Fight Aging! Newsletter, November 12th 2012

November 12th 2012

The Fight Aging! Newsletter is a weekly email containing news, opinions, and happenings for people interested in aging science and engineered longevity: making use of diet, lifestyle choices, technology, and proven medical advances to live healthy, longer lives. This newsletter is published under the Creative Commons Attribution 3.0 license. In short, this means that you are encouraged to republish and rewrite it in any way you see fit, the only requirements being that you provide attribution and a link to Fight Aging!



- More Researchers Should Talk About Bold Goals in Human Longevity
- The Greatest Instance of the Broken Window Fallacy
- Regenerative Medicine Timelines from Anthony Atala
- Many Longevity Manipulations Appear to Work Via Insulin Signaling
- Discussion
- Latest Headlines from Fight Aging!
    - Work on Better Understanding Oxidative Damage in Aging
    - Towards Tissue Engineered Large Intestines
    - Lower Vitamin D Levels Correlated to Human Longevity
    - Hypothesizing a Link Between Taste Receptors and Longevity
    - Some Visible Signs of Aging Reflect Biological Age
    - Quantifying Gains in Life Expectancy Correlated With Exercise
    - Compression of Morbidity Through Physical Activity
    - The Mechanism of Blind Mole Rat Cancer Immunity
    - Lifestyle Choices and the Pace of Age-Related Memory Decline
    - Another Example of a Mitochondrially Targeted Antioxidant


It's been a good few years since Aubrey de Grey first put forward his view of the political and social processes that inhibit progress in longevity science: the short summary is that a sort of logjam is created and sustained by the silence of researchers. When scientists don't talk openly about bold goals in their field then there can be no broad public support for funding of those goals, and conservative funding organizations will assign resources to other projects. There are many players in the grand game of scientific progress, but it ultimately falls to the researchers to define the bounds of the possible in the public eye, and it is their pronouncements - or lack thereof - that set the limits of what can be easily funded.

When researchers sit back and say nothing, or restrict themselves to visions of incremental gain when far more is possible, then progress suffers. There are many reasons as to why members of the aging research community were for decades very reluctant to talk about extending human life at all: fear of being associated with the fraudulent "anti-aging" marketplace, the normal reluctance to place a flag far out on the field even in an age of radical change, and so forth. Until very recently, the ethos of aging research was observation and little more, amounting to a stifling of research into extending the healthy human life span. Who can say how much of an opportunity was lost? Certainly the chance to build an aging research community with the same breadth and eagerness to produce measurable results as the cancer research community; that opportunity was squandered, and that task still lies ahead.

The old attitudes have largely thawed, however, in the face of a combination of persistent advocacy (such as that of the Methuselah Foundation and supporters) and many demonstrations of extended healthy life in laboratory animals. It has been welcome, these past few years, to see more researchers willing to step up to the plate to talk in public about radical life extension and pushing the boundaries of what can be achieved through biotechnology.


We as a species are defined by our ability to create: given time we will build new wonders from all the matter we can lay our hands on. The true legacy of every generation is the new advances they create in technology - that progress in creation is the only thing likely be recalled in the distant future. Yet despite a history of creation piled upon creation, the urge to destroy is also strong; a certain love of destruction seems a hardwired part of human nature. See the broken window fallacy, for example, which is the 19th century formulation of an ancient truth: that people look upon the consequences of destruction selectively, and call it beneficial.

"Suppose it cost six francs to repair the [window broken by a child], and you say that the accident brings six francs to the glazier's trade - that it encourages that trade to the amount of six francs - I grant it; I have not a word to say against it; you reason justly. The glazier comes, performs his task, receives his six francs, rubs his hands, and, in his heart, blesses the careless child. All this is that which is seen. ... It is not seen that as [the owner of the window] has spent six francs upon one thing, he cannot spend them upon another. It is not seen that if he had not had a window to replace, he would, perhaps, have replaced his old shoes, or added another book to his library. In short, he would have employed his six francs in some way, which this accident has prevented."

The lesson of the broken window is that destruction is never beneficial. It is a cost, and that cost must be paid at the expense of some other benefit. This lesson is needed: the broken window fallacy was widespread two centuries ago and remains so now. You will hear commentary after every natural disaster suggesting that the resulting expenditures on repair will benefit the economy, for example.

