StemCell Therapy

Annual herd turnover rates and reported reasons for culling may be misleading, and the timing of culling during the lactation can be a more useful indicator of potential management problems on a given farm. Conformation traits are often used to select for improved cow longevity, but these traits account for only a modest proportion of differences in cow survival. Significant genetic variation exists between sires in the length of productive life of their daughters, as well as susceptibility to specific health disorders. Genetic improvement of cow survival should focus on direct measures of longevity, fertility, and health.

Dairy cow survival is influenced by many factors. Non-genetic factors include stall size, bedding type, degree of overcrowding, heat abatement devices, nutrition, veterinary care, herd expansion plans, milk quota restrictions, and availability and affordability of replacement heifers. As shown below, genetic improvement of longevity involves breeding animals that can produce a live calf without assistance; cycle normally, show visible heat, and conceive when inseminated; maintain adequate body condition and resist metabolic disorders; avoid udder injuries and fight off infection by mastitis pathogens; walk and stand comfortably without frequent hoof trimming, and efficiently produce milk of desirable composition. Many cows fail to complete these tasks and leave the herd prematurely. In some cases, the cow is genetically flawed, while in other cases her environment is lacking. Significant genetic variation exists between sire families for longevity, fertility, calving performance, and disease resistance. Therefore, we can improve longevity directly by selecting families that resist culling, or we can improve longevity indirectly by selecting families that excel for each of its component traits.

Please check this link first if you are interested in organic or specialty dairy production

Much negative attention has been given to the annual turnover or replacement rates on commercial dairy farms. However, the overall replacement rate for a given herd doesnt provide enough information to indicate whether or not a problem exists; one needs to know which cows left the herd, as well as the reasons for and timing of their removal. Suppose that 35% of the milking cows in each of two dairies were replaced last year. In one herd, the majority of these were low-producing, older animals that were culled late in lactation and subsequently replaced by younger, genetically superior heifers grown from within the operation. In the other herd, the majority were young, high-producing cows that were culled or died early in lactation due to calving problems, mastitis, lameness, ketosis, and other metabolic disorders, and the owner was forced to buy springing heifers from a cattle dealer at the prevailing market price. Thus, even though the replacement rates on these farms are identical, ones interpretation of each herd's management success is vastly different. Replacement rates can also be misleading in herds that have an excess of replacement heifers. Suppose one herd sells its extra animals as springing heifers prior to first calving, while another herd calves all of its heifers and culls stringently for low production within the milking herd. Both may be successful in terms of managing the health, fertility, and productivity of their cattle, but the former will have a substantially lower annual replacement rate. In general, herds with lower replacement or turnover rates tend to be more successful in terms of cow comfort, health, and productivity. However, replacement rates can be misleading, and more detailed information about the reasons for culling and the timing of culling is needed. Furthermore, herd turnover rates are influenced heavily by external factors, such as expansion plans and replacement heifer prices.

Dairy producers routinely report reasons for disposal as part of the national milk recording program. Animals can be recorded as died, sold for dairy, or sold for beef, with the latter category broken down into low production, mastitis, infertility, and so on. These descriptive reasons for disposal can be useful when studying the general demographics of a national dairy herd. For example, one might use such data to conclude that mastitis and infertility are the most common causes of culling on most dairy farms. However, reported reasons for disposal can be misleading when one attempts to compare the management level of various dairy farms, or when one attempts to draw conclusions about the genetic merit of certain animals or sire families. Many animals are culled for multiple offenses. For example, a cow might have a difficult calving, followed by a case of ketosis, and a displaced abomasum. She may then fail to breed back in a timely manner and be culled from the herd when her daily milk production drops below a profitable level. The farmer might code her as sold for low production, sold for infertility, or sold due to disease. Thus, the reported reason for disposal is often a vague indicator of the actual problem. Furthermore, inconsistencies may exist between reported reasons for disposal and the actual health and reproductive history of the culled animals.

