Fight Aging! Newsletter, September 14th 2015

September 14th 2015

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 2015 Fight Aging! Matching Fundraiser for SENS Rejuvenation Research Starts on October 1st
  • SENS Research Foundation 2015 Annual Report
  • Omics Data in Aging: the Rat Hole of Metabolism Runs Very Deep Indeed
  • Apply Common Sense and Caution When Reading About Aging, Longevity, and Rejuvenation Biotechnology
  • Radical Life Extension: an Interview with Aubrey de Grey
  • Latest Headlines from Fight Aging!
    • Investigating the Mechanisms of Remyelination
    • Circulating Nucleic Acids in Blood Cause DNA Damage?
    • AMRITA Initiative at the Regenerative Sciences Institute
    • The Ethics of Using Plastination to Save Lives
    • Atlas Regeneration Launches, Yet More Focus on Drug Discovery to Slow Aging
    • A Novel Mechanism Impairing Blood Flow with Aging
    • Searching for a Biomarker of Aging in Gene Expression Patterns
    • Developing Stem Cell Therapies for Parkinson's Disease
    • Engineered Macrophages Deliver GDNF to the Brain
    • Wnt Signaling in Aging and Regeneration


This year's Fight Aging! matching fundraiser to support the work of the SENS Research Foundation starts on October 1st, just a few weeks away. The SENS Research Foundation is a noted California nonprofit organization that coordinates work in US and European laboratories with the aim of ending frailty and disease in aging. From October 1st until the end of 2015 for we will match every donation with an equal amount from this year's 125,000 matching fund. We welcome all assistance in meeting our goal, with the aim of speeding the end of aging as a threat to health.

Aging is caused by an accumulation of cell and tissue damage, and these forms of damage are well cataloged and understood. To kickstart meaningful progress in the treatment of aging the research community must focus on therapies capable of repairing this damage. We stand now in the opening years of a process of development: philanthropic fundraising and early stage research coordinated by the SENS Research Foundation over the past decade have led to the first startups and established companies that are today working on new medical technologies that will treat the causes of aging. Senescent cell clearance and preventing the consequences of mitochondrial DNA damage are starting to turn into going concerns, for example, but there is much more left to do.

We want to support and expand this progress, leading the way to human rejuvenation. It is us up to us to shine the lantern and call more attention to this field of research, to fund the prototypes, to speak in public, and call for others to do the same. With this in mind, Fight Aging!, Josh Triplett, Christophe and Dominique Cornuejols,, and an anonymous donor have collaborated to create this year's 125,000 matching fund for SENS donations. From October 1st to December 31st 2015 we will match every donation to SENS rejuvenation research with an equal amount from the fund. This is our challenge to the community: we came together to raise 60,000 in 2013 and 150,000 in 2014, so let us see if we can hit the target of 250,000 for 2015. You never know the limits of fundraising and support for a worthy cause unless you reach for them.

Much has changed over the past few years in the public view of aging research and the prospects for development of first generation rejuvenation therapies. Researchers are more openly talking about treating aging as a medical condition, and influential backers are also using their soapboxes to discuss this cause. This is the slow tipping point of influence. Ultimately, we want to see the average fellow in the street think of research to treat aging in the same way as he thinks of research to treat cancer today, and that isn't so far away now. To eliminate the suffering, frailty, and death caused by aging is the greatest of goals; aging and its consequences are by far the largest cause of pain in the world. This is in our hands; it is our fundraising and support for organizations like the SENS Research Foundation that enabled the networking and persuasion needed to make rejuvenation research a respected goal, with growing awareness and support.

So, once again, I ask you to join me in helping to speed things along this October 1st. To fund the research, to tell your friends, to put up the posters, and to assist in whatever other way you can. The clock is ticking for all of us, but if the right lines of research are just funded more aggressively, then the widespread availability of therapies that can prevent and cure all age-related disease is just a few decades away now, and the first prototype treatments are considerably closer than that. We have made a difference in the past, we are making a difference now, and the wheel is starting to turn as a result of efforts just like this one.


The SENS Research Foundation staff have released their annual report for 2015, and as you can no doubt see it marks the beginning of a new phase for the organization, as well as for the field of rejuvenation research as a whole. Everyday people such as you and I have materially supported SENS research programs over the past decade, initially at the Methuselah Foundation and later at the SENS Research Foundation. The most advanced of these lines of research are now beginning to transfer out to startup companies for development of the first round of therapies. Over the next five to ten years we will see at least a few examples make it into trials and clinical practice, and the data on effectiveness will start to roll in.

This is the first of many steps that will see the SENS approach of periodic repair of cell and tissue damage broaden far beyond the SENS Research Foundation and its present allies. The prevention of age-related frailty and disease via these means will eventually become one of the principal pillars of medicine. As this year's Fight Aging! SENS fundraiser nears its launch, it is important to remember that we helped to make this happen: all of us together, over the years. Take a long look at the progress reported by the SENS Research Foundation and see what you have helped to create: meaningful steps towards a world without frailty and suffering.

SENS Research Foundation 2015 Annual Report (PDF)

Creating partnerships and collaborations to accelerate research

As the landscape of rejuvenation biotechnology broadens, we are seeing increasing opportunities for technology transfer and infrastructure-building efforts, across several categories of transaction.

1) We provide small seed funds - alone or with other funding sources - to companies able to perform mission-related research and development, saving costs against expanding our internal programs. Our research program on Advanced Macular Degeneration has been transferred using this approach, allowing further investigation whilst freeing up our own resources to focus on our next priority.

2) We have supplied small amounts of loan funding to private companies that are developing infrastructure for the rejuvenation biotechnology industry. This includes a loan to assist in the establishment of a tissue cryopreservation company that is working towards the creation of a supply chain for artificial organs.

3) We transfer appropriately mature research to well funded start-up companies pursuing specific disease fields, in return for a stake in those companies.

Case study: technology transfer to Human Rejuvenation Technologies, Inc.

SENS Research Foundation's LysoSENS program had been investigating methods of removal of unwanted intracellular aggregates since 2009. One project focused on aggregates that are the key drivers of the damage underlying plaque formation in atherosclerosis. Removing these aggregates from the immune cells that they disable would reduce plaque formation and dramatically lower the prevalence of heart disease. The project had successfully identified a non-human enzyme that was effective at eliminating some of these aggregates. It became clear that the research was at a stage where significant further investment could greatly accelerate progress, and that such investment could be achieved by transferring the research into a private company. This was done in 2014, when Jason Hope - himself a longterm supporter of the Foundation - formed Human Rejuvenation Technologies, Inc. (HRT). The technologies developed by the Foundation were transferred to HRT in return for a 10% stake in the company.

