The adaptation of muscle to endurance or resistance exercise is a highly variable trait in humans and animals. As a means to discover the molecular mechanisms that regulate endurance adaptations in skeletal muscle, our previous work utilized rodent models generated by selective breeding for low- or high-adaptive response to endurance exercise. The failure to improve aerobic capacity in low responders to endurance training occurred in conjunction with a less oxidative muscle phenotype and deficiencies in exercise-induced angiogenesis in skeletal muscle. Importantly, blunted endurance remodeling in the skeletal muscle of low responders to endurance exercise was associated with increased risk for chronic metabolic disease. Our data demonstrated that hyper-activation of the mitogen-activated protein kinase, c-Jun N-terminal kinase (JNK), was associated with the failure of muscle to undergo endurance remodeling with exercise. Thus, we hypothesized that JNK activation during exercise is a negative regulator of endurance adaptations in muscle.

The present investigation aimed to directly test the hypothesis that JNK is a critical mediator of muscle remodeling. We employed a multi-disciplinary approach to determine the effect of JNK hyper-activation and loss of function on muscle phenotype and remodeling, including tissue culture systems, animal models, and human subjects. This work identifies JNK as a molecular switch that, when active, stimulates muscle fibers to grow, leading to increased muscle mass. Conversely, when JNK is inhibited, an alternative adaptive program is induced, leading to endurance adaptations and enhanced aerobic capacity.

We find that JNK exerts its effects on muscle phenotype via phosphorylation of the transcription factor, SMAD2, at specific linker-region residues. JNK-mediated SMAD2 phosphorylation results in negative regulation of the myostatin/TGFβ pathway, thus allowing for muscle growth. In addition, we demonstrate that in human skeletal muscle, this JNK/SMAD signaling axis is activated by resistance exercise, but not endurance exercise, therefore identifying JNK/SMAD signaling as a target to induce muscle remodeling. These data enhance our understanding of the fundamental mechanisms that mediate muscle reprogramming and remodeling in vivo.

Polyamines including spermidine play an essential role in intermediate metabolism. Since they are synthesized by higher eukaryotic cells, they are not vitamins. However, the levels of polyamines are profoundly influenced by their external supply. Our groups have shown over the past decade that supplementing spermidine by adding it to culture media (as we did for the yeast Saccharomyces cerevisiae, the nematode Caenorhabditis elegans and the fruit fly Drosophila melanogaster) or to the drinking water (as we did for the rodent Mus musculus) is sufficient to extend longevity and to improve health span at multiple levels. Thus, in mice, the supplementation was able to suppress the age-related decline in cardiovascular function (as measured at 24 months of age) and increased overall longevity by approximately 10%.

The molecular and cellular mechanisms through which spermidine delays age-related disease and death have been elucidated to some extent. Spermidine can act as an inhibitor of EP300. EP300 acts as an inhibitor of autophagy by acetylating lysine residues within multiple proteins that are involved in autophagy-regulatory or autophagy-executing circuitries. As a result, the inhibition of EP300 by spermidine stimulates autophagy. Autophagy is required for the anti-aging effect of spermidine as indicated by the fact that genetic inhibition of autophagy abolishes the longevity-extending effects of spermidine on yeast, worms, and flies.

Until now the literature on the longevity-enhancing effects of spermidine has been limited to model organisms. Now, two prospective population-based studies report for the first time that nutritional spermidine uptake is also linked to reduced overall, cardiovascular and cancer-related mortality in humans. Both studies were based on the use of food questionnaires that allowed to calculate for each individual the nutritional uptake of polyamines including spermidine. Importantly, high spermidine uptake constituted an independent favourable prognostic parameter for reduced mortality, meaning that this variable predicted a reduced incidence of death even after correction for possible confounding factors.