Stewart (Steve Stewart, Univ. of Minnesota, 2002, unpublished) proposed the idea of using the timing of culling within the lactation as an indirect indicator of the reason for disposal. He constructed a graph showing the proportion of total culled animals that were removed within certain time periods during the lactation. An example of this type of graph is shown below, where the percentage of culled cows that left during each 3-week period from calving to 440 d postpartum is shown for 59,390 cows that calved in 2001-2003 and were subsequently culled from 151 herds that participate in the Alta Genetics (Watertown, WI) Advantage Progeny Testing Program. One can hypothesize that cows that were culled between 0 and 62 d postpartum may have left due to calving problems or early lactation metabolic disorders, while cows that were culled between 63 and 293 d postpartum may have left due to mastitis or lameness, and cows that were culled after 294 d postpartum may have left due to infertility. Exceptions to the rule exist, as a cow that is culled today may actually reflect the outcome of a do not breed decision that occurred many months earlier. Nonetheless, an analysis of the timing of culling events within a dairy herd may provide a more objective description of management on a given farm than one can obtain by inspecting the overall turnover rate or reported reasons for disposal. Furthermore, genetic evaluation of dairy sires based on the proportion of daughters that were culled during each period of the lactation may provide a useful indicator of differences in susceptibility to various diseases or disorders. For example, one could compute sire predicted transmitting abilities for early lactation survival, and this might identify bulls whose daughters avoid calving complications and resist early postpartum metabolic disorders.

Initial attempts to improve dairy cow longevity through artificial selection began in the 1970s and early 1980s when breed associations and AI studs first developed linear type appraisal programs. For the next two decades, type and longevity were considered as synonymous. Bulls that sired daughters with high, wide rear udders, strong median suspensory ligaments, well-attached fore udders, and correct teat placement were considered to transmit superior longevity. Likewise, bulls that sired daughters with strong pasterns, a steep foot angle, and correct set to the hock were expected to improve longevity.

Numerous studies have addressed the genetic relationships between linear type traits and longevity (e.g., Caraviello et al., 2004a; Sewalem et al, 2004; Short and Lawlor, 1992). Early studies relied on the estimation of genetic correlations between longevity and linear type traits, and these studies typically invoked a 60-, 72-, or 84-month opportunity period for longevity. However, these studies suffered from two major limitations. First, the use of genetic correlation parameters to assess trait-longevity relationships limited these studies to measurement of linear relationships only. Few traits have a strictly linear relationship with longevity, and the role of traits with intermediate optima or traits that offer diminishing returns as scores increase cannot be evaluated properly using genetic correlations. Second, the use of a long opportunity period, to allow each cow to fully express her genetic potential for longevity, resulted in a tremendous time lag between the birth of animals in the study group and eventual publication of results. For example, the youngest cows in the Short and Lawlor (1992) study were born in 1982, so more than a decade of additional genetic and management improvements occurred prior to publication of results of the study. The use of survival analysis methodology in more recent studies (e.g., Caraviello et al., 2004b) alleviated several of the aforementioned limitations. In many of these studies, linear type scores were grouped into categories, and no restrictions were placed on the form of the trait-longevity relationship. Furthermore, because survival analysis allows proper modeling of censored records from animals that are still alive (Ducrocq, 1994), these studies used much more timely data than previous studies that invoked a long opportunity period. Results indicated that many type traits, such as rear leg set, rump angle, or dairy form, have intermediate optima, while many others, such as udder support, teat placement, or foot angle, seem to display a pattern of diminishing returns. More importantly, these studies demonstrated that udder depth, fore udder attachment, rear udder attachment, and udder support were of primary importance with respect to longevity, while rear leg set and foot angle were of secondary importance, and stature had no importance. Despite the importance of physical conformation, a significant proportion of the genetic variation in longevity remained unexplained by existing type or production traits well into the 1990s. Numerous examples were noted of bulls that transmitted outstanding production and type to their daughters but whose daughters nonetheless tended to leave the herd prematurely. Thus, type traits can be used as an indirect indicator of the expected longevity of a bull's daughters, and actual culling and fertility data are needed to explain the rest of the story.