What is the greatest ongoing disaster, the cause of the greatest destruction? The answer is degenerative aging. Aging destroys human capital: knowledge, skills, talents, the ability to work, the ability to create. It does so at a ferocious rate, a hundred thousand lives a day, and all that they might have accomplished if not struck down. If translated to a dollar amount, the cost is staggering - even shifts in life expectancy have gargantuan value. And why shouldn't they? Time spent alive and active is the basis of all wealth.

It is unfortunate, but many people advocate for the continuation of aging, for relinquishment of efforts to build medicines to extend health life. Among these are people who welcome aging and death because to their eyes it gives a young person the chance to step into a role vacated by an older person. This is another form of the broken window, however: the advocate for aging looks only at the young person, and dismisses what the older person might have done were they not removed from the picture by death or disability. So too, any apologism for aging based on clearing out the established figures because it provides a greater opportunity for younger people to repeat the same steps, follow the same paths, relearn the same skills, redo the same tasks ... these arguments are the broken window writ large.

Vast wealth and opportunity bleeds into the abyss on a daily basis, destroyed because the people who embody that wealth and opportunity decay and die. We would all be wealthier by far given the medical means to prevent these losses. In your thoughts on aging, don't ignore the vast invisible costs - the work never accomplished, the wonders never created, because those who could have done so never had the chance. The enforced absence of the age-damaged, the frail, the disabled, and the dead is in and of itself a form of damage; the loss of their skills and knowledge is something that must be repaired. That requires work and resources that might have gone to new creations, rather than catching up from loss.

So this continues, and the perpetual devotion of resources to repair and recover from the losses of death and disability is a great ball and chain shackled to our ability to create progress. But most people don't think of at all - it is invisible to them. Nonetheless, the costs of aging that we labor under are so vast that the introduction of ways to rejuvenate the old will lead to an blossoming of wealth and progress the likes of which has never before been seen.


Anthony Atala is one of the present luminaries of tissue engineering, or at least that part of the field focused on building replacement organs and pseudo-organs - the latter being tissue structures that are not exactly the same as what they replace, but still get the job done, such as the substitute bladder tissue manufactured by Tengion. Atala is also on the SENS Foundation research advisory board, and so can be seen to look favorably on the agenda of engineering longer healthy human life spans.

I notice that a recent article has Atala giving some thoughts on timelines for organ regrowth, which you might compare to similar thoughts from another figure in the field, and to speculative timelines for the use of animal organs, such as those grown in engineered chimeras. Researchers are usually fairly reticent to put times and timelines on the table in public, for all the obvious reasons, so I think it worth taking note when they do:

Right now, more than 116,000 people are on the U.S. organ transplant waiting list. But what if they could just regrow their own livers, hearts, and kidneys, even 3-D print them? Anthony Atala, the director of the Wake Forest Institute for Regenerative Medicine, is working to make that a reality. Speaking today at Ciudad de las Ideas, an annual conference about big ideas held in Puebla, Mexico, and sponsored by Grupo Salinas, Atala asked, "If a salamander can do it, why can't we?"

So how long until regenerative medicine can make the agonizingly long transplant waiting list a thing of the past? Within the next decade, Atala predicts, "we will see partial replacements of [some] organs - not the entire replacement, but many times that's all we need." Of course, [the] regulatory process will have to be carried out before there is widespread use of regenerated organs. Atala notes that the average drug takes 15.5 years to be approved in the United States, and regenerative medicine is neither drug nor medical device, but a combination thereof, which makes approval even more complicated.


There are many ways to manipulate a single protein or gene in lower animals in order to modestly slow aging and extend life, and new ones are discovered on a regular basis. This process of discovery tends to proceed more rapidly for short-lived laboratory species like flies and nematode worms, where evaluating alterations in life span requires less time and fewer resources. Thus more and more diverse studies can be conducted within a given budget in comparison to, say, work in mice.

So: genes can be mutated via genetic engineering, or removed, or doubled up. An individual protein produced from a genetic blueprint can be created more rapidly so as to boost its presence in cells or its production dialed back to lower levels. This is not an exhaustive list. Any of these possibilities can be targeted to specific cell types or portions of anatomy, if so desired. There are far more combinations to tinker with than the research community has capacity for, so researchers tend to work in areas that have already demonstrated some promise, or where the maps of function and interaction between protein machinery are better understood.