In addition to the aforementioned epidemiological results, there are further, though admittedly indirect arguments in favour of a health-improving role for spermidine in human health. Thus, spermidine has been classified as a "caloric restriction mimetic" that has broad health-promoting effects due to its capacity to induce similar biochemical changes as does caloric restriction. Second, the proximal pharmacological target of spermidine is the same as that of salicylic acid, the active metabolite of aspirin (both inhibit EP300). The health-improving effects of aspirin have been initially attributed to act as an anti-coagulant. Since spermidine has not been reported to have similar anti-coagulant activity, we prefer the hypothesis that aspirin may mediate its broad pro-health effects via the inhibition of EP300.

Following Alzheimer's Disease (AD), synucleinopathies such as Parkinson's disease (PD) and dementia with Lewy bodies (DLB) are the second most common group of neurodegenerative disorders of the aging population. Overall, they represent heterogeneous group of neurological conditions, characterized by progressive accumulation of α-synuclein in neuronal and glial cells. The mechanisms through which the various species of α-synuclein aggregates lead to selective neurodegeneration and neuroinflammation is not completely understood. Transmission of α-synuclein aggregates from neuron-to-neuron and neuron-to-glia has been suggested as the underlying mechanism of the neurodegeneration and neuroinflammation in synucleinopathy.

We have previously shown that the oligomeric forms of extracellular α-synuclein interact with Toll-like receptor 2 (TLR2) on the surface of neurons and glial cells. This results in neuro-inflammatory responses with TNFα and IL-6 production. TLR2 belongs to a family of pattern recognition receptor which modulate responses to exogenous pathogens as well as endogenous misfolded proteins released following damage and cellular stress. In the central nervous system, TLR2 is expressed in glial cells and neuronal populations, and recent studies have shown that the levels of TLR2 are elevated in neurodegenerative disorders such as AD and PD.

We have recently shown that inhibition of TLR2 by gene deletion or siRNA-mediated knock down rescues the pathology associated with α-synuclein accumulation in cellular models and transgenic mice. Therefore, TLR2 and downstream signaling have been suggested a new therapeutic target for synucleinopathy. Neutralizing TLR2 with a monoclonal antibody has been recently shown to ameliorate the pathology in a murine model of AD.

The main objective of this study was to evaluate the therapeutic effects of targeting TLR2 with a functional inhibitory antibody (anti-TLR2). We show that the administration of anti-TLR2 was able to decrease the accumulation of neuronal and astroglial α-synuclein, resulting in reduced neuroinflammation, neurodegeneration, and behavioral deficits in an α-synuclein transgenic mouse model of PD/DLB. Moreover, the anti-TLR2 blocked neuron-to-neuron and neuron-to-astrocyte α-synuclein transmission and reduced pro-inflammatory responses in a cell based model. Therefore, TLR2 might be a viable target and TLR2 immunotherapy is a novel therapeutic strategy for synucleinopathies of the aging population.

Although sensorineural hearing loss (SNHL) can involve damage to either sensory cells or sensory neurons of the inner ear, a longstanding dogma in acquired SNHL was that loss of sensory cells is the primary event, and that degeneration of auditory nerve fibers (ANFs) occurs only secondarily to the loss of peripheral targets. This view arose because, after cochlear insults such as acoustic injury or ototoxic drugs, the degeneration of sensory cells can be seen within hours post-exposure, whereas degeneration of spiral ganglion cells (SGCs), the cell bodies of the ANFs, is not visible for weeks to months.

Animal work challenged the dogma by showing that hair cell loss in acquired SNHL is neither necessary nor sufficient for loss of ANFs. Firstly, in acoustic injury models, overexposures causing only reversible threshold shifts, and no hair cell loss, can nevertheless cause significant ANF degeneration. The neural damage is visible immediately as loss of synaptic connections between ANFs and inner hair cells (IHCs). In the aging mouse ear, as in the noise-damaged ear, it is the connections between SGCs and IHCs that degenerate first, rather than the hair cells themselves. This primary neural degeneration, or partial de-afferentation of IHCs, has negligible effect on thresholds until it exceeds 80-90%, thus it "hides" behind the audiogram.