In 1994, the USDA Animal Improvement Programs Laboratory (Beltsville, MD) introduced national genetic evaluations for length of productive life (PL), which was measured as the total number of months in milk from first calving until 84 mo of age, with a limit of 10 mo per lactation (VanRaden and Klaaskate, 1993). Because the vast majority of cows are culled by 84 mo of age, this seems to provide a reasonable opportunity period. In fact, the additional gain in accuracy that could be achieved by waiting for a few, highly selected daughters to complete 8, 10, or 12 yr of PL would be negligible. Because the starting point of the opportunity period (date of first calving) can vary, it is possible that this definition of PL may favor animals that calve at a young age. However, the phenotypic variation in age at first calving on most commercial dairies is rather limited. The limit of 10 mo of PL per lactation was applied for two reasons: because it seemed desirable to penalize cows that have a long dry period and an extended calving interval and because test-day production data beyond 305 d postpartum were unavailable historically. However, this restriction may have some unintended consequences, in terms of the genetic relationships between PL and other traits in the breeding goal. Tsuruta et al. (2005) showed that the genetic correlation between milk yield and PL changed from -0.11 with a 305 d limit, to +0.08 with a 500 d limit, and to +0.14 with a 999 d limit. Corresponding genetic correlations between days open and PL were -0.62, -0.36, and -0.27 for per lactation PL limits of 305 d, 500 d, and 999 d, respectively, while genetic correlations with dairy form were -0.25, -0.12, and -0.08, respectively. An extension of the current 305 d limit to a value that is more closely aligned with the management of modern commercial dairies, such as 365 d or 400 d, has been discussed. An additional argument for extending, or even removing, a limit on PL credits per lactation is that national dairy sire evaluations for daughter pregnancy rate (DPR) are now routinely available, and indirect selection for fertility using PL information is no longer necessary. An important aspect of current national genetic evaluations for PL is that records of cows that are still alive can be extended or projected to obtain an estimate of the total months in milk that such animals will accumulate by culling or 84 mo of age (VanRaden and Klaaskate, 1993). Thus, the 84-mo opportunity period does not cause a major delay or time lag in computing sire PTA for PL. On the other hand, the accuracy of such projections is low much lower than the accuracy of projected 305 d milk production records based on the first two or three test-day yields.

The primary concern with regard to genetic evaluation of PL is the substantial period of time required to obtain complete culling data for daughters of a given bull. Because a short generation interval is desirable in genetic selection programs, AI studs and pedigree breeders like to make sire selection decisions as quickly as possible. However, when a recently tested sire is being considered as a sire of sons or as an embryo transfer sire, most of his daughters are still alive. Therefore, reliability of PL evaluations is often low at the most critical points in life. This can lead to errors in selection decisions, particularly for bulls whose daughters fail to follow a typical maturity pattern. If a particular bull's daughters mature more or less gracefully than daughters of an average bull, his PTA can change significantly over time. Weigel et al. (1998) developed a procedure by which correlated traits, such as type, production, and somatic cell score, can be used to compute an indirect prediction of a bulls PTA for PL. The indirect prediction for a given bull can then be combined with his direct prediction, which is based on actual culling data, using weights that depend on the REL of direct and indirect predictions. The combined PTA will have higher REL than either the direct or indirect prediction, especially early in life. Although the combined PL predictions tend to be more accurate than direct predictions for the majority of sires, there are exceptions. The most disturbing cases are bulls whose daughters appear promising in first lactation but mature less gracefully than daughters of an average bull. These bulls tend to have a high indirect prediction early in life, but their combined PTA tends to decrease over time, as daughters mature and get culled from the herd more rapidly than anticipated.

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Genetic Improvement of Dairy Cow Longevity - eXtension

A handful of genes that control the body's defenses during hard times can also dramatically improve health and prolong life in diverse organisms. Understanding how they work may reveal the keys to extending human life span while banishing diseases of old age

By David A. Sinclair and Lenny Guarente

You can assume quite a bit about the state of a used car just from its mileage and model year. The wear and tear of heavy driving and the passage of time will have taken an inevitable toll. The same appears to be true of aging in people, but the analogy is flawed because of a crucial difference between inanimate machines and living creatures: deterioration is not inexorable in biological systems, which can respond to their environments and use their own energy to defend and repair themselves.

At one time, scientists believed aging to be not just deterioration but an active continuation of an organism's genetically programmed development. Once an individual achieved maturity, "aging genes" began to direct its progress toward the grave. This idea has been discredited, and conventional wisdom now holds that aging really is just wearing out over time because the body's normal maintenance and repair mechanisms simply wane. Evolutionary natural selection, the logic goes, has no reason to keep them working once an organism has passed its reproductive age.

Yet we and other researchers have found that a family of genes involved in an organism's ability to withstand a stressful environment, such as excessive heat or scarcity of food or water, have the power to keep its natural defense and repair activities going strong regardless of age. By optimizing the body's functioning for survival, these genes maximize the individual's chances of getting through the crisis. And if they remain activated long enough, they can also dramatically enhance the organism's health and extend its life span. In essence, they represent the opposite of aging genes--longevity genes.