Even seemingly trivial functions in the metabolism of lower animals are enormously complex in their details. Anything of the subsystems involved in how food is converted into something that cells can use for energy, for example, or how body temperature is regulated. These evolved systems make use of overlapping feedback loops that might involve dozens or hundreds of proteins, and any given protein might be promiscuously involved in several quite different systems; if our biology teaches us anything it is that evolution favors the reuse of existing materials. A great example is p53, which shows up as a player in many of the central, crucial processes of cellular biology.

Alter the amount of a protein in circulation and that ripples out through all the networks of protein machinery that it is in involved with. You can't flip any switch in isolation. This diversity of components in every biological system is one of the reasons why there are seemingly so many different ways to alter life span in lower animals. There might be only a few important networks of proteins tightly coupled to determination of life span, such as that involved in the calorie restriction response, but within each network there are possibly dozens of proteins that can be tweaked to produce some form of beneficial effect on the whole - and of course varying degrees of side-effects.

So when researchers uncover yet another life extending methodology, they must then chase cause and effect through networks of interacting protein machineries until they get to something that looks familiar - which they usually do. One very well studied area is the network of insulin and insulin-like growth factor (IGF) signaling, and as is the case for increased autophagy, many diverse longevity enhancing alterations touch on this machinery.


The highlights and headlines from the past week follow below. Remember - if you like this newsletter, the chances are that your friends will find it useful too. Forward it on, or post a copy to your favorite online communities. Encourage the people you know to pitch in and make a difference to the future of health and longevity!



Friday, November 9, 2012
Oxidative stress is a term you'll see a lot when reading the literature of aging research. The more reactive oxidant compounds there are in a cell, the more they will react with important proteins, modifying them and thus causing cellular machinery to run awry or require repair. Aging is characterized by rising levels of oxidative stress, caused by things such as increased presence of metabolic byproducts that are ever more inefficiently removed, accumulating damage to mitochondria, and so forth. This is still something of a high level picture, however, and there is still a lot of room left for researchers to expand the understanding of how exactly oxidative damage progresses, or how it contributes to specific manifestations of aging, such as increased cellular senescence. Hence we see work of this nature: "Protein damage mediated by oxidation, protein adducts formation with advanced glycated end products and with products of lipid peroxidation, has been implicated during aging and age-related diseases, such as neurodegenerative diseases. Increased protein modification has also been described upon replicative senescence of human fibroblasts, a valid model for studying aging in vitro. However, the mechanisms by which these modified proteins could impact on the development of the senescent phenotype and the pathogenesis of age-related diseases remain elusive. In this study, we performed in silico approaches to evidence molecular actors and cellular pathways affected by these damaged proteins. A database of proteins modified by carbonylation, glycation, and lipid peroxidation products during aging and age-related diseases was built and compared to those proteins identified during cellular replicative senescence in vitro. Common cellular pathways evidenced by enzymes involved in intermediate metabolism were found to be targeted by these modifications, although different tissues have been examined. ... An important outcome of the present study is that several enzymes that catalyze intermediate metabolism, such as glycolysis, gluconeogenesis, the citrate cycle, and fatty acid metabolism have been found to be modified. These results indicate a potential effect of protein modification on the impairment of cellular energy metabolism. Future studies should address this important issue by combining metabolomics and targeted proteomic analysis during cellular and organismal aging."

Friday, November 9, 2012
Last year a research group demonstrated that they could build tissue engineered sections of small intestine in mice. That same group is also working on producing structures of the large intestine using human cells, and here is an update on their progress: "[Researchers] have for the first time grown tissue-engineered human large intestine. ... Our aim is exact replacement of the tissue that is lacking. There are many important functions of the large intestine, and we can partially compensate for that loss through other medical advances, but there are still patients for whom this technology might be revolutionary if we can cross the translational hurdles. This is one of the advances that brings us toward our goal. The human tissue-engineered colon includes all of the required specialized cell types that are found in human large intestine. The research team grew the tissue-engineered large intestine from specific groups of cells, called organoid units that were derived from intestinal tissue normally discarded after surgery. The organoid units grew on a biodegradable scaffold. After 4 weeks, the human tissue-engineered colon contained the differentiated cell types required in the functioning colon, and included other key components including smooth muscle, ganglion cells, and components of the stem cell niche. ... This proof-of-concept experiment is an important step in transitioning tissue-engineered colon to human therapy."

