Beyond the era of biotechnology lies the era of pervasive computation and advanced nanotechnology, starting around 2030, I would imagine. Processing cycles will be ten thousand times more abundant than now and applications of molecular manufacturing will be tentatively emerging from the labs. This is the era in which the human brain will be reverse-engineered, the first strong artificial intelligences constructed, and perhaps most importantly, inroads made into the grail of radical life extension: incrementally replacing the biology of the brain with something more robust and damage-resistant.

I would get my neurons replaced (slowly, one at a time over time, to ensure continuity of the self) with some form of much more robust, easily maintained nanomachinery. That allows these sorts of engineering possibilities:

• Swapping out the body for whatever machinery of transport and support best minimizes risk
• Moving most of the business of life into simulation
• Physically separating my neurons while still remaining alive, conscious and active

It's that last point that's key, as physical locations have the same sort of issues with time, probability and bad events as people do. Meteorites happen, as do landslides, earthquakes and volcanoes. The way to reduce your risk function dramatically is to spread out. You can imagine a wireless brain (using whatever the most robust communications technology of the time happens to be be) scattered in a thousand separate locations across a continent, or the whole planet.

I notice that the Future of Humanity Institute has published a (PDF) roadmap to whole brain emulation (WBE) - a tiny step towards the visions outlined above. In intent it could be compared to SENS, or the work of Drexler, Freitas and others on the design of medical nanomachinery: a foundation of theory on which research strategies can be built.

As this review shows, WBE on the neuronal/synaptic level requires relatively modest increases in microscopy resolution, a less trivial development of automation for scanning and image processing, a research push at the problem of inferring functional properties of neurons and synapses, and relatively business‐as‐usual development of computational neuroscience models and computer hardware.

This assumes that this is the appropriate level of description of the brain, and that we find ways of accurately simulating the subsystems that occurs on this level. Conversely, pursuing this research agenda will also help detect whether there are low‐level effects that have significant influence on higher level systems, requiring an increase in simulation and scanning resolution.

There do not appear to exist any obstacles to attempting to emulate an invertebrate organism today. We are still largely ignorant of the networks that make up the brains of even modestly complex organisms. Obtaining detailed anatomical information of a small brain appears entirely feasible and useful to neuroscience, and would be a critical first step towards WBE. Such a project would serve as both a proof of concept and test bed for further development.

If WBE is pursued successfully, at present it looks like the need for raw computing power for real‐time simulation and funding for building large‐scale automated scanning/processing facilities are the factors most likely to hold back large‐scale simulations.

Posted by Reason at 8:03 PM
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A couple of papers to compare and contrast:

Melatonin in relation to the "strong" and "weak" versions of the free radical theory of aging:

While the data supporting a role for melatonin in forestalling aging and prolonging life span per se is not compelling, the findings related to melatonin's ability to reduce the severity of a variety of age-related diseases that have as their basis free radical damage is convincing.

Melatonin prevents age-related mitochondrial dysfunction in rat brain via cardiolipin protection

Melatonin has been shown to possess antioxidant properties and to reduce oxidant events in brain aging. .... We found [that a number of] mitochondrial parameters were significantly altered with aging, and that melatonin treatment completely prevented these age-related alterations. These effects appear to be due, at least in part, to melatonin's ability to preserve the content and structural integrity of cardiolipin molecules, which play a pivotal role in mitochondrial bioenergetics.

Which is interesting to say the least; I would have lumped melatonin in with all the other antioxidant supplements - just because a chemical happens to affect some aspects of your biochemistry doesn't mean that ingesting it is going to have any positive benefit.

I have to wonder at what complexity is hidden here: a mechanism completely prevents alterations in mitochondrial parameters, and yet doesn't do anything for life span? Compare that with antioxidant chemicals targeted directly to mitochondria, which lead to significant extensions of healthy life. Mitochondria are complex objects, and (a) the state of their membranes, (b) the working of their inner processing mechanisms, and (c) the effects they have on their cell are not linked in straightforward ways.