Case study: seed funding for Oisin Biotech

SENS Research Foundation was considering the creation of an internal project to investigate novel rejuvenation biotechnology solutions to the ablation of senescent cells. Instead we helped in the creation of Oisin Biotech, providing seed funding along with the Methuselah Foundation. Oisin is using licensed liposome technology matched with their own patent-pending DNA construct to perform apoptosis-induced eradication of senescent cells. They have demonstrated that their construct can selectively target senescent cells in vitro.

Delivering a mature and engaged research program

SENS Research Foundation supports a global research effort. Our own scientists are based in our Mountain View, California facility and we fund researchers at field-leading institutions around the world. As we age, we accumulate decades of unrepaired damage to the cellular and molecular structures of our bodies. The types of damage are few in number - we count seven, currently - but cause a great many diseases of aging, including cancer, Alzheimer's and atherosclerosis. Rejuvenation biotechnologies target this underlying damage, restoring the normal functioning of our bodies' cells and essential biomolecules. As preventative interventions they halt the harmful accumulation of damage, stopping disease before it ever starts. Damage and disease have a many-to-many relationship. That simply means that sometimes one type of damage can cause multiple diseases and sometimes one disease is caused by multiple types of damage.

Foundation-funded research includes teams which are:

1) Developing a regenerative medicine approach to treating inflammatory bowel disease, creating underlying technologies vital for future approaches to cancer.

2) Creating therapeutic approaches to intracellular aggregates which build up over time and compromise the functioning of cells in the brain, heart, and muscles.

3) Engineering healthy new tissue for the thymus, helping to restore the vigorous immune response of youth.

4) Engineering new mitochondrial genes to restore function to damaged mitochondria - a source of age-related disease and currently incurable inherited disorders.

5) Exploring non-invasive approaches to the diagnosis and monitoring of certain underdiagnosed forms of heart disease - avoiding the need for cardiac biopsy - and identifying.

6) Ways to remove aggregates which lead to impaired heart function.

7) Understanding the genetic basis of certain cancers which rely on a mechanism called ALT (alternative lengthening of telomeres), to pave the way for new cancer treatments.

8) Developing the tools needed to create therapies which reduce hypertension, stroke and
kidney disease by breaking molecular crosslinks which cause arteries to stiffen with age.

The report contains much longer summaries of current research programs, which are well worth reading. These are exciting times we live in, and it is very welcome to see the work and support of past years beginning to pay off today. As we gear up for this year's fundraiser, starting on October 1st, bear this all in mind. Donating to the SENS Research Foundation this year helps to build the foundation for tomorrows' advances in treating aging. There is no better way I know of to put money to good use.


Here I'll point out a review paper on the "omics," the younger fields of the life sciences, including genomics, proteomics, and so forth, and their role in aging research. These fields encompass the study of biological molecules and their roles in cellular metabolism and tissue function, broken down by type and class. The study of genes, the study of proteins, the study of proteins only applicable to the immune system, the study of proteins involved in transcription, and many more divisions besides. There are now dozens of omics fields, and they continue to proliferate and specialize, this growth a reflection of the accelerating capabilities and falling costs of biotechnology. Mountains of ever more detailed data are produced each year, and merely focusing on analysis and application occupies much of the field. Indeed it might be argued that the production of omics data far outstrips its productive use at the present time, that there is something of a land grab underway now that commercial ventures focused on omics data are entering the fray, and that we are due a lengthy phase of consolidation and analysis in the years ahead. For now data is the zeitgeist of the life sciences: data on genes, on proteins, on specific clades of proteins, closely followed by the search for relevance and meaning in vast databases.

All of this is entirely in line with the goals of the scientific method: learn everything, discover everything, analyze everything. Take in all that the tools can provide. When it comes to aging, however, I think that the present zeitgeist is a distraction from an existing road to effective treatments for the causes of degeneration, frailty, and disease. It is a very effective distraction: the bulk of the field is turning in that direction, and their activities are best understood as firstly addressing the goal to comprehensively map all of our biology, and then as a distant second trying to make something of that new knowledge. Our biology is fantastically complex when operating in its standard, undamaged, youthful state. When it is disarrayed by the cell and tissue damage of aging, it can fall into a much wider range of dysfunctional operation, every older individual a special snowflake within the broader statistical patterns of disease and organ failure that we observe across populations. There is data enough here to keep the omics organizations busy for the foreseeable future, exploring the limitless differences in biochemistry found between billions of individuals as they age.

This is not the path to treating aging. It is the path to understanding exactly why there are variations in outcome when the initial types of damage that cause aging are the same for everyone. These two end goals are not the same thing at all. You cannot take the complete understanding of how aging progresses and then use it to make an effective therapy by adjusting the biochemistry of person A to make it more like the biochemistry of person B. That changes the outcome in only minor ways, at best slightly slowing the generation of damage that causes aging, or slightly improving its ongoing repair. Yet this is pretty much exactly what the mainstream of the research community is trying to do. As a goal it is enormous and challenging, and yet it will produce few benefits in the grand scheme of things.

The only effective therapy for aging and age-related disease, the only way to add decades or longer to healthy, vital life spans, is to repair the damage that causes aging. We don't need omics data or much in the way of further transformative advances in the life sciences in order to accomplish that goal. The types of damage that cause aging and all of its manifestations are well cataloged and identified. The biotechnologies to repair them could be built with no major new breakthroughs, just painstaking work on the details. Yet this path of repair, to restore the undamaged youthful metabolism that we know works, is still largely overlooked.

The open access paper quoted below is an educational look at the omics fields, and illustrates just how much data there is yet to gather and analyze. The rat hole extends down for a very long way indeed. To plumb its depths will be one of the great works of this century, and I expect to be underway still decades from now. Yet even if none of that happened, the research community could still effectively cure aging and create robust and reliable rejuvenation treatments on much the same timescale, starting from where we are and what we know today about the damage that causes aging. Changing the focus of the field to fall upon periodic repair of damage is the most important thing we can help to achieve.