The observation that ANF degeneration precedes and/or exceeds hair cell loss in animal models of acquired SNHL has suggested why two people with the same threshold audiogram, whether normal or abnormal, can have very different abilities to understand speech in a noisy environment. i.e. that partial de-afferentation of IHCs, a.k.a. "hidden hearing loss", compromises hearing ability in complex listening environments without changing the ability to detect a pure tone in quiet.

Here we take a direct approach to the question of whether hidden hearing loss is as important in humans as in animal models. We study temporal bones from a group of 20 "normal-aging" humans, ranging in age from birth to 86 years, without any explicit history or ear diseases or ototoxic exposures. We prepare these autopsy specimens in ways that allow us to accurately quantify the survival of hair cells and ANF peripheral axons in the same cochlear regions.

Mean loss of outer hair cells was 30-40% throughout the audiometric frequency range in subjects over 60 yrs, with even greater losses at both apical (low-frequency) and basal (high-frequency) ends. In contrast, mean inner hair cell loss across audiometric frequencies was rarely more than 15%, at any age. Neural loss greatly exceeded inner hair cell loss, with 7 of 11 subjects over 60 years showing more than 60% loss of peripheral axons, and with the age-related slope of axonal loss outstripping the age-related loss of inner hair cells by almost 3:1. The results suggest that a large number of auditory neurons in the aging ear are disconnected from their hair cell targets. This primary neural degeneration would not affect the audiogram, but likely contributes to age-related hearing impairment, especially in noisy environments. Thus, therapies designed to regrow peripheral axons could provide clinically meaningful improvement in the aged ear.

You have been an advocate for quite some time now; how successful do you think collective advocacy efforts have been over the years?

Not enough yet and not fast enough. The "pro-aging" narrative is, sadly, powerful. Defeating aging looks "too good to be true" and makes people feel uneasy. However, there are changes. For example, in the French-speaking world, sometimes we see articles about "amortalité" (life without senescence) in the press; a few years ago, you would see only articles speculating about billionaires wanting "immortality" (which makes people afraid).

In November, HEALES will organize the next Eurosymposium on Healthy Ageing (EHA). EHA and Undoing Aging each have a section focused on advocacy. Why did you decide to include it?

I think most scientists wanting big progress for longevity know that having public opinion on our side will help. Also, PR is useful in order to raise money. However, many scientists feel uneasy about these issues. That's why we decided to have a day dedicated to social aspects. Not all scientists will stay for the last day, and we will also try to reach a larger public on the last day. Another aspect is that Brussels is the European capital. One of our goals is to convince people there. Let's be honest: there is a long way to go. However, for a year or two now, some European civil servants who have been promoting "healthy aging" (we know it is an oxymoron) seem to be very interested in big data on health and scientific research. We will be keeping an eye on these developments.

You don't need to convince people that saving the lives of children is a good thing to do; however, you do need to convince them that saving elderly lives is a good thing. Why do you think this difference exists?

Nor do you need to convince people that defeating cancer or Alzheimer's disease would be good, but death by old age is a step too far. For me, the fundamental reason is a variant of Stockholm syndrome called the terror management theory. Death by old age is awful and unavoidable. We must think that longevity is not better, otherwise it would be too awful to die. This process is unconscious.

How far do you think we are from the point when people won't need persuading anymore, if ever?

Aubrey de Grey said it will be when a mouse becomes "immortal", because people will feel that rejuvenation therapies will be available soon. I think that it could be sooner if more and more scientists start to speak out more about it.

With some luck, the effects of first-generation rejuvenation therapies, such as senolytics, will be tangible soon. Assuming that the effects are measurably positive, how do you think the world will react to the news, and how do you think that this will affect advocacy?

It would be interesting even if senolytics have only a moderate effect. I think some groups who are not in the "longevity camp" will start asking to use them. Maybe, in some countries, they will even start asking for reimbursement from social security programs. Some groups on the other side will probably ask not to use these products or will stress risks, but it will be especially difficult for "deathists" to fight against senolytics, which are, in a way, very classical drugs.