Thursday, November 8, 2012
This research result is noted because it stands in opposition to the present consensus on vitamin D and long term health in humans; the evidence to date supports a correlation between higher levels of vitamin D, a lower risk of age-related disease, and a longer life expectancy. But here we see the opposite result. This sort of outright contradiction is usually indicative of some greater complexity under the hood yet to be outlined and understood - and there's certainly no shortage of complexity in metabolism: "Low levels of 25(OH) vitamin D are associated with various age-related diseases and mortality, but causality has not been determined. We investigated vitamin D levels in the offspring of nonagenarians who had at least one nonagenarian sibling; these offspring have a lower prevalence of age-related diseases and a higher propensity to reach old age compared with their partners. We [assessed] vitamin D levels, [dietary] vitamin D intake and single nucleotide polymorphisms (SNPs) associated with vitamin D levels. We included offspring (n = 1038) of nonagenarians who had at least one nonagenarian sibling, and the offsprings' partners (n = 461; controls) from the Leiden Longevity Study. The offspring had significantly lower levels of vitamin D (64.3 nmol/L) compared with controls (68.4 nmol/L), independent of possible confounding factors. ... Compared with controls, the offspring of nonagenarians who had at least one nonagenarian sibling had a reduced frequency of a common variant in the CYP2R1 gene, which predisposes people to high vitamin D levels; they also had lower levels of vitamin D that persisted over the 2 most prevalent genotypes. These results cast doubt on the causal nature of previously reported associations between low levels of vitamin D and age-related diseases and mortality."

Thursday, November 8, 2012
Since calorie intake has a comparatively large impact on natural variations in life expectancy, any genetic difference that systematically reduces calorie intake in some way should be correlated with increased longevity. So how about differences in the genes that determine taste? Here researchers search for signs of that correlation: "Several studies have shown that genetic factors account for 25% of the variation in human life span. On the basis of published molecular, genetic and epidemiological data, we hypothesized that genetic polymorphisms of taste receptors, which modulate food preferences but are also expressed in a number of organs and regulate food absorption processing and metabolism, could modulate the aging process. Using a tagging approach, we investigated the possible associations between longevity and the common genetic variation at the three bitter taste receptor gene clusters on chromosomes 5, 7 and 12 in a population of 941 individuals ranging in age from 20 to 106 years from the South of Italy. We found that one polymorphism, rs978739, situated 212 bp upstream of the TAS2R16 gene, shows a statistically significant association with longevity. In particular, the frequency of A/A homozygotes increases gradually from 35% in subjects aged 20 to 70 up to 55% in centenarians. These data provide suggestive evidence on the possible correlation between human longevity and taste genetics." Given the broad role of this gene, the correlation with longevity may or may not have anything to do with a tendency to reduce calorie intake through differences in food preference.

Wednesday, November 7, 2012
As one might expect, some of the easily measurable, more visible signs of aging tend to reflect a correspondingly greater risk of age-related conditions. Aging is a body-wide process, after all. Different people age at modestly different rates, predominantly due to lifestyle choices involving diet and exercise these days, now that the burden of infectious disease is greatly reduced. Genetic differences do contribute to some degree, but appear to be more important in survival at old age. The aim of any meaningful advance in longevity science is to make all of these natural differences irrelevant, washed out by the benefits of therapies that can slow or reverse various aspects of degenerative aging: "In a new study, those who had three to four aging signs - receding hairline at the temples, baldness at the head's crown, earlobe crease, or yellow fatty deposits around the eyelid (xanthelasmata) - had a 57 percent increased risk for heart attack and a 39 percent increased risk for heart disease. ... "The visible signs of aging reflect physiologic or biological age, not chronological age, and are independent of chronological age." Researchers analyzed 10,885 participants 40 years and older (45 percent women) in the Copenhagen Heart Study. Of these, 7,537 had frontoparietal baldness (receding hairline at the temples), 3,938 had crown top baldness, 3,405 had earlobe crease, and 678 had fatty deposits around the eye. In 35 years of follow-up, 3,401 participants developed heart disease and 1,708 had a heart attack. Individually and combined, these signs predicted heart attack and heart disease independent of traditional risk factors. Fatty deposits around the eye were the strongest individual predictor of both heart attack and heart disease. Heart attack and heart disease risk increased with each additional sign of aging in all age groups and among men and women. The highest risk was for those in their 70s and those with multiple signs of aging."