Integration of 'omics' data in aging research: from biomarkers to systems biology

Age is the strongest risk factor for many diseases including neurodegenerative disorders, coronary heart disease, type 2 diabetes and cancer. Due to increasing life expectancy and low birth rates, the incidence of age-related diseases is increasing in industrialized countries. Therefore, understanding the relationship between diseases and aging and facilitating healthy aging are major goals in medical research. In the last decades, the dimension of biological data has drastically increased with high-throughput technologies now measuring thousands of epigenetic, expression and metabolic variables.

Omics technologies provide valuable tools to study aging on the molecular level. Reductionist data analyses, testing the measured variables separately for association with age, have been extensively applied. Such studies successfully identified hundreds of epigenetic mutations, gene expression levels, metabolite concentrations to be linked with chronological and/or biological age (see below for details). Even though these results improved our understanding of aging as a complex phenotype, the mechanisms underlying these associations and the impact of interactions between different biological entities remain elusive in most cases. In contrast to reductionist approaches, systems biology aims to analyse all components of a biological process simultaneously taking into account their interactions and their intrinsic hierarchical structure. With more and more high-throughput data becoming available, systems biology has led to many new methods and their successful application on age and age-related phenotypes.


Genomics was the first omics field for which high-throughput measurements became available. While aging (or rather longevity) itself was found to be only about 20% heritable, many age-related diseases are highly heritable. For instance, Alzheimer's disease (AD) shows a heritability above 70% and osteoarthritis or cataract show 50% heritability.


Epigenomics describes the study of heritable changes in the genome that are not caused by DNA sequence mutations. The most common epigenetic mechanism is DNA methylation, which is known to often silence gene expression. The epigenome is influenced by environmental and lifestyle factors and is associated with many complex diseases such as neurodegenerative disorders and cancer. Nearly 500 differentially methylated regions were found to be associated with chronological age and age-related phenotypes such as lung function, cholesterol levels and maternal longevity. A recent study showed that methylation patterns of just three sites are sufficient to predict chronological age.


Genes are transcribed into RNA molecules, which are further processed in a tightly controlled process. The entirety of the RNA transcripts is referred to as the transcriptome. Similar to the epigenome, gene expression was shown to dramatically change with age. A pioneer study comparing postmortem human frontal cortex tissue samples between 30 individuals of different ages yielded 463 differentially expressed genes. Despite the small sample size, results were replicated in subsequent experiments.


Proteins are translated from coding transcripts. Due to alternative splicing and post-translational protein modifications, the number of proteins is estimated to be two orders of magnitudes higher than the number of genes. However, current proteomic techniques based on immunoassays, protein arrays or mass spectrometry can measure only a small fraction of the proteome. Due to these technicalities, 'proteomics' studies in aging research so far focused on smaller sets of proteins and small sample sizes. A recent study by our group analysed over 1000 proteins in 200 plasma samples. Eleven proteins were found to strongly associate with chronological age as well as age-related phenotypes such as lung function and blood pressure. The results were replicated in an independent cohort. Even though comprehensive proteomics studies are still missing, proteins are likely to be associated with several age-related diseases.

Post-translational modifications - glycomics

Post-translational modifications are important elements of proteins, which can alter their biochemical properties such as protein structure, binding preferences and enzyme activity. There are many different modifications ranging from addition of small molecules (e.g. acetylation or phosphorylation), over addition of larger molecules such as lipids or sugar chains (e.g. glycosylation), to the addition of whole proteins (e.g. ubiquitination). The application of this technology on epidemiological cohorts revealed that glycan structures are stable for one individual over time but very diverse within a population. Differences in glycomes were found to be related with various cancers. Recently, researchers showed that IgG glycans are strongly associated with age: a linear combination of three glycans explained 58% of the observed variance of chronological age in a study of four independent populations with 5117 participants in total.


Metabolomics investigates the low-molecular-weight molecules in a biological system. The measured molecules are often referred to as metabolites as many of them act as educts, products and intermediates of the cellular metabolism. Currently, the Human Metabolome Database contains more than 40,000 distinct metabolites from different tissues. Similar to proteomics, to date, there is no analytical method available to determine and quantify all metabolites in a single experiment. In 2008, the first metabolome-wide association study on age analysed the plasma metabolome of 269 individuals using an untargeted approach. The authors found 100 of 300 compounds to correlate with chronological age.


The human microbiome describes the complete set of microbial species (and their genomes) hosted by the human body. The largest microbial community resides in the gut, where microbial cells and their genes outnumber human cells (10:1) and genes (100:1). More than 10,000 different species with millions of protein-coding genes were identified by the Human Microbiome Project. The composition of the microbe flora varies a lot across individuals and even between different parts of the body. It has a huge influence on many biological processes such as immune response, metabolism and disease. While the microbiome seems to be relatively stable during adulthood, it changes significantly in later life. Researchers have observed drastic changes in the gut microbiome of centenarians compared with young adults as well as elderly, namely a general loss of diversity and increased abundance of bacilli and proteobacteria.


Simultaneously with omics data, the dimension of clinical and lifestyle traits, particularly clinically used intermediate traits, keeps increasing. Epidemiological studies collected thousands of clinically relevant phenotypes beyond omics data types. These range from anthropometric measures to health and lifestyle questionnaires. Collecting high-dimensional clinical data is important to unveil pleiotropy of genes and interactions amongst clinical phenotypes such as comorbidities. Phenomics is especially important for aging research. Dozens of clinical phenotypes, such as Parkinson's, AD, body mass index, blood pressure and bone mineral density, as well as lifestyle parameters, such as nutrition, smoking and physical activity, are strongly related to age. Only extensive collection of data and their joint analysis will help to unveil these dependencies and find causal relationships.


This is an era of near effortless communication, in which anyone with anything to say can publish to the world at next to no cost. As it turns out nearly everything that is said or written on any given topic is garbage. Back when the cost of communication was much higher, that cost served as a filter to block most casually created junk from widespread propagation, leaving only the earnest or well-backed junk to surround the small proportion of useful and accurate works. Truth is always a small selection at the back of the global library, dwarfed by the reams of propaganda, error, wishful thinking, and irrelevance.