Ageing in worms mainly results from the direct action of genes and not from random wear and tear or loss of function, and the same is likely to be true in humans, according to research. The study shows that normal biological processes which are useful early on in life, continue to 'run-on' pointlessly in later life causing age-related diseases. The deteriorative part of ageing, called 'senescence', is the main cause of disease and death worldwide as it leads to dementia, cancer, cardiovascular disease, and chronic obstructive pulmonary disease, but scientists have struggled to identify what causes it.

To address this, researchers have focused on discovering the basic principles of ageing by studying simple animals such as Caenorhabditis elegans, a nematode worm used in this study which lives on fruit, and dies of old age after only 2-3 weeks. Specifically, they focused on autophagy, where body cells consume their own biomass to recycle components and extract energy. They found that the worms' intestine consumes itself (autophagy) to create the yolk needed for eggs, and in elderly worms, this process causes severe deterioration of the intestine and obesity from a build-up of pooled fats. In turn, this further impacts on the health of the worm by promoting growth of tumours in the uterus, and shortens lifespan.

"This really surprised us since autophagy is usually thought to protect against ageing rather than cause it. It seems that worms crank-up autophagy, which is considered good, to maximise reproductive success, which is good too, but they end up overdoing it, causing senescence." When useful biological programmes run-on in later life, they can become disease-causing 'quasi-programmes'. Such programmes were recently proposed and the findings support that they are indeed a major underlying cause of ageing. This does not mean that aging is programmed but instead, that it is a continuation of developmental growth driven by genetic pathways to the point where these becomes harmful. Other examples include an increase in blood pressure causing hypertension and an increase to the eyes' near vision point causing long-sightedness and a need for reading glasses.

Autophagy is a process of destruction and processing of damaged cell components by the cells themselves. It is used by a cell to clean itself of excessive organelles and sometimes for programmed cell death. This adaptive mechanism supports a healthy phenotype on the cellular level. Autophagy is activated in certain cases of acute kidney failure (e.g., caused by the administration of antibiotics or anti-cancer drugs), sepsis, or kidney ischemia. Scientists already know that it is the activation of autophagy that reduces kidney damage manifestation.

However, while an organism is aging, the efficiency of autophagy declines as well. Though the number of lysosomes (the organelles that digest damaged cell components) is increased in old cells, they fail to perform their function. Oxidized proteins and damaged organelles (including mitochondria that participate in the respiration and energy production) start to pile up.

A team of scientists considered kidney pathologies that accompany aging - first of all, acute kidney failure that is several times more likely to be observed in patients over 60. "In our article we demonstrated that aging is associated with the accumulation of damaged biological structures (proteins, lipids, nucleic acids, organelles) in the kidney. The replacement of a young (healthy) phenotype with an old one takes place when a certain threshold level of such changes is reached."

Adults in their early 60s, who spend less time sitting and more time engaged in light to vigorous physical activity, benefit with healthier levels of heart and vessel disease markers. Physical inactivity is a well-known risk factor for cardiovascular disease and premature death from cardiovascular disease. Physical activity's protective effect is likely due in part to its impact on biomarkers in the blood that help predict atherosclerosis risk.

"The 60 to 64 age range represents an important transition between work and retirement, when lifestyle behaviors tend to change. It may, therefore, be an opportunity to promote increased physical activity. In addition, cardiovascular disease risk is higher in older adults. It's important to understand how activity might influence risk in this age group. We found it's important to replace time spent sedentary with any intensity level of activity."

Researchers studied more than 1,600 British volunteers, age 60 to 64, who wore heart rate and movement sensors for five days. The sensors revealed not only how much physical activity, in general, they were doing, but also how much light physical activity, such as slow walking, stretching, golfing, or gardening, versus moderate-to-vigorous activity, such as brisk walking, bicycling, dancing, tennis, squash, lawn mowing, or vacuuming.