We began investigating this idea nearly 15 years ago by imagining that evolution would have favored a universal regulatory system to coordinate this well-known response to environmental stress. If we could identify the gene or genes that serve as its master controllers and thereby act as master regulators of an organism's life span, these natural defense mechanisms might be turned into weapons against the diseases and decline that are now apparently synonymous with human aging.

Many recently discovered genes, known by such cryptic names as daf-2, pit-1, amp-1, clk-1 and p66Shc, have been found to affect stress resistance and life span in laboratory organisms, suggesting that they could be part of a fundamental mechanism for surviving adversity. But our own two laboratories have focused on a gene called SIR2, variants of which are present in all organisms studied so far, from yeast to humans. Extra copies of the gene increase longevity in creatures as diverse as yeast, roundworms and fruit flies, and we are working to determine whether it does the same for larger animals, such as mice.

As one of the first longevity genes to have been identified, SIR2 is the best characterized, so we will focus here on its workings. They illustrate how a genetically regulated survival mechanism can extend life and improve health, and growing evidence suggests that SIR2 may be the key regulator of that mechanism.

One of us (Guarente) began by screening yeast colonies for unusually long-lived cells in the hope of finding genes responsible for their longevity. This screen yielded a single mutation in a gene called SIR4, which encodes part of a complex of proteins containing the Sir2 enzyme. The mutation in SIR4 caused the Sir2 protein to gather at the most highly repetitive region of the yeast genome, a stretch containing the genes that encode the protein factories of the cell, known as ribosomal DNA (rDNA). More than 100 of these rDNA repeats exist in the average yeast cell's genome, and they are difficult to maintain in a stable state. Repetitive sequences are prone to "recombining" with one another, a process that in humans can lead to numerous illnesses, such as cancer and Huntington's disease. Our yeast findings suggested that aging in mother cells was caused by some form of rDNA instability that was mitigated by the Sir proteins.

In fact, we found a surprising kind of rDNA instability. After dividing several times, yeast mother cells spin off extra copies of the rDNA as circular rings that pop out of the genome. These extrachromosomal rDNA circles (ERCs) are copied along with the mother cell's chromosomes prior to cell division but remain in the mother cell's nucleus afterward. Thus, a mother cell accumulates an ever increasing number of circles that eventually spell her doom, possibly because copying the ERCs consumes so many resources that she can no longer manage to replicate her own genome.

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Longevity genes - Supercentenarian

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In July last year I wrote about some fairly glaring flaws in a paper published in Science on the genetics of extreme longevity. At the time, potential problems with the paper had been flagged in an excellent Newsweek piece by Mary Carmichael.

Today, after a year in advance online limbo without ever progressing to the print edition of the journal, and a formal Expression of Concern last November, the paper was fully retracted. Theres solid coverage of the announcement at the Boston Globe (including quotes from my Genomes Unzipped colleague Jeff Barrett), Nature, and of course the superb Retraction Watch.

Heres the retraction notice in full:

After online publication of our Report Genetic signatures of exceptional longevity in humans (1), we discovered that technical errors in the Illumina 610 array and an inadequate quality control protocol introduced false-positive single-nucleotide polymorphisms (SNPs) in our findings. An independent laboratory subsequently performed stringent quality control measures, ambiguous SNPs were then removed, and resultant genotype data were validated using an independent platform. We then reanalyzed the reduced data set using the same methodology as in the published paper. We feel the main scientific findings remain supported by the available data: (i) A model consisting of multiple specific SNPs accurately differentiates between centenarians and controls; (ii) genetic profiles cluster into specific signatures; and (iii) signatures are associated with ages of onset of specific age-related diseases and subjects with the oldest ages. However, the specific details of the new analysis change substantially from those originally published online to the point of becoming a new report. Therefore, we retract the original manuscript and will pursue alternative publication of the new findings.

In a statement quoted over at Retraction Watch, the journal makes it more clear how the retraction decision was actually reached:

Sebastiani and colleagues submitted the corrected data to Science in December 2010, where the work underwent careful peer-review. Although the authors remain confident about their findings, Science has concluded on the basis of peer-review that a paper built on the corrected data would not meet the journals standards for genome-wide association studies. One such standard, for example, is the inclusion of a reliable replication sample that shows comparable results to those in the initial experiments.

The authors have therefore agreed to retract their paper.