Posted by Reason at 6:27 PM
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The rational actor looks at risks to life and health ahead and acts to minimize those risks. Since we all have limited time and resources, we have to prioritize: we make lists, in our heads if nowhere else, putting the most likely and terrible outcomes up at the top. Highly unlikely but terrible outcomes don't receive much attention: meteors, lightning strikes, that sort of thing. Likely but merely unpleasant events might just be suffered as a cost of getting on with life: catching the flu is an obnoxious happenstance, but not particularly threatening for most of us. There are more important things to worry about while buying insurance and otherwise taking care of essentials.

So you end up with a list involving fires, car accidents, sudden implosion of the company you work for, that sort of thing. In that, most of us are not being terribly rational, as aging isn't on the list. It is absolutely going to happen, and it leads to the most terrible personal consequence possible - death - via numerous other very nasty personal consequences. Alzheimer's, heart disease, cancer, and all the rest. We all have a 100% chance of aging as things stand, and it's the worst thing that will happen to most of us. So why isn't it up near the top of that priority list?

On that subject, thoughts from a bioethicist I seem to be linking to a lot of late. Replace "we" with "I" and "society" with "an individual" and it works just fine:

the following four issues are vital:

1. The certainty of the harm (e.g. 0.1% vs 70% chance)
2. The severity of the harm (e.g. broken leg vs death)
3. The likelihood of mitigating the harm (e.g. 0.1% vs 70%)
4. The cost of mitigating the harm ($1 billion vs $1 trillion)

...

Aging increases one’s risk of disease and death. So the empirical evidence clearly shows that aging scores very high on (1) and (2). These facts alone show that aging is a BIG problem.

How about issues (3) and (4)? People are most likely to (mistakenly) assume aging research scores low on both these fronts. That is, people are skeptical that we can actually modify the biological processes of aging. But there are countless experiments in a variety of organisms that show aging is not immutable. And so the goal of retarding human aging scores reasonably well on (3). And once you add considerations (1) and (2) into the mix, it becomes evident that the current neglect of aging research is unjustified.

People will also falsely assume that (4) will require vast amounts of money. But here one must put things in their proper context. A lot of money compared to what? What we spend on national defence? National defense spending in the U.S. has reached approximately $1,600 per capita, compared to $97 per capita for federal spending on biomedical research (source)

Which I think is a fair summary of where things stand - aging is terrible, but those who would act to materially support longevity science don't believe that progress is possible, or that progress is cost-effective. Meanwhile, individuals pledge significant time and money for food, entertainment, and geopolitical machinations. You might want to refresh your memory as to the Strategies for Engineered Negligible Senescence (SENS) cost breakdown: a billion dollars over ten years to develop the medical technologies capable of rejuvenating aged mice in the laboratory, each of the seven branches of SENS requiring something like $15 million per year over that time.

Effective research is cheap compared to almost everything else connected with aging: the loss of wealth, deteriorating health, loss of contributing members of society, the elderly care infrastructure, and more. It's a great pity that support and fundraising lags so far behind the potential of longevity science.

Posted by Reason at 7:30 PM
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Mainstream research on the biochemistry of aging and longevity - with an eye to slowing down aging rather than repairing it - is at this time primarily focused on a small number of areas. One is the cluster of mechanisms and signaling pathways associated with insulin and insulin-like growth factor 1 (IGF-1). You might recall that a tenfold increase in nematode life span was engineered via manipulation of IGF-1, for example:

Reis' team discovered that a mutant in the insulin/ IGF-1 pathway of C. elegans slows development but ultimately produces adults he described as "super survivors," able to resist levels of toxic chemicals that would kill an ordinary worm. Although the adult lifespan of C. elegans is normally only two to three weeks, half of the mutant worms were still alive after six months, with some surviving to nine months.

While perusing PubMed, I noticed a couple of papers on insulin, IGF-1, and aging:

Insulin and aging

In invertebrates, signaling pathways homologous to mammalian insulin and insulin-like growth factor (IGF-1) signal transduction have a major role in the control of longevity. There are numerous indications that these pathways also influence aging in mammals, but separating the role of insulin from the effects of IGF-1 and growth hormone (GH) is difficult.

In mice, selective disruption of the insulin receptor in the adipose tissue extends longevity. Increases in lifespan were also reported in mice with deletion of insulin receptor substrate 1 (IRS1) in whole body or IRS2 only in the brain. GH deficiency or resistance in mutant mice leads to hypoinsulinemia and enhanced insulin sensitivity along with remarkably extended longevity.