Have you ever noticed that when the popular press publishes on a topic that you know well, such articles are near always easily identified as being misleading and wrong in a dozen ways in as many sentences? It is that way for everything that is published by professional journalists, and for every topic. Yet we go on believing what we read; it is an interesting phenomenon. Popular news of scientific research into human longevity is distorted in many ways between laboratory and press room, and then further degraded in the echo chambers of the media and the online world. This is especially true of anything that the "anti-aging" marketplace takes an interest in; that industry is a font of lies and misdirection, ranging from the blatant to the very subtle, all in service of liberating the gullible from their money. To sift all of this you have to first and foremost always seek out the primary materials, the original published works. Then apply common sense; be skeptical; be somewhat familiar with what researchers are up to in the field; know of a few reputable publications that cover medical progress and the life sciences. Try to fit what you read into the framework of what you know, and be ever ready to throw out whatever looks suspect.

Even within the specialist area of peer reviewed scientific publications and research papers there is a lot of earnest junk, things worth neither time nor attention, and theories hanging out there on the edge, entirely unsupported. Science is a messy process, generating just as much in the way of wildly wrong dead-ends as it does new truths and useful progress. There is a post way back in the Fight Aging! archives on how to read the out of the scientific method. It covers some of the basics, but in essence the advice boils down to a matter of following the numbers and the consensus - unless you happen to be one of those knowledgeable enough to contribute to the fray with papers of your own. The rest of us, as laypeople, should only believe a position to be likely plausible or defensible when many researchers agree.

In any case, here I'll point out an article with a click-bait title that nonetheless manages to say a few sensible things on the topic. At some point everyone investigating the science of human longevity and the prospects for the future has the realization that most of what is written on the topic isn't worth the time it will take to recognize it as junk:

When the science of living longer doesn't make sense

A lot of bizarre things get put on the internet these days. However, given that almost anyone can contribute practically anything they like to the worldwide web of information, it's getting increasingly difficult to separate fact from fiction. Due to the misinterpretation, misuse or misunderstanding of scientific evidence, many minor studies are often seized upon, and portrayed as concrete fact in spite of a lack of basis. One scientific area which is particularly affected by this issue is the field of healthy life extension. There are literally thousands of websites and articles out there which offer advice on how to overcome age-related diseases or radically increase lifespan, many of which are highly misleading. By following some simple rules however, it can be relatively easy to identify what is legitimate and what is not.

Rather than focusing solely on the results of a scientific study, journalists would do well to pay some attention to the methods which have been used to generate them, since this can provide a good indication of how valid and applicable such results might be for their readers. Too often, articles imply that the results of a scientific study are of far greater relevance to the reader than they actually are. When it comes to examining the association between an exposure and an outcome, the most widely trusted approach is the randomized controlled trial. However, it is not always possible to conduct randomized trials. Alternatively, researchers can turn to "nonexperimental" or "observational" database studies. These database studies make use of large sets of data collected from past surveys. Ultimately, no single study is perfect - be it a randomized trial or a non-experimental one. This is why it is better to wait until enough evidence to support a particular hypothesis has accumulated from multiple studies, which make use of a range of methods and have been applied to different populations.

In the absence of studies which test out a specific hypothesis, it can be tempting for journalists to make inferences from other studies, or worse still, attempt to conduct their own 'scientific' research. Be wary of claims which rely on anecdotes rather than scientific studies. Similarly, know that meanings can be distorted through the use of language. Sometimes, for the sake of artistic licence, non-experts reporting the outcomes of a scientific study choose to alter the wording of the phrases being used to describe the results. Whether it is intentional or not, such alterations can grossly distort the implied meaning.

Ultimately, providing a platform for the most unlikely and strange pieces of advice can damage the reputation of any scientific field. In the case of research into increasing healthy lifespan, the spreading of misinformation serves only to slow the rate of progress and acceptance of this relatively new branch of science.


"Life extension" and "radical life extension" are declining terms these days, less frequently used now that the scientific community is stepping closer to being able to build the means of greatly extending healthy life spans. The original overarching visions of far longer lives achieved through medical progress, laid out in the 70s and 80s and vague on the details, will fade away in the face of increasing specificity and concrete implementations. The communities who will in the years ahead launch companies and make money by building and distributing actual, working rejuvenation therapies: it is these people who will coin the new terms we use for the next few decades. For now there are intermediary categories: longevity science; rejuvenation biotechnology; an expansion of regeneration medicine to include treatment of aging. But I have no more idea than you as to what we'll be calling the rejuvenation therapies of the 2030s when those years are upon us. Language is a river, and you take it as it comes.

Aubrey de Grey is the cofounder of the Methuselah Foundation and SENS Research Foundation. He devotes half of his time to the coordination of research needed to speed progress towards working rejuvenation treatments and the other half traveling and speaking to persuade the rest of the world to help. If you ever find yourself doubting that we all live in a madhouse society, blind to what really matters, then consider that it is in fact very hard to persuade people to help with medical research that will prevent their future selves from suffering horribly. The population at large veers between disinterest in ensuring their future health and hostility to the idea that anyone else might be trying to better maintain their health by treating aging as a medical condition. No matter that more than 100,000 lives are lost to aging every day, while millions of others are in pain, decrepit and frail, most people still instinctively defend that status quo.

Here I'll link to a recent interview with de Grey in the technology press. The highly networked venture capital, entrepreneur, and technology community centered in California - but with growing outposts across the US - has been very supportive of SENS rejuvenation research over the years, at least in comparison to the rest of the population. Many of the most influential donors are from this community, and there is no doubt a retrospective to be written at some point at some point in the future, a work that will outline the connections and explain just why it is that the prospect of radically enhanced longevity achieved through medical progress strikes a chord so effectively with programmers and technology entrepreneurs.

Radical lifespan extension: A chat with Aubrey de Grey

Reese: What's the current state of the effort to "cure death"?

de Grey: Well, first off, let's be perfectly clear. I don't work on "curing death." I work on health. I work on keeping people healthy. And, yes, I understand that success in my work could translate into an important side effect, which is that people would, on average, live longer. But ultimately, the main thing people die of is being unhealthy, being sick. And if you can keep people less sick, it means that they're going to live longer. Now, it happens that the particular way in which I am working on stopping people from getting sick is a really comprehensive one that applies to all aspects of the ill health of old age, so the side effect is going to be bigger than people are used to. But still, it's just a side effect. I don't work on longevity. I work on health.

And another big thing to understand is that even if you think, well, this is just words, and I really do work on longevity, the fact is I still don't work on "curing death," because you can die of a whole bunch of other things. You can die by being hit by a truck. We can all die if we get hit by an asteroid. So it's all about health.