In other words, the authors were still willing to stand by their results, but the journal wasnt.

Questions remain about how the study managed to pass through peer review in the first place virtually every complex trait geneticist I spoke to was immediately, massively skeptical about the articles findings from the moment of publication but it appears that Science has conducted a thorough investigation of the authors amended manuscript and made an appropriate decision. It will be intriguing to see if, when and in what form the studys authors manage to republish their results.

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Longevity genetics study retracted from Science | WIRED

Genetics of Human Longevity: New Ideas & Findings

Natalia Gavrilova

Center on Aging, NORC at the University of Chicago

(Abstract of presentation at the International Conference on Longevity, Sydney, Australia, March 5-7, 2004)

In contrast to the remarkable progress in the genetics of yeast and nematode aging, little is known about genes that control human longevity. What is behind the records of extreme human longevity: just lucky chance, favorable environment, or 'good' genes? How to resolve the apparent controversy between strong familial clustering of human longevity, and poor resemblance in lifespan among blood relatives?

We applied methods of genetic epidemiology and survival analysis to family-linked data on human lifespan. Special efforts were undertaken to collect detailed and reliable human genealogies an important data source for genetic studies of human longevity. We found that the dependence of offspring lifespan on parental lifespan is essentially non-linear, with very weak resemblance before parental lifespan of 80 years and very steep offspring-parent dependence (high narrow-sense heritability) for longer lived parents. There is no correlation between lifespan of spouses, who share familial environment. These observations suggest that chances to survive beyond age 80 are significantly influenced by genetic factors rather than shared familial environment. These findings explain the existing longevity paradox: although the heritability estimates for lifespan are rather low, the exceptional longevity has a strong familial association.

We also tested the prediction of mutation theory of aging that accumulation of mutations in parental germ cells may affect progeny lifespan when progeny was conceived to older parents. We found that daughters conceived to older fathers live shorter lives, while sons are not affected. Maternal age effects on lifespan of adult progeny are negligible compared to effects of paternal age, which is consistent with the notion of higher rates of DNA copy-errors in paternal germ cells caused by more intensive cell divisions during spermatogenesis.

Genealogical data also are useful for testing the prediction of the disposable soma theory that human longevity comes with the cost of impaired reproductive success. We found that in contrast to previous reports by other authors, woman's exceptional longevity is not associated with infertility. Thus, the concept of heavy infertility cost for human longevity is not supported by data, when these data are carefully cross-checked, cleaned and reanalyzed. These results demonstrate the importance of high quality genealogical data for genetic studies of human longevity.

Relevant Publications:

Gavrilov, L.A., Gavrilova, N.S. Early-life factors modulating lifespan. In: Rattan, S.I.S. (Ed.).Modulating Aging and Longevity. Kluwer Academic Publishers, Dordrecht, The Netherlands, 2003, 27-50.

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Genetics of Human Longevity - Longevity Science

Chromosomes and DNA. adam.about.net

Updated December 30, 2014.

What is a Telomere?:

A chromosome is a long strand of DNA. At the end of a chromosome is a telomere, which acts like a bookend. Telomeres keep chomosomes protected and prevent them from fusing into rings or binding with other DNA. Telomeres play an important role in cell division.

What Happens When a Cell Divides?:

Each time a cell divides, the DNA unwraps and the information in the DNA is copied. The process does not copy all of the DNA information - the telomeres are not copied.

When the cell is finished dividing, the DNA comes back together. The telomeres lose a little bit of length each time this happens.

Why Do They Get Shorter?:

When a cell divides and copies DNA, the strands of DNA get snipped to enable the copying process. The places that are snipped are the telomeres. Since the telomeres do not contain any important information, more important parts of the DNA are protected. The telomeres get shorter each time a cell divides, like a pencil eraser gets shorter each time it's used.

Can Telomeres Become Too Short?:

The rest is here:
Telomeres and Aging - Understanding Cellular Aging

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With several companies on the verge of mass-marketing genetic tests that claim to read agings cellular clock, some researchers say the science isnt yet ready for prime-time use.

The tests measure telomeres, or protein sheaths that prevent the tips of chromosomes from fraying. As time passes, they grow shorter, a process hastened by stress, environmental insult and disease. If they get too short, cell breakdown follows. A large body of research links telomere deterioration to deteriorating health.

That makes telomeres an alluring target for quantifying the ravages of aging, which have proved surprisingly difficult to measure. But the clinical use of telomeres has yet to be determined.