These characteristics resemble animals subjected to calorie restriction. Studies of physiological characteristics and polymorphisms of insulin-related genes in exceptionally long-lived people suggest a role of insulin signaling in the control of human aging.

Role of the GH/IGF-1 axis in lifespan and healthspan: Lessons from animal models

Consistently, two interventions, caloric restriction and repression of the growth hormone (GH)/insulin-like growth factor-1/insulin axis, have been shown to increase lifespan in both invertebrates and vertebrate animal model systems. Caloric restriction (CR) is a nutrition intervention that robustly extends lifespan whether it is started early or later in life. Likewise, genes involved in the GH/IGF-1 signaling pathways can lengthen lifespan in vertebrates and invertebrates, implying evolutionary conservation of the molecular mechanisms.

Specifically, insulin and insulin-like growth factor-1 (IGF-1)-like signaling and its downstream intracellular signaling molecules have been shown to be associated with lifespan in fruit flies and nematodes. More recently, mammalian models with reduced growth hormone (GH) and/or IGF-1 signaling have also been shown to have extended lifespans as compared to control siblings. Importantly, this research has also shown that these genetic alterations can keep the animals healthy and disease-free for longer periods and can alleviate specific age-related pathologies similar to what is observed for CR individuals. Thus, these mutations may not only extend lifespan but may also improve healthspan, the general health and quality of life of an organism as it ages.

With the level of interest presently devoted to this subject, I imagine that a decade from now researchers will fully understand how IGF-1, insulin, growth hormone, and calorie restriction all fit together into the bigger picture of the natural range of metabolic processes in response to circumstances. Your diet and exercise choices change the way your biochemistry operates: the biochemical mechanisms by which this happens have a deep evolutionary history.

It seems evident that some large portion of the research community will continue to forge ahead with strategies to shift your metabolism into a better state for your long term health - replicating calorie restriction, or mutations known to be beneficial. This is not a path to radical extension of the healthy human life span, however. It will only produce modest gains. To move beyond the small goals, we have to aim to repair the damage of aging rather than just slow down its accumulation. It will be no harder to achieve from where we are now, and the rewards are far greater.

Posted by Reason at 7:17 PM
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The latest Rejuvenation Research is available online; I'm interested to note the contribution of another "social justice"-style bioethicist. Regular positive engagement with the ideas and goals of longevity science is a fairly recent phenomenon for that portion of the social studies crowd; while their ideas are just as contemptuous of freedom as the root of progress here as everywhere else, I view diversification as progress. There is some truth in the view that libertarian cliques get things started, but their goal only becomes a movement when the socialist masses finally join in with a clamor of "you must," "we should," and "there ought to be a law!"

It is usually the case that you will see sentences containing "should" and "we" in this way when you're being sold up the river. There exists some group of people who think you should live your life a certain way, regardless of your opinions on the matter, and this is a little of the manner in which they build up a rhetoric to justify their eventual use of force and constraint of law. Assumptions of inclusion and unity via "we" and assumptions of authority via "should." Neither are true; you're not a member of their little group unless you choose to be, and there is no authority beyond that which you grant them of your own choice.

Here's the social science paper that prompted this line of discussion:

The Normative Dimensions of Extending the Human Lifespan by Age-Related Biomedical Innovations:

The current normative debate on age-related biomedical innovations and the extension of the human lifespan has important shortcomings. Mainly, the complexity of the different normative dimensions relevant for ethical and/or juridicial norms is not fully developed and the normative quality of teleological and deontological arguments is not properly distinguished.

This article addresses some of these shortcomings and develops the outline of a more comprehensive normative framework covering all relevant dimensions. Such a frame necessarily has to include conceptions of a good life on the individual and societal levels. Furthermore, as a third dimension, a model for the access to and the just distribution of age-related biomedical innovations and technologies extending the human lifespan will be developed. It is argued that such a model has to include the different levels of the general philosophical theories of distributive justice, including social rights and theories of just health care. Furthermore, it has to show how these theories can be applied to the problem area of aging and extending the human lifespan.

It is unfortunate that human cultures seem so hardwired for inefficiency and waste - so much time spent on trying to justify coercion of others to attain your personally favored goals. Human nature is what it is, for now at least: best to keep plugging away at the problems you care about and do your best to hold up a decent set of standards by persuading rather than coercing.