Reese: If you achieved all of your aims of curing all disease and promoting health, do you think the human body then has a natural limit to its life span?

de Grey: Absolutely not. I think that as things stand today, before the medicines that we are working on have come to fruition, that there is definitely a natural maximum life span, because there are various types of damage that the body does to itself as a side effect of the way the body works. The best example of this is breathing. Breathing is pretty damn nonnegotiable. But the effect of breathing is the creation of free radicals, which cause a lot of damage. So yes, damage is always happening, and right now there is only so much that we can do to minimize that rate, and there's only so much accumulated damage that we can tolerate.

But our work revolves around repairing that ongoing damage. And that will completely transcend any such limits. It's just like a vintage car. Vintage cars were not designed to last more than ten or 15 years, but preventive maintenance, so long as it's comprehensive, can completely transcend any such limits.

Reese: What do you think are going to be the social impacts of extending people's lives?

de Grey: There will be enormous social consequences, no question. But I think we need to look at this question a little bit more objectively than most people do. The fact is that, yes, we need to figure out issues like, how will we pay the pensions, and so forth, so everybody gets these therapies. But these are not new questions. Think about the Industrial Revolution. We didn't know what we were doing, we figured it out. We've got to remember that the main purpose is to stop people from getting sick just because they were born a long time ago. Ultimately, if you ask anyone - if you ask an audience, whether they want to get Alzheimer's disease, you're going to get a fairly unanimous "no."

And if you ask them whether they would like to get Alzheimer's disease when they reach the age of a hundred, you're still going to get the unanimous "no," and it's the same for cancer. It's the same for all of the diseases of old age. The real reason we get these crazy questions - you know, like "how will we make sure that this is available to everybody?" - is because they have this crazy, crazy idea in their heads that there is this thing called aging, that is in some way completely separate, completely unconnected with any disease. In biological reality, there is no such distinction.


Monday, September 7, 2015

Researchers here uncover a potential drug target to spur the remyelination of nerves. Accelerated degradation of the myelin sheathing required for correct nervous system function underlies a range of medical conditions, including multiple sclerosis. Evidence suggests that everyone suffers demyelination to a lesser degree over the course of aging, however, and that this may contribute towards the noticeable loss of cognitive function that occurs in even the fittest of older people. So it is worth keeping an eye on progress towards methods of restoring myelin:

In vertebrates, axons extending from nerve cells are covered by insulating sheets called the myelin sheath, made with the cell membranes of oligodendrocytes, enabling fast electrical signaling through saltatory conduction. Normally, myelin is repaired, even if damaged, but the mechanism that controls remyelination was not well understood. In addition, in demyelinating diseases such as multiple sclerosis, the myelin sheath does not recover from damage and gets worse, finally leading to symptoms such as vision loss, limb numbness, and movement disorders.

Researchers performed a detailed examination of the remyelinating process of damaged myelin using disease model mice. Their results show that a growth factor called pleiotrophin is secreted from nerve axons injured by demyelination, and this pleiotrophin inhibits the function of the receptor molecule PTPRZ of oligodendrocyte precursor cells, stimulating cellular differentiation into oligodendrocytes which form the myelin sheath, thereby promoting remyelination.

This achievement shows that it is possible to encourage the regeneration of the myelin sheath by inhibiting the action of PTPRZ in endogenous oligodendrocyte precursor cells, indicating a new potential treatment for demyelinating diseases. "This was made possible by establishing oligodendrocyte precursor cell lines. Pleiotrophin is an endogenous PTPRZ inhibitor, but if synthetic PTPRZ inhibitors were obtained, then effective treatments for multiple sclerosis should become possible. We are currently directing our research in that direction".

Monday, September 7, 2015

Researchers here propose a novel method by which stochastic nuclear DNA damage can occur over the course of aging. The paper is open access, but only available in PDF format at the moment:

Whether nucleic acids that circulate in blood have any patho-physiological functions in the host have not been explored. We report here that far from being inert molecules, circulating nucleic acids have significant biological activities of their own that are deleterious to healthy cells of the body. Fragmented DNA and chromatin (DNAfs and Cfs) isolated from blood of cancer patients and healthy volunteers are readily taken up by a variety of cells in culture to be localized in their nuclei within a few minutes. The intra-nuclear DNAfs and Cfs associate themselves with host cell chromosomes to evoke a cellular DNA-damage-repair-response (DDR) followed by their incorporation into the host cell genomes. Whole genome sequencing detected the presence of tens of thousands of human sequence reads in the recipient mouse cells. Genomic incorporation of DNAfs and Cfs leads to dsDNA breaks and activation of apoptotic pathways in the treated cells.

When injected intravenously into Balb/C mice, DNAfs and Cfs undergo genomic integration into cells of their vital organs resulting in activation of DDR and apoptotic proteins in the recipient cells. Cfs have significantly greater activity than DNAfs with respect to all parameters examined, while both DNAfs and Cfs isolated from cancer patients are more active than those from normal volunteers. All the above pathological actions of DNAfs and Cfs described above can be abrogated by concurrent treatment with DNase I and/or anti-histone antibody complexed nanoparticles both in vitro and in vivo. Taken together, our results suggest that circulating DNAfs and Cfs are physiological, continuously arising, endogenous DNA damaging agents with implications to ageing and a multitude of human pathologies including initiation of cancer.

Tuesday, September 8, 2015

A growing number of scientists and scientific organizations are willing to advocate for, and work towards, the treatment of aging. A great deal of effort over the past decade on the part of organizations like the Methuselah Foundation and SENS Research Foundation and their supporters has helped to change the culture of aging research and increase public awareness of the present state of aging science. This has created a much more receptive environment, one in which more such organizations can thrive.

Painting with very broad strokes, you might think of there being two camps in the aging research community: firstly the majority who see aging as caused by accumulated cell and tissue damage, and secondly a growing minority who see aging as an evolved program caused by epigenetic changes. There are of course a great many opposing factions and different viewpoints within those two large groupings, but I see this as the most important division in the field. With greater progress towards working therapies, we should have a good idea as to which side is correct within the next decade - it will be the one that can produce meaningful prototype rejuvenation treatments.