Researchers analyzed participants' blood levels for markers of cardiovascular disease, including inflammatory markers and cholesterol markers. Each additional 10-minutes spent in moderate-to-vigorous intensity activity was associated with leptin levels that were 3.7 percent lower in men and 6.6 percent lower in women. Each additional 10-minutes spent sedentary was associated with 0.6 percent higher IL-6 levels in men and 1.4 percent higher IL-6 levels in women. Each additional 10-minutes spent in light intensity activity was associated with around 0.8% lower tissue-plasminogen activator levels in both men and women. Based on the study's findings, physical activity might lower cardiovascular disease risk by improving blood vessel function. Increased sedentary time may be adversely related to endothelial function.

One of the biggest risk factors for glaucoma is elevated pressure in the eye, which often occurs as people age and the ducts that allow fluid to drain from the eye become blocked. The disease often goes undetected at first; patients may not realize they have the disease until half of their retinal ganglion cells have been lost. Most treatments focus on lowering pressure in the eye (also known as intraocular pressure). However, in many patients, the disease worsens even after intraocular pressure returns to normal.

"That led us to the thought that this pressure change must be triggering something progressive, and the first thing that came to mind is that it has to be an immune response." To test that hypothesis, the researchers looked for immune cells in the retinas of mice exhibiting glaucoma and found that indeed, T cells were there. This is unusual because T cells are normally blocked from entering the retina, by a tight layer of cells called the blood-retina barrier, to suppress inflammation of the eye. The researchers found that when intraocular pressure goes up, T cells are somehow able to get through this barrier and into the retina.

The researchers generated high intraocular pressure in mice that lack T cells and found that while this pressure induced only a small amount of damage to the retina, the disease did not progress any further after eye pressure returned to normal. Further studies revealed that the glaucoma-linked T cells target proteins called heat shock proteins, which help cells respond to stress or injury. Normally, T cells should not target proteins produced by the host, but the researchers suspected that these T cells had been previously exposed to bacterial heat shock proteins.

The researchers then turned to human patients with glaucoma and found that these patients had five times the normal level of T cells specific to heat shock proteins, suggesting that the same phenomenon may also contribute to the disease in humans. The researchers' studies thus far suggest that the effect is not specific to a particular strain of bacteria; rather, exposure to a combination of bacteria can generate T cells that target heat shock proteins.

A recent publication shows that Cytomegalovirus (CMV) infection increases the risk of cardiovascular death by over 20% but no specific mechanisms explaining this effect were identified. CMV infection, however, is notorious for promoting large expansions of terminally differentiated effector T-cells, including CD4 T-cells. This is particularly observable in older people. Moreover, there is good evidence that terminally differentiated T-cells may cause vascular damage, to the extent that therapies specifically targeting T-cells in advanced atherosclerosis are being developed.

Among activated CD4 T-cells, cardiologists are particularly interested in CD28null CD4 T-cells. These terminally differentiated effector cells do not express CD28, a co-stimulatory receptor molecule, which antigen-presenting cells engage during early T-cell activation. CD28null CD4 T-cells were initially discovered in rheumatoid arthritis, but later associated with unstable angina and coronary artery plaque instability. Multiple links between these cells and cardiovascular complications have since been reported. Down-regulation of CD28 on CD4 T-cells is thought to be triggered by continuous/repetitive antigen exposure, which could be the result of a persistent viral infection, for example with CMV.

CD28null CD4 T-cells accumulate in older people and show reduced proliferative capacity among many other signs of cellular senescence. Large frequencies of these cells are, therefore, primarily attributed to normal (immune system) aging. While an association of CMV infection with increased numbers of CD28null CD4 T-cells was repeatedly reported in the literature, this link is generally considered to be indirect and explained by the fact that older people are more likely to be CMV infected. Nobody has yet studied CD28null CD4 or CD8 T-cells in a large enough number of CMV-seronegative (CMV-) older people to resolve this issue. However, several smaller studies in the fields of autoimmune and cardiovascular disease offer some insight.