Even if we could draft the masses to work to defeat aging, we should not do it; that would make us no better than those deathists who would set the agency of government to block research and mandate age-related death to their schedule.

Posted by Reason at 7:26 PM
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The human body is not a homogeneous mass, but rather a networked collection of very different structures and systems. Unsurprisingly, then, aging affects different tissues at different rates. This is just the same as in any engine, simple or complex: some components tend to fail due to accumulated damage more rapidly than others. For example:

The 80-year-old Norwegian received a cornea transplant fifty years ago, a piece of tissue now 123 years old that still works today. It could be the oldest eye, or even human body part, still functioning or to have ever been in use for so long. ... He had a cornea transplanted into his right eye in 1958, from a man born in June 1885. At the time it was expected to work for only 5 years. However, Reuters report that the procedure has been in use since the early 20th century. That means there could be even older corneas out there.

There is no profound lesson to be learned here, but this another useful example to present to people unfamiliar with the bounds of life span and survival in the natural world. If tortoises, whales, and this cornea can all manage such lengthy survival, it encourages the belief that medical research can engineer the same for human life in general. It is easier for people to accept that a goal can be accomplished based upon the evidence of a near example already in existence than in the absence of any example at all.

Posted by Reason at 6:47 PM
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What biological systems trigger the beneficial effects of calorie restriction? The response to limited calorie intake is an evolutionary adaptation to periods of famine that extends longevity in most species tested so far. The mechanisms that determine whether or not to trigger this response are still under investigation, but some intriguing results are surfacing. Last year, scientists demonstrated that sense of smell is important for calorie restriction in flies:

A team of scientists [found] that the average life span of fruit flies on restricted diets decreased when they were exposed to food odors. The findings [suggest] that the flies are "actually perceiving the environment," thinking they are in a nutrient-rich place and then their bodies are "adaptively responding to it."

A recent experiment demonstrates the opposite effect in nematode worms, another favored experimental animal:

Many animals live longer when raised on low calorie diets. But now [researchers] have shown that they can extend the life spans of roundworms even when the worms are well fed - it just takes a chemical that blocks their sense of smell.

...

it's possible that sensory perception cues have important metabolic consequences independent of what we actually eat. "Emerging evidence suggests that core metabolic pathways that modulate lifespan in worms also modulate lifespan in vertebrates such as mice and perhaps humans. Sensory pathways might also be fairly universal. In an ancient common ancestor, these pathways might have caused metabolic adjustments that affect lifespan. That could be reflected in our own biology."

It wouldn't be surprising to uncover some influence on the metabolic changes of calorie restriction from sensory systems in more complex animals like us - but whether or not it exists and is significant is pure speculation at this stage. It does present another possible place to start looking for ways to trick the body into enacting these changes independently of diet, however.

Posted by Reason at 6:17 PM
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Another thoughtful post from In Search of Enlightenment; always interesting to see how the other half of the healthy life extension community presents and interprets the ideas we hold in common:

When people ask me what I am working on I inevitably mention aging and the aspiration to retard human aging. This provokes many different responses. The most common response is a sense of surprise that we might actually be able to do something about aging. This is of course understandable, for if one had not been following the field of biogerontology for the past few years one might assume that aging is immutable, for that was a common belief. But this belief has been proven wrong- aging is not immutable.

Once I note this people often persist in their scepticism, and express doubt that we could actually develop a technology that could slow aging in humans (rather than just in mice). Again, this scepticism is understandable, indeed some scepticism is warranted. But I often ask them how much scepticism they have about finding a cure for cancer, or reversing climate change. And when it comes to these issues they are pretty optimistic about the likelihood that these goals could be achieved.

It's a long post and covers a lot of ground, so read the whole thing. The more people writing seriously on these issues, the better - and even more so when the community of writers displays a wide plurality of backgrounds and philosophies. These are signs of progress in the breadth of support for longevity research.

Posted by Reason at 7:40 PM
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One of the more interesting recent developments in tissue engineering is recellularization: removing all the cells from an organ, leaving only the extracellular matrix as a blueprint, and then repopulating that blueprint with cells from the patient who will receive the finished tissue. It's a clever way around our present inability to grow organs from scratch, or generate nanoscale scaffolds as complex as the extracellular matrix. As an added bonus, organs and tissue from animals can be used as the basis for a transplant.