While SENS research programs are based on damage repair as the ideal approach to therapies for aging, the path that I favor, the Regenerative Sciences Institute takes an epigenetic focus for their otherwise quite similar advocacy for human rejuvenation. In terms of organizational development they are in their very early stages, but then so were the SENS initiatives a decade ago. In an ideal world, there would be scores of young organizations akin to these, pulling in funding for the science and helping to raise awareness for longevity science:

The AMRITA (Abolishing Morbidity by Regeneering and Integrated Technology Advancement) Initiative is RSI's long-term strategy to develop and enhance the regenerative capacity of human beings to live healthier, disease-free lives and transform aging into a benign, beneficial process during which health and vigor are maintained. Aging results primarily from reversible loss of epigenetic/epigenomic information with cell divisions and with chronological time. The key to differences in longevity among mammals is varying fidelities of the biomolecular machines that maintain the epigenome. AMRITA is developing methods to restore a youthful state of the epigenome and enhance regeneration. AMRITA is the logical next step for regenerative medicine - to engineer enhanced regeneration into human beings.

Closely integrated with our innovative education projects, the AMRITA Initiative is divided into three parallel tracks. The first track will identify ways to slow or reverse aging in the immediate future by using systems biology and targeted research to identify aging pathways amenable to intercession. The second track develops the technology to reprogram human cells and tissue in vivo to effectively rejuveneer them, based on breakthroughs in stem cell biology. Our own cells and tissues will be programmed to: 1) undergo a cycle of rejuvenative cell division, 2) remove old dysfunctional cells, and 3) replace them with rejuvenated youthful cells. Increased regenerative power will be a beneficial side effect. In the third track, micro- and nanotechnology are being developed to create biological automatons (biomatons) and robots (biobots) that will be able to carry out repair throughout the body and effectively complement the pure biology based approaches.

Tuesday, September 8, 2015

Plastination is a potential alternative to cryonics for the long-term preservation of the brain following death, a way to maintain the fine neural structure that encodes the data of the mind. Given the pace of technological progress, preserved individuals can expect some unknown chance at restoration to active life in the future. The types of technology required for that feat are well understood, and include a near complete control over cellular biochemistry, along with a molecular nanotechnology industry capable of reconstruction of cells and sequestration of preservation chemicals. Whatever the odds for survival turn out to be, they are considerably better than the other option, which is the grave and oblivion. There is no better path to longevity for the billions who will age to death prior to the widespread availability of rejuvenation therapies, and it is perhaps the greatest shame of our age that cryonics and plastination remain niche concerns.

Plastination has been shown to be feasible as the basis for a preservation technology to much the same degree as cryonics, but unlike cryonics it has not yet developed into a practicing industry. While this lengthy article focuses on plastination, the points are also applicable to cryopreservation:

For the most part bioethics is understandably a conservative business. In the past there has been little tolerance for taking life extension seriously. If the possibility was not scorned as wishful thinking it was dismissed as being selfish and a grave danger to society, usually without any real argument. Yet a new generation of scientists and bioethicists are no longer willing to dismiss radical life extension and have begun to seriously examine these issues. The techno-progressive community as well as the general public are also much more informed about the every increasing pace of technology and are less willing to dismiss potential life extension technologies.

Once the information-theoretic definition of death and the fact that a person is their connectome are accepted, any technique that can preserve the information in the brain has the potential for life extension. In chemical brain preservation, rather than using low temperatures to lock the brain in place as is done in cryonics, the brain is placed in stasis by chemical bonding, a procedure also known as plastination. However, the difference between cryonics and chemical brain preservation is no absolute. Newer forms of cryonics use a process called vitrification. Vitrification uses low temperatures and cryoprotectants to turn tissue into a glass like state where decay is extremely slow. Therefore it may be possible to develop hybrid procedures involving elements of both cryonics and chemical brain preservation.

It may seem obvious to some, but we need ask the question of why would anyone pursue brain preservation? Assuming it works, the obvious answer it that the person wishes to continue living. Many bioethicists argue it is wrong to "unnaturally" extend life and that we need to accept death. This may be good advice if there is nothing we can do about death, but it rings hollow when something can be done. After all, no one argued about refusing public health measures beginning in the late nineteenth century which was arguably the first case of significant life extension.

If the world continues its accelerated pace there is every reason to expect that in a few hundred years we will have a complete science of how the brain gives rise to mind, and the technological prowess to routinely upload memories and minds. Citizens of that future world will have conquered disease and death and overcome countless other biological limitations. And they will viscerally understand what today's neuroscience textbooks try to convey: The mind is computational, and a person's unique memories and personality are encoded in the pattern of physical connections between neurons. From that vantage point, future generations will ask: "Why didn't humanity preserve its most priceless possession -the human brain?"

Wednesday, September 9, 2015

Anthony Atala, known for his work on tissue engineering is launching a new company, Atlas Regeneration to focus on pharmacology related to aging. This is in many ways similar to Human Longevity Inc., and it seems a pity to me that someone who was doing something more useful is now going to focus on something less useful when it comes to advancing the state of medicine for healthy longevity.

Numerous groups are now getting into the field of longevity-related genetics and drug discovery with the aim of very modestly slowing down aspects of the aging process. It is probably the case that there is money to be made here, and there is certainly much more data to be gathered on the precise details of the operation of cellular metabolism and its relationship with natural variations in longevity. I do not see it as a viable path towards meaningfully lengthening human life spans, however. Few if any of these initiatives are involved in attempts on the damage repair approach to aging that characterizes SENS, and thus I expect their work to do little but add to our knowledge of metabolism, or move the research community a few steps closer to being able to capture some of the well-established benefits of calorie restriction or exercise through drug treatments. These are small potatoes compared to the rejuvenation that might be achieved through periodic repair of the cell and tissue damage that causes aging, rather than merely slowing down its accumulation.

Atlas Regeneration Inc, a company dedicated to developing novel software platforms and algorithms for drug discovery relating to regenerative medicine and stem cell research, has officially launched. Atlas has partnered with InSilico Medicine, a bioinformatics company, which employs its state of the art Geroscope platform to select and rate personalized anti-aging therapies and identify new drug candidates in longevity.

Aging is an issue that effects all people around the globe universally, but as the babyboomer generation ages, the stress that it places on society becomes greater and the need develop methods for people to remain productive as they age rises in turn. Aging is a very complex multifactorial process that cannot be stopped or reversed by a simple combination of drugs, which is why it is important to develop personalized treatments tailored to individual subjects. The pharmaceutical industry needs a platform to effectively utilize and clinically implement stem cells technology.