It was not the purpose of our work to show that CD28null CD4 T-cells are associated with cardiovascular (CV) morbidity or mortality, since there is overwhelming evidence for this association in the literature. Instead, we examined the frequencies of CD28null CD4 T-cells in 93 CMV- and 122 CMV+ generally healthy older people and a corresponding cohort of young people; CD28null CD8 T-cells were evaluated in parallel. Our investigation was focused on the intriguing possibility that, independently of aging, CMV infection is a major risk factor for the expansion of the highly pro-atherogenic CD28null CD4 T-cell subset.

Our results show that CMV infection is significantly associated with the accumulation of CD28null CD4 T-cells. Our data further suggest that CMV may directly drive this subset with a significant proportion of these cells recognizing CMV-antigens. The frequencies of CD28null CD4 T-cells were an order of magnitude higher in CMV+ compared to CMV- individuals, but only marginally affected by age. These observations seem to refute the idea that accumulation of CD28null CD4 T-cells is a result of normal immune system aging.

Alzheimer's disease (AD) is the most frequent type of dementia. The pathological hallmarks of the disease are extracellular senile plaques composed of beta-amyloid peptide (Aβ) and intracellular neurofibrillary tangles composed of phosphorylated tau (pTau). These findings led to the "beta-amyloid hypothesis" that proposes that Aβ is the major cause of AD. Clinical trials targeting Aβ in the brain have mostly failed, whether they attempted to decrease Aβ production by BACE inhibitors or by antibodies. These failures suggest a need to find new hypotheses to explain AD pathogenesis and generate new targets for intervention to prevent and treat the disease.

Many years ago, the "infection hypothesis" was proposed, but received little attention. However, the recent discovery that Aβ is an antimicrobial peptide (AMP) acting against bacteria, fungi, and viruses gives increased credence to an infection hypothesis in the etiology of AD. We and others have shown that microbial infection increases the synthesis of this AMP. Here, we propose that the production of Aβ as an AMP will be beneficial on first microbial challenge but will become progressively detrimental as the infection becomes chronic and reactivates from time to time. Furthermore, we propose that host measures to remove excess Aβ decrease over time due to microglial senescence and microbial biofilm formation. We propose that this biofilm aggregates with Aβ to form the plaques in the brain of AD patients.

Samumed, LLC, announced today that it has closed its A-6 Round of equity issuance with 438 million, bringing its total equity raised to date to more than 650 million.The pre-money valuation for the round was 12 billion. "We appreciate the strong support from our investors, and we are now in a fortunate position to both move our later stage programs to commercialization, as well as expand on our earlier stage science and clinical portfolio."

Samumed is developing small-molecule drugs that target the regenerative potential of the Wnt pathway in order to reverse the progression of various age-related diseases. Its development pipeline includes therapies focused on osteoarthritis, degenerative disc disease, idiopathic pulmonary fibrosis, and Alzheimer's disease. A number of these therapies are currently in human trials, and some of them are currently in phase 2 testing.

The Wnt pathway is a primary signaling pathway that regulates the self-renewal and differentiation of adult stem cells. It plays a key role in tissue repair and upkeep, and it helps the body repair and regenerate following injury. As we age, the Wnt pathway becomes deregulated, which leads to a decline of tissue regeneration and supports the progression of various age-related diseases. Samumed is focused on modulating the Wnt pathway in order to promote the restoration and health of diseased tissues by spurring effective regeneration.

An estimated 17 percent of humans worldwide die from cancer, but less than five percent of captive elephants - who also live for about 70 years, and have about 100 times as many potentially cancerous cells as humans - die from the disease. Humans, like all other animals, have one copy of the master tumor suppressor gene p53. This gene enables humans and elephants to recognize unrepaired DNA damage, a precursor of cancer. Then it causes those damaged cells to die. Unexpectedly, however, researchers found that elephants have 20 copies of p53. This makes their cells significantly more sensitive to damaged DNA and quicker to engage in cellular suicide.