I noticed a press release today that delves a little more into ongoing recellularization work outside the US, by a different group to that receiving the more recent press attention:

The three scientists were nominated for the development and successful transplantation of tissue engineered biological cardiac valves for children, which grow with the patients ... The "decellularised and re-colonised pulmonary valves" developed by Haverich and his team provide child patients with significantly improved chances of survival and a better quality of life. In Europe around 1,200 heart valve transplants a year are performed on children. The mechanical heart valves normally used in these operations have the disadvantage that they require lifelong blood thinning treatment and are susceptible to infections. The biological heart valves from pigs or cows used as an alternative are again only of limited durability. Children with heart valve defects therefore normally have to undergo multiple operations - with all the physical and psychological pressures and risks this entails.

Haverich and his colleagues, on the other hand, use heart valves that are "grown" from the young patient's natural body cells. To do this, a valve from a human or animal donor is removed of all cells using tissue engineering, so that only its outer framework remains. This valve matrix is then colonised with cells that have been obtained from the blood of the recipient and propagated. Within a few weeks, a quasi-natural heart valve then emerges in this bioreactor, that exhibits no rejection response or other faults, but instead grows with the patient after the implantation.

Recellularization makes xenotransplantation a much more viable technology to fill the tissue engineering gap prior to the ability to grow complex organs from scratch. Transplanting complex organs on demand is still a secondary target in the grand scheme of things, however - transplants are traumatic affairs, as for any major surgery. What we really want is sufficient control over our own cells that we can direct them to completely repair and regenerate existing organs.

Posted by Reason at 7:24 PM
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One of the effects of oppressive regulation in medical research is that animals have better access to cutting edge therapies than people:

Veterinary science continues to provide the shining example of where we could be with even just a little less waste, less socialism and less pointless, self-serving bureaucracy.

In the race to perfect 'regenerative medicine,' stem cell therapy for animals is ahead of treatment for humans because it is not so strictly regulated. It's not experimental - it's here. ... There are no side effects and no problems with rejection, because the patient is also the cell donor. ... I don't see any reason why humans aren't doing it."

Here is another example of the sort of work presently taking place in veterinary medicine, but that is many (government-enforced, largely unnecessary) trials away from reaching human clinics:

Tendon injuries can be career-killers for horses: only 5 to 15 percent of those with damaged tendons will ever make it back to the track, he says. But a novel treatment that Casey developed - injecting adult tendon cells grown in a lab into horses’ injured core lesions - has had remarkable success. The first 10 of 14 horses treated have returned to intensive training, and seven of these racers are back in full competition, he says. “We’re putting back natural tissue into a defect that has formed,” says Casey. “It’s minimally invasive. So far so good.”

...

They’re looking to take their findings in regenerative medicine in animals and apply them to humans. Think new treatments for stubborn injuries to areas like the Achilles tendon and rotator cuff. “Before the rotator cuff goes, we would be able to put tenocytes back into the tear and help heal,” says Casey.

Before that happens, however, there’s work to do, Casey says, including safety studies to determine that once injected, cells stay where they’re supposed to and don’t travel. Another would be to determine that the cellular signaling message to “turn on” or divide gets “turned off” again. Therapy Cells has hired a legal team in Washington, D.C. to work toward approval from the U.S. Food and Drug Administration. “It will revolutionize how you treat tendon injuries,” predicts Casey.

Casey says he and his team will await guidance from the FDA about the next steps to take. “But our first target is to hopefully gain FDA approval and in short order have human applications in human tendons,” he says. If that day arrives, he may finally end up with patients who can actually talk to him about their treatment.

Posted by Reason at 7:34 PM
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Following up on a post from a few days back on the benefits that the discovery of induced pluripotency is bringing to stem cell research, I thought I'd point out this article:

The first reports of the successful reprogramming of adult human cells back into so-called induced pluripotent stem (iPS) cells, which by all appearances looked and acted liked embryonic stem cells created a media stir. But the process was woefully inefficient: Only one out of 10,000 cells could be persuaded to turn back the clock.