Aging is extremely complex. Its going to involve many behavioral and genetic factors, said Boston University gerontologist Thomas Perls, who runs the worlds largest study of centenarian health. Its going to be unwise to try and pin it down on one particular marker. There are going to be many different factors.

Telomere tests came to public notice this week after an article in The Independent described a test being developed by Life Length, a Madrid startup company. In the article, University of Texas Southwestern geneticist and Life Length consultant Jerry Shay extolled the tests potential.

When youre looking at a whole bunch of people, you conclude that shorter telomeres are bad. But that doesnt mean you can take an individual and tell them their risk.

Telomere length is actually a pretty good representation of your biological age, he said. People might say If I know Im going to die in 10 years, Ill spend all my money now. Or, If Im going to live for 40 more years Ill be more conservative in my lifestyle.'

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To Measure Longevity, Common Sense Trumps Genetic Test

More than 400 mutations were found in the healthy white blood cells of a 115-year-old woman, according to a new study that may advance what is known about limits of the human life span.

Genetic mutations have been linked to diseases such as cancer, but these findings suggest that mutations in white blood cells are largely harmless over a lifetime, the researchers said.

Blood is continually replenished by hematopoietic (meaning "to make blood") stem cells that are inside the bone marrow and divide to produce different types of blood cells.

Cell division can lead to genetic mutations and hundreds of mutations have been found in patients with blood cancers. However, little was known about white blood cells and mutations.

The woman in the study - whose name was not revealed - was the oldest person in the world when she died in 2005. She is thought to be the oldest person ever to donate her body to science. The hundreds of mutations identified in her white blood cells appeared to be tolerated by the body and did not cause disease.

The researchers also found possible new insight into the limits of human longevity, according to the authors of the study published online April 23 in the journal Genome Research.

"To our great surprise we found that, at the time of her death, the peripheral blood was derived from only two active hematopoietic stem cells (in contrast to an estimated 1,300 simultaneously active stem cells), which were related to each other," lead author Dr. Henne Holstege said in a journal news release.

The researchers also found that the woman's white blood cells' telomeres were extremely short. Telomeres, which are at the ends of chromosomes and protect them from damage, get a bit shorter each time a cell divides.

"Because these blood cells had extremely short telomeres, we speculate that most hematopoietic stem cells may have died from 'stem cell exhaustion,' reaching the upper limit of stem cell divisions," Holstege said.

Further research is needed to learn whether such stem cell exhaustion is a cause of death in extremely old people.

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Scientists seek genetic clues to longevity from 115-year ...

Updated May 21, 2014.

What It Is:

The genetic theory of aging believes that lifespan is largely determined by the genes we inherit. According to the theory, our potential age is primarily determined at the moment of conception.

The Evidence Behind the Theory:

There is some evidence to support this theory. People with parents who have lived long lives are more likely to live long themselves (though this could be partially explained by learned behaviors, such as food preferences).

Also, identical twins (who have the exact same genes) have closer lifespans than siblings.

How Genes Impact Lifespan:

Some genes are beneficial and enhance longevity -- a gene that helps a person metabolize cholesterol would reduce a person's risk of heart disease, for example. But some genes are harmful, like those that increase the risk cancer. Some gene mutations are inherited, too, and may shorten lifespan. (Mutations also can happen after birth, since exposure to toxins, free radicals and radiation can cause gene changes.)

The Bottom Line:

It is estimated that genes can explain a maximum of 35 percent of lifespan. The other determinants are your behaviors, exposures, and just plain luck. So don't think that you are doomed just because your family members tend to die young -- and also don't think that you can ignore your health if your family members tend to live long.

See more here:
Genetics and Aging - The Genetic Theory of Aging

The purpose of our studies: to understand the mechanisms of aging and longevity in order to extend healthy and productive human lifespan. This scientific and educational website contains over a hundred of scientific and reference documents relevant to longevity and aging studies. It is receiving about 1000 visits per day from many prestigious organizations including the US Library of Congress, the US National Institutes of Health (NIH), the US Centers for Disease Control (CDC), and from the Royal Society - the UK National Academy of Science. This website is rated as the top # 1 website on longevity science topic in such major search engines as Google, Yahoo!, Alltheweb, etc. (when searching for longevity science term).Breaking News:

Table of Contents:

