectional study - in other words, a study that looks at data from individuals at one point in time - researchers looked at the impact of obesity on brain structure across the adult lifespan to investigate whether obesity was associated with brain changes characteristic of ageing. The team studied data from 473 individuals between the ages of 20 and 87.

The researchers divided the data into two categories based on weight: lean and overweight. They found striking differences in the volume of white matter in the brains of overweight individuals compared with those of their leaner counterparts. Overweight individuals had a widespread reduction in white matter compared to lean people. The team then calculated how white matter volume related to age across the two groups. They discovered that an overweight person at, say, 50 years old had a comparable white matter volume to a lean person aged 60 years, implying a difference in brain age of 10 years. Strikingly, however, the researchers only observed these differences from middle-age onwards, suggesting that our brains may be particularly vulnerable during this period of ageing.

Despite the clear differences in the volume of white matter between lean and overweight individuals, the researchers found no connection between being overweight or obese and an individual's cognitive abilities, as measured using a standard test similar to an IQ test. "We don't yet know the implications of these changes in brain structure. Clearly, this must be a starting point for us to explore in more depth the effects of weight, diet and exercise on the brain and memory."

Contradictory Results on New Neurons and Old Memories

The adult brain adds new neurons at a very slow pace. Exercise increases that pace, so it is a place to start when trying to determine the likely outcome of therapies that greatly increase the generation of new neurons. As they are developed, such therapies will likely come to have an important place in the near future toolkit of rejuvenation therapies. The generation of new neurons diminishes with age, and is an important part of the plasticity of the brain, determining the ability to learn, change, and heal minor damage. At this point, many of the possible outcomes of a greater supply of new neurons remain debated, with studies still taking place. The contradictory animal data covering effects on memory noted here is just one example.

Research has found that exercise causes more new neurons to be formed in a critical brain region, and contrary to an earlier study, these new neurons do not cause the individual to forget old memories. Exercise is well known for its cognitive benefits, thought to occur because it causes neurogenesis, or the creation of new neurons, in the hippocampus, which is a key brain region for learning, memory and mood regulation. Therefore, it was a surprise in 2014 when a research study found that exercise caused mice to forget what they'd already learned. "It was a very well-done study, so it caused some concern that exercise might in some way be detrimental for memory."

The animal models in the exercise group - in the previous study - showed far more neurogenesis than the control group, but contrary to what one might think, these additional neurons seemed to erase memories that were formed before they started the exercise regimen. To test this, the researchers removed the extra neurons, and the mice suddenly were able to remember again. "The mice who exercised had a large number of new neurons, but somehow that seemed to break down the old connections, making them forget what they knew."

Researchers decided to replicate this earlier research, using rats instead of mice. Rats are thought to be more like humans physiologically, with more-similar neuronal workings. They found that - luckily for runners everywhere - these animal models showed no such degradation in memories. "We had completely contradictory findings from the 2014 study. Now we need to study other species to fully understand this phenomenon." The researchers trained their animal models to complete a task over the course of four days, followed by several days of memory consolidation by performing the task over and over again. Then, half the trained animal models were put into cages with running wheels for several weeks, while the control group remained sedentary. The rats who ran further over the course of that time had much greater neurogenesis in their hippocampus, and all rats who had access to a wheel (and therefore ran at least some), had greater neurogenesis than the sedentary group. On an average, they ran about 48 miles in four weeks, and neuron formation doubled in the hippocampus of these animals.

Importantly, despite differing levels of increased neurogenesis, both moderate runners and brisk runners (those who ran further than average) in the new study showed the same ability as the sedentary runners to recall the task they learned before they began to exercise. This means even a large amount of running (akin to people who perform significant amount of exercise on a daily basis) doesn't interfere with the recall of memory.


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