Wednesday, November 7, 2012
In recent years a number of studies have tried to put numbers to the gains in life expectancy that might accompany exercise. Here is another: "In pooled data from six prospective cohort studies, the researchers examined associations of leisure-time physical activity of a moderate to vigorous intensity with mortality. They analyzed data from more than 650,000 subjects and followed subjects for an average of ten years - analyzing over 82,000 deaths. Participation in a low level of leisure time physical activity of moderate to vigorous intensity, comparable to up to 75 min of brisk walking per week, was associated with a 19 percent reduced risk of mortality compared to no such activity. Assuming a causal relationship, which is not specifically demonstrated in this research, this level of activity would confer a 1.8 year gain in life expectancy after age 40, compared with no activity. For those who did the equivalent to 150 min of brisk walking per week - the basic amount of physical activity currently recommended by the federal government - the gain in life expectancy was 3.4 years. Participants faring best were those who were both normal weight and active: among normal weight persons who were active at the level recommended by the federal government, researchers observed a gain in life expectancy of 7.2 years, compared to those with a BMI of 35 or more who did no leisure time physical activity." You might compare these results to those obtained from a study of highly trained athletes and work examining jogging and life expectancy.

Tuesday, November 6, 2012
Compression of morbidity is a hypothesis suggesting that advances in medical science are causing, or will cause, a compression of the terminal period of frailty, illness, and disability at the end of life, squeezing it into an ever-shorter fraction of the overall human life span. In colloquial use compression of morbidity is often spoken of as a practical goal by medical researchers who do not wish to talk openly about extending human life for political or funding reasons. There is data to support the existence of compression of morbidity with respect to the effects of lifestyle choices on longevity, such as exercise. When it comes to advances in medical science, however, it seems unlikely that gains in life expectancy will forever lag behind gains in health. Consider aging in terms of accumulated damage, for example: if we find ways to repair that damage, then the overall life expectancy will increase, just as it does for any complex machine that is better maintained. In any case, here is an example of present data supporting a compression of morbidity through increased physical activity: ""Active aging" connotes a radically nontraditional paradigm of aging which posits possible improvement in health despite increasing longevity. The new paradigm is based upon postponing functional declines more than mortality declines and compressing morbidity into a shorter period later in life. This paradigm (Compression of Morbidity) contrasts with the old, where increasing longevity inevitably leads to increasing morbidity. We have focused our research on controlled longitudinal studies of aging. The Runners and Community Controls study began at age 58 in 1984 and the Health Risk Cohorts study at age 70 in 1986. We noted that disability was postponed by 14 to 16 years in vigorous exercisers compared with controls and postponed by 10 years in low-risk cohorts compared with higher risk. Mortality was also postponed, but too few persons had died for valid comparison of mortality and morbidity. With the new data presented here, age at death at 30% mortality is postponed by 7 years in Runners and age at death at 50% (median) mortality by 3.3 years compared to controls. Postponement of disability is more than double that of mortality in both studies. These differences increase over time, occur in all subgroups, and persist after statistical adjustment."

Tuesday, November 6, 2012
Blind mole rats, like naked mole rats, do not appear to suffer from cancer - an aspect of their biology that probably drives more research interest at the moment than their exceptional longevity. The cancer suppression mechanism in naked mole rats has been explored in recent years, but here researchers discover that blind mole rats have evolved a different method of achieving the same end: "Blind mole rats and naked mole rats - both subterranean rodents with long life spans - are the only mammals never known to develop cancer. Three years ago, [researchers] determined the anti-cancer mechanism in the naked mole rat. Their research found that a specific gene - p16 - makes the cancerous cells in naked mole rats hypersensitive to overcrowding, and stops them from proliferating when too many crowd together. "We expected blind mole rats to have a similar mechanism for stopping the spread of cancerous cells. Instead, we discovered they've evolved their own mechanism." [The researchers] made their discovery by isolating cells from blind mole rats and forcing them to proliferate in culture beyond what occurs in the animal. After dividing approximately 15-20 times, all of the cells in the culture dish died rapidly. The researchers determined that the rapid death occurred because the cells recognized their pre-cancerous state and began secreting a suicidal protein, called interferon beta. The precancerous cells died by a mechanism which kills both abnormal cells and their neighbors, resulting in a "clean sweep." [The next step is] to find out exactly what triggers the secretion of interferon beta after cancerous cells begin proliferating in blind mole rats. "Not only were the cancerous cells killed off, but so were the adjacent cells, which may also be prone to tumorous behavior. While people don't use the same cancer-killing mechanism as blind mole rats, we may be able to combat some cancers and prolong life, if we could stimulate the same clean sweep reaction in cancerous human cells.""