Now, researchers describe a second element of this process: an anti-cancer gene that returned from the dead. "Genes duplicate all the time. Sometimes they make mistakes, producing non-functional versions known as pseudogenes." While studying p53 in elephants, researchers found a former pseudogene called leukemia inhibitory factor 6 (LIF6) that had somehow evolved a new on-switch. LIF6, back from the dead, had become a valuable working gene. Its function, when activated by p53, is to respond to damaged DNA by killing the cell. The LIF6 gene makes a protein that goes, quite rapidly, to the mitochondria, the cell's main energy source. That protein pokes holes in the mitochondria, causing the cell to die.

LIF6 seems to have emerged around the time when the fossil record indicates that the small groundhog-sized precursors of today's elephants began to grow bigger. This started about 25 to 30 million years ago. This supplementary method of suppressing cancer may have been a key element enabling enormous growth, which eventually led to modern elephants. Bigger animals have vastly more cells, and they tend to live longer, which means more time and opportunities to accumulate cancer-causing mutations. When those cells divide, their DNA makes copies of itself. But those copies don't match the original. Errors get introduced and the repair process can't catch up. "Large, long-lived animals must have evolved robust mechanisms to either suppress or eliminate cancerous cells in order to live as long as they do, and reach their adult sizes."

Researchers report that women whose mothers lived to at least age 90 were more likely to also live to 90, free of serious diseases and disabilities. The study found women whose mothers lived into their ninth decade enjoyed 25 percent increased likelihood of also doing so without suffering from serious or chronic illness, including heart disease, stroke, diabetes, cancer, hip fractures or other debilitating disabilities.

Interestingly, the study also found that if only the father lived to 90, it did not correlate to increased longevity and health in daughters. However, if both the mother and father lived to 90, the likelihood of the daughter achieving longevity and healthy aging jumped to 38 percent. The study did not address parental life span effects on sons. Rather, it analyzed data from approximately 22,000 postmenopausal women participating in the Women's Health Initiative, a large, national study investigating major risk factors for chronic diseases among women. Limitations included no knowledge of the health or cause of death of the participants' parents.

Researchers believe a combination of genetics, environment, and behaviors passed to subsequent generations may influence aging outcomes among offspring. At baseline, the women in the study whose mothers lived to at least 90 were more likely to be college graduates, married with high incomes and incorporated physical activity and a healthy diet into their lives. "We now have evidence that how long our parents live may predict our long-term outcomes, including whether we will age well, but we need further studies to explore why. Although we cannot determine our genes, our study shows the importance of passing on healthy behaviors to our children. Certain lifestyle choices can determine healthy aging from generation to generation."

The Buck Institute for Research on Aging, Insilico Medicine, and Juvenescence Ltd announced today that they have formed Napa Therapeutics, Ltd to develop drugs against a novel aging-related target. The Buck Institute is one of the leading research centers in the world focused solely on research on aging and the elimination of age-related disease. Insilico Medicine is an AI company focused on a range of verticals devoted to aging. Juvenescence is a company focused on developing drugs to modify aging and the diseases of aging.

Napa Therapeutics is based on groundbreaking research in NAD metabolism conducted in the lab of Eric Verdin, MD, President and CEO of the Buck Institute. The Verdin lab will collaborate with Napa, using Insilico's drug development engine to speed the discovery of new compounds. "I am most excited by this model and the ability to combine the quality science of the Buck Institute with the remarkable deep learning engine at Insilico Medicine. To me this is another big step in the evolving process of using AI with human intelligence to extract the best of both systems. Napa Therapeutics lets Juvenescence deepen our collaboration with the Buck Institute and with Insilico Medicine. We hope to shorten the time required to identify molecules that can be brought to the clinic and most importantly help patients."