"We built our platform, Regeneration Intelligence, on years of experience in regenerative medicine and pharmacology, de novo organ regeneration, body-on-the chip technology just to mention a few of them with a one single goal: develop a reliable tool to convert multi-omics data from individual patient's tissues into unified drug score to predict the effectiveness of targeted compounds and improve clinical decision making, unified iPSC lines score to predict differentiation potential and evaluate clinical safety. We are reinventing this system for drug discovery in regeneration medicine and aging to more effectively employ big data to find solutions for aging, competing with the Google's Calico and Human Longevity companies, to deliver hope that we may see the time when our mutual efforts will start saving lives and increase life span via regeneration in adult humans."

Some of the ideas behind the company's bioinformatics platforms for both regeneration, iPS and aging are rather simple: analyze all available omics profiles of "cells-in-progress" (iPSC line under evaluation, cells/tissues under treatment and so on) and targeted counterpart cells in mature healthy tissues or organs, run computer simulations based on proprietary pathway map to see what drugs or treatments make the old or undifferentiated cell get as close to the norm/healthy counterparts as possible and then validate the results on human cells and model organisms. The same approach may be employed to personalize the drug regimen for individual patients. The core parts of the technology are proprietary signaling pathway map, a unique scoring algorithm along with well-developed biological models which allows us to use all-inclusive gene expression analysis, including microRNA, methylation and proteomics modules among others, and a comprehensive constantly updated drug database.

The position that aging needs personalized treatments is something I see as nonsense, and a symptom of the research community being focused on entirely the wrong approach to the problem. We all age for the same reasons, the damage that causes aging is the same in all of us. The therapies to repair that damage can be the same for all of us, mass produced and cheap once established. Only if you are trying to mess around with the operation of metabolism to slow aging or compensate for damage without actually repairing it - a futile effort, doomed to expensive failure and marginal benefits - do you need to care about exactly how the spiral of simple damage creating complex consequences takes place in any given individual.

Wednesday, September 9, 2015

Researchers here find a possible neurological contributing cause to the characteristic dysfunction in blood vessels that occurs with aging. This is distinct from the age-related increases in tissue stiffness that sabotage blood vessel flexibility in response to circumstances:

"Aging affects everyone and causes changes throughout our bodies. The purpose of our study was to understand how blood vessels are affected by this process. We found that older arteries had a significantly lower number of sensory nerves in the tissues surrounding them and they were less sensitive to an important neurotransmitter responsible for dilation."

The study focused on mesenteric arteries - a type of artery that supplies blood to the small intestines - of mice that were 4 months and 24 months old. These ages correspond to humans in their early 20s and mid-60s, respectively. Without stimulation, the diameter of the blood vessels of both younger and older mice was approximately the same. However, when stimulated to induce dilation, differences between the age groups became apparent. "The younger arteries dilated as expected. However, when we performed the same stimulation to the arteries of older mice, the vessels did not dilate. When we examined the presence of sensory nerves, we noted a 30 percent decrease in the amount surrounding the older arteries compared to the younger arteries."

Additionally, the researchers found that even when purposefully exposing older mesenteric arteries to defined amounts of the neurotransmitter calcitonin gene-related peptide, or CGRP, the arteries' ability to dilate was greatly reduced. "Poor neurotransmitter function and a reduced presence of sensory nerves surrounding older vessels lead to age-related dysfunction of mesenteric arteries. The importance of this discovery is that if we can identify why this happens to mesenteric arteries, it may be possible to prevent the same thing from happening to other blood vessels throughout the body."

Thursday, September 10, 2015

A reliable biomarker for biological age would be some measure that reflects the level of cell and tissue damage present in an individual. The existence of such a biomarker would greatly speed up work on treatments for aging, allowing at least preliminary evaluation of the effectiveness of potential rejuvenation therapies based on damage repair very soon after their application in a test subject. The only presently available option is to run life span studies, to take the wait and see approach, which is very expensive and time-consuming, even in mice.

Researchers have made inroads towards a biomarker for aging by looking at DNA methylation patterns, and here is news of an analogous project that analyzes changes in gene expression levels. By the sound of it this new methodology only captures a slice of the wide-ranging cellular responses to accumulating damage, missing some of the important changes related to, for example, deterioration of the cardiovascular system:

Researchers used a process called RNA-profiling to measure and compare gene expression in thousands of human tissue samples. Rather than looking for genes associated with disease or extreme longevity, the researchers discovered that the "activation" of 150 genes in the blood, brain and muscle tissue were a hallmark of good health at 65 years of age. The researchers were then able to create a reproducible formula for "healthy ageing," and use this to tell how well a person is ageing when compared to others born the same year.

The researchers found an extensive range in "biological age" scores of people born at the same time indicating that a person's biological age is separate and distinct to his or her chronological age. Importantly, a low score was found to correlate with cognitive decline, implying that the molecular test could translate into a simple blood test to predict those most at risk of Alzheimer's disease or other dementias and suitable for taking part in prevention trials. A person's score was not, however, found to correlate with common lifestyle-associated conditions, such as heart disease and diabetes, and is therefore likely to represent a unique rate of ageing largely independent of a person's lifestyle choices.

However, the study does not provide insight into how to improve a person's score and thus alter their "biological age." While a low score could be considered as "accelerated ageing," an important aspect of the work suggests that ageing does not now need to be defined only by the appearance of disease. "Given the biological complexity of the ageing process, until now there has been no reliable way to measure how well a person is ageing compared with their peers. Physical capacity such as strength or onset of disease is often used to assess healthy ageing in the elderly but in contrast, we can now measure ageing before symptoms of decline or illness occur. We now need to find out more about why these vast differences in ageing occur, with the hope that the test could be used to reduce the risk of developing diseases associated with age."