Now, a team of researchers led by Juan Carlos Izpisua Belmonte at the Salk Institute for Biological Studies, succeeded in boosting the reprogramming efficiency more than 100fold, while cutting the time it takes in half. In fact, they repeatedly generated iPS cells from the tiny number of keratinocytes attached to a single hair plucked from a human scalp.

For a variety of reasons, technical and otherwise, inducing pluripotency in adult cells is within the present capacity of many more laboratories and researchers than embryonic stem cell research. More researchers means faster progress - as illustrated above. I expect to see a great deal of progress in the broader field of controlling our cells resulting from this line of work over the next few years.

Ultimately, the aim is to be able to understand and control the mechanism of potency - thus enabling any cell to be transformed into any other type of cell. The result of all this work would be low cost, efficient regenerative medicine. Age-damaged or injured tissue? No problem, just grow a fresh, undamaged replacement in culture from your own healthy cells.

Posted by Reason at 7:42 PM
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While differences in mitochondria are clearly very important to aging and longevity, this is not the case for all specific differences between your mitochondria and those of the person next to you. For example, take a look at this paper that draws on the Ashkenazi Jewish centenarian study:

Association of mitochondrial haplogroup J with longevity has been reported in several population subgroups. While studies from northern Italy and Finland, have described a higher frequency of haplogroup J among centenarians in comparison to non-centenarian, several other studies could not replicate these results and suggested various explanations for the discrepancy.

...

There does not exist a universal association of mitochondrial haplogroup J with longevity across all population groups.

It is not at all unreasonable to expect differences in mitochondria between genetic subgroups of the same species to influence longevity - even for the comparatively tiny biochemical changes involved in differentiating one haplogroup from another. Mitochondria are the engines of our cells, and numerous experiments have shown that altering their effective output of damaging free radicals can greatly influence healthy life in mammals. I can envisage future decades in which mitochondrial replacement is not just a matter of preventing the age-related degeneration caused by damaged mitochondria, but also upgrades your birth mitochondria to a more robust version - either discovered somewhere else in the human species or engineered de novo based on what is known at the time.

For all that, these are early days in the underlying science, and haplogroup J doesn't appear to be an important difference.

Posted by Reason at 8:20 PM
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There closer scientists look, the more ways they find for our aging stem cells to fail. Since stem cells are necessary to repair ongoing wear in our tissues, their loss of function is an important contributer to degenerative aging. My attention was drawn today to a novel discovery: a malfunction in the mechanisms of cell replication and differentiation that doesn't look much like any of the more familiar ways in which cells fail with age.

Asymmetric division of adult stem cells generates one self-renewing stem cell and one differentiating cell, thereby maintaining tissue homeostasis. A decline in stem cell function has been proposed to contribute to tissue ageing, although the underlying mechanism is poorly understood. Here we show that changes in the stem cell orientation with respect to the niche during ageing contribute to the decline in spermatogenesis in the male germ line of Drosophila.

Throughout the cell cycle, centrosomes in germline stem cells (GSCs) are oriented within their niche and this ensures asymmetric division. We found that GSCs containing misoriented centrosomes accumulate with age and that these GSCs are arrested or delayed in the cell cycle. The cell cycle arrest is transient, and GSCs appear to re-enter the cell cycle on correction of centrosome orientation.

On the basis of these findings, we propose that cell cycle arrest associated with centrosome misorientation functions as a mechanism to ensure asymmetric stem cell division, and that the inability of stem cells to maintain correct orientation during ageing contributes to the decline in spermatogenesis. We also show that some of the misoriented GSCs probably originate from dedifferentiation of spermatogonia.

So, translated to English from the Scientese: there is a fiddly, complex structure within stem cells upon which their most vital function - the generation of new cells - depends. This structure, the centrosome, only works when in the right relationship with the surrounding stem cell niche. As flies get older, more and more of stem cells fall out of this correct relationship.

Interestingly, we already know that the stem cell niche, the tissue in which stem cells are sustained, is important in the decline of stem cell function with aging - it's wrong to think of stem cells in isolation. The real mechanism in your body consists of an entire stem cell population plus the signaling and support mechanisms of the niche in which they are sustained. It's all connected.

This new finding will no doubt have scientists scratching their heads and digging in deeper. Are misaligned centrosomes a cause or effect - a symptom of other cellular damage, or a stand-alone form of decline? It will be interesting to find out.