Monday, November 5, 2012
Longitudinal studies generally show the anticipated results when it comes to physical activity and age-related decline - if you are more active, you tend to exhibit a slower pace of decline. Education, intelligence, and wealth are also correlated with longer life and slower onset of frailty and disability, but unlike physical activity it is less clear as to what the root causes of these correlations might be: "[Data on] one thousand nine hundred fifty-four healthy participants aged 35 to 85 at baseline from the Betula Project [was used] to reveal distinct longitudinal trajectories in episodic memory over 15 years and to identify demographic, lifestyle, health-related, and genetic predictors of stability or decline. Memory was assessed according to validated episodic memory tasks in participants from a large population-based sample. ... Of 1,558 participants with two or more test sessions, 18% were classified as maintainers and 13% as decliners, and 68% showed age-typical average change. More educated and more physically active participants, women, and those living with someone were more likely to be classified as maintainers, as were carriers of the met allele of the catechol-O-methyltransferase gene. Less educated participants, those not active in the labor force, and men were more likely to be classified as decliners, and the apolipoprotein E ɛ4 allele was more frequent in decliners."

Monday, November 5, 2012
Mitochondria, the powerplants of the cell, generate damaging reactive oxygen species as a side-effect of their operation. Unfortunately, they are vulnerable to those very same reactive compounds, and some forms of resulting damage to proteins and genes can create dysfunctional cells that contribute to degenerative aging. The longer you live, the more of these dysfunctional cells you have, and the larger their harmful effects. This contribution to aging can be modestly slowed by use of antioxidants targeted to the mitochondria, as they will soak up some fraction of the oxidants generated before they cause damage. It is also the case that the effects of mitochondrial damage could be reversed entirely by some form of repair or replacement technology, and that would be a far better outcome. Nonetheless, a number of research groups are working on targeted antioxidants, compounds that are very different from generic antioxidants sold in stores. Ingested antioxidants that you can buy today do nothing for this issue of mitochondrial damage, and are arguably a net negative for long-term health because they interfere with the signaling processes that produced increased cellular maintenance in response to exercise or other forms of mild stress. Here is news of a recent addition to the research groups working on mitochondrially targeted antioxidants: "[Researchers] have designed a compound that suppresses symptoms of [Huntington's] disease in mice. The compound is a synthetic antioxidant that targets mitochondria, an organelle within cells that serves as a cell's power plant. Oxidative damage to mitochondria is implicated in many neurodegenerative diseases including Alzheimer's, Parkinson's, and Huntington's. The scientists administered the synthetic antioxidant, called XJB-5-131, to mice that have a genetic mutation that triggers Huntington's disease. The compound improved mitochondrial function and enhanced the survival of neurons. It also inhibited weight loss and stopped the decline of motor skills, among other benefits. In short, the Huntington's mice looked and behaved like normal mice. Defending mitochondria from reactive oxygen species is a tall order. That's because mitochondria are both the main target of these molecules, and a cell's primary source of them. In other words, mitochondria produce the very thing that damages them. Researchers have studied whether dietary supplements of natural antioxidants such as vitamin E and coenzyme Q can mitigate the harmful effects of reactive oxygen species on mitochondria. Natural antioxidants don't target specific tissue within the body, however. And they've been shown to yield only marginal benefits in human clinical trials. These lackluster results have driven scientists to develop synthetic antioxidants that specifically target mitochondria. A few years ago, [researchers] synthesized an antioxidant called XJB-5-131 that zeroes in on bacterial membranes, which are very similar to mitochondrial membranes. The scientists first injected Huntington's mice with XJB-5-131 and tested the mice's motor skills. ... We saw improvements across the board. The difference was amazing. XJB prevented the onset of weight loss and the decline in motor skills. Next, the researchers removed neurons from the Huntington's mice and cultured the cells in the presence of XJB-5-131. They found that XJB-5-131 significantly improved the survival of neuronal cultures compared to untreated neuronal cultures. [Researchers] studied the impacts of the compound on the mice's mitochondrial DNA. They discovered that XJB-5-131 dramatically lowered the number of lesions on the DNA, which is a sign of oxidative damage. They also tallied the number of mitochondrial DNA copies, which plummets in diseased mice. This number was restored back to normal in XJB-treated mice."



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