Thursday, September 10, 2015

This open access review covers attempts by the research community to produce a cell therapy to treat Parkinson's disease, a condition driven by the accelerated loss of a small but vital population of brain cells. This loss happens to everyone over the course of aging to a much lesser degree, and thus progress towards treatments is of general interest. In theory these lost cells could be replaced, but in practice getting to the point of a reliable treatment along those lines is entwined with the ongoing development of stem cell medicine as a whole. Robust methods of cell production, transplant, and engineering, along with sufficiently comprehensive knowledge of cell biology to steer this work are all still in progress, further along for some types of cell and tissue, less well advanced for others:

Parkinson's disease (PD) is one of the most common neurodegenerative disorders of aging, affecting about 1% of the population aged 60 years and older and 3-5% of the population above the age of 85. The various disruptions in motor control typically appear when 60-80% of dopamine (DA) neurons in the substantia nigra are degenerated. Because DA neurons degenerate to cause a drop in dopamine release, current treatments for PD include dopamine replacement drugs and deep brain stimulation (DBS) to the nucleus subthalamicus. Even though dopamine replacement drugs and DBS are effective in improving the symptoms of the patients, they cannot stop the disease progression. Moreover, current medications can cause the development of involuntary muscle movements, effectively "overshooting" the clinical symptoms of PD.

Recent research progress has provided treatment potential through replacing lost DA neurons using neural stem cells (NSCs) or fully differentiated DA neurons from fetal brain tissue, embryonic stem cells (ESCs), mesenchymal stem cells (MSCs) sourced from adults or fetuses, and induced pluripotent stem cells (iPSCs) reprogrammed from patients' somatic fibroblasts or blood cells. Much work has been done to adapt cells from various sources to potential clinical applications to improve treatments for neurodegenerative diseases including PD. NSCs and DA neurons from fetal brain and hESCs are not suitable for clinical use because of their immune-rejections and ethical issues. The availability of iPSCs and iDA neurons paved the road for autologous cell-based therapy of PD. However, several aspects of iPSCs need to be resolved before they go to clinical use. These include low yields of DA neurons, genetic and epigenetic abnormalities, and the safety of iPSC-derived cells.

Cell replacement therapy is a promising avenue for the treatment of PD and other neurodegenerative disorders. The use of all cell sources derived is fraught with ethical, logistical, and safety concerns. However, scientific research is making great progress in the development and characterization of iPSC derived cells for PD. iPSCs and their derivatives injected into animal models have shown promise in treatment of disorders such as PD; however, iPSCs have not been used in clinical trials for PD. There are some limitations/disadvantages associated with iPSCs. A relevant therapeutic progenitor or mature cell type may be identified and grafted in such treatments; in the case of PD, the options are, of course, iPSC-derived NSCs and iPSC-derived DA neurons. Theoretically, these two should act just like their non-iPSC derived counterparts - in actuality, because of the concerns mentioned above, the unique iPSC heritage of such cells sometimes poses its own unique set of problems.

Pre-clinical studies on viability might also be necessary to establish the scope of the treatment. iPSCs would not be moved to clinical trials at least until iPSCs are better understood and efficient and safe methods for reprogramming and gene correction are developed. The pace of progress will no doubt continue to speed along in the years to come, and it is therefore quite likely that within our lifetime we will witness the jump from dish to clinic.

Friday, September 11, 2015

This is one example of many new approaches to delivering therapeutic proteins into the brain. In this case the aim is to spur greater regeneration and cell resilience in order to compensate for neurodegenerative processes underlying diseases such as Parkinson's:

Researchers genetically modified white blood cells called macrophages to produce glial cell-derived neurotrophic factor, or GDNF, and deliver it to the brain. Glial cells provide support and protection for nerve cells throughout the brain and body, and GDNF can heal and stimulate the growth of damaged neurons. "Currently, there are no treatments that can halt or reverse the course of Parkinson's disease. There are only therapies to address quality of life, such as dopamine replacement. However, studies have shown that delivering neurotrophic factor to the brain not only promotes the survival of neurons but also reverses the progression of Parkinson's disease." In addition to delivering GDNF, the engineered macrophages can "teach" neurons to make the protein for themselves by delivering both the tools and the instructions needed: DNA, messenger RNA and transcription factor.

Successfully delivering the treatment to the brain is the key to the success of GDNF therapy. Using immune cells avoids the body's natural defenses. The repurposed macrophages are also able to penetrate the blood-brain barrier, something most medicines cannot do. The reprogrammed cells travel to the brain and produce tiny bubbles called exosomes that contain GDNF. The cells release the exosomes, which then are able to deliver the proteins to neurons in the brain.

Friday, September 11, 2015

Here I'll point out an open access paper on Wnt signaling in aging. The full paper is PDF format only at the present time. The Wnt signaling pathway plays a range of important roles in embryonic development, cancer, and regeneration. It also changes over the course of aging, one of countless specific reactions to accumulated cell and tissue damage, and these changes are thought to be a part of the characteristic decline in stem cell activity that takes place in later life. Less stem cell activity means less tissue maintenance and the gradual failure of organ function and integrity. There is considerable interest in the scientific community in finding ways to restore tissue maintenance, but most of those involved do not address the underlying damage that causes aging, instead seeking to override some of the reactions to that damage.

Here, however, researchers are looking at the merits of exercise in the context of Wnt signaling and tissue maintenance in old age. There is ample evidence to show that regular exercise is beneficial for even extremely old individuals, and its effects on Wnt signaling may be one of the reasons why this is the case:

Aging is an inevitable physiological process that leads to the dysfunction of various tissues, and these changes may contribute to certain diseases, and ultimately death. Recent research has discovered biological pathways that promote aging. This review focuses on Wnt signaling, Wnt is a highly conserved secreted signaling molecule that plays an essential role in the development and function of various tissues, and is a notable factor that regulates aging. Although Wnt signaling influences aging in various tissues, its effects are particularly prominent in neuronal tissue and skeletal muscle. In neuronal tissue, neurogenesis is attenuated by the downregulation of Wnt signaling with aging. Skeletal muscle can also become weaker with aging, in a process known as sarcopenia. A notable cause of sarcopenia is the myogenic-to-fibrogenic transdifferentiation of satellite cells by excessive upregulation of Wnt signaling with aging, resulting in the impaired regenerative capacity of aged skeletal muscle.

However, exercise is very useful for preventing the age-related alterations in neuronal tissue and skeletal muscle. Upregulation of Wnt signaling is implicated in the positive effects of exercise, resulting in the activation of neurogenesis in adult neuronal tissue and myogenesis in mature skeletal muscle. Although more investigations are required to thoroughly understand age-related changes and their biological mechanisms in a variety of tissues, this review proposes exercise as a useful therapy for the elderly, to prevent the negative effects of aging and maintain their quality of life.


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