Dr. Natalia S. Gavrilova Center on Aging NORC at theUniversity of Chicago 1155 East 60th Street Chicago, IL 60637-2745 E-mail: Brief Biographical Sketch, NIH Biosketch Detailed Curriculum Vitae Resume Expertise Profile Statement of Research Interests

We also maintain close scientific contacts with Dr. Bruce A. Carnes at the University of Oklahoma. Dr. Yulia Kushnareva at Burnham Institute, La Jolla, CA

What we have found and published:

Available at:

THE RELIABILITY THEORY OF AGING AND LONGEVITY Journal of Theoretical Biology, 2001, 213(4): 527-545. Abstract To download full text click here For Press Release click here For Media Coverage click here

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Longevity Science: Unraveling the Secrets of Human ...

Welcome to the LongevityMap, a database of human genetic variants associated with longevity. Negative results are also included in the LongevityMap to provide visitors with as much information as possible regarding each gene and variant previously studied in context of longevity. As such, the LongevityMap serves as a repository of genetic association studies of longevity and reflects our current knowledge of the genetics of human longevity.

Searching the LongevityMap can be done by gene or genetic variant (e.g., refSNP number). You can enter one or more words from the gene's name or use the gene's HGNC symbol. Note that the search is case insensitive. It is also possible to search for a specific cytogenetic location but for this you need to tick the box below.

To search for a specific study in the LongevityMap, you may browse or search its literature:

You may download a zipped tab-delimited ASCII dataset with the raw data, derived from the latest stable build of the LongevityMap.

If you find an error or wish to propose a study or variant to be included in the database, please contact us. To receive the latest news and announcements, please join the HAGR-news mailing list.

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LongevityMap: Genetic association studies of longevity

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Posted May 21, 2012

Noted Pathologist PhD in Human Genetics Added to Existing Member Expertise in Stem Cell Maternal Fetal Medicine and Stem Cell Cardiology

CLEARWATER, FL -- Biostem U.S., Corporation, (OTCQB: HAIR) (PINKSHEETS: HAIR) (Biostem, the Company), a fully reporting public company in the stem cell regenerative medicine sciences sector, today announced that Jeanne Ann Lumadue, MD, PhD, MBA, has been appointed to its Scientific and Medical Board of Advisors (SAMBA).

Dr. Lumadue currently is Medical Director at the Mount Nittany Physician Group Laboratory in State College, PA. She also serves as Medical Director of the Central Pennsylvania Blood Bank and is a member of the medical staff of the Mount Nittany Medical Center, all in State College.

Dr. Lumadue stated, "Biostem's international technology development and licensing approach is well planned. Stem cell regenerative medicine is a rapidly expanding field that has the potential to affect every human being in a positive way. I am delighted to be part of this highly promising company."

Biostem CEO Dwight Brunoehler said, "I am thrilled for the opportunity to work with Jeanne again. She is an innovative thinker, a tireless contributor, and a great team player."

Dr. Lumadue received her undergraduate degree magna cum laude from the Pennsylvania State University and her PhD in Genetics from Yale University. She received an MD degree from the Johns Hopkins University in Baltimore, MD, where she also did residency and fellowship training in anatomic and clinical pathology. She has served as Pathologist and Assistant Medical Director of Transfusion Medicine at the Johns Hopkins Hospital, the Medical Director of Laboratory Hematology and Stem Cell Processing at Children's National Medical Center in Washington, DC, and the Medical Director of Transfusion Services and Stem Cell Processing at the Inova Fairfax Hospital in Falls Church, Virginia.

She is a member of the American Society of Hematology, the College of American Pathologists, the American Society of Clinical Pathologists and the AABB, for which she serves as a facility assessor.

About Biostem U.S., Corporation

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Biostem U.S., Corporation Adds Jeanne Ann Lumadue, MD, PhD, MBA to Its Scientific and Medical Board of Advisors

CLEARWATER, FL--(Marketwire -03/19/12)- Biostem U.S., Corporation (OTCQB: BOSM.PK - News) (Pinksheets: BOSM.PK - News) (Biostem, the Company), a fully reporting public company in the stem cell regenerative medicine sciences sector, announced today the addition of Perinatologist Sanford M. Lederman, MD to its Scientific and Medical Board of Advisors (SAMBA).

As Chairman of the Department of Obstetrics and Gynecology at New York Methodist Hospital in Brooklyn, Dr. Lederman is consistently recognized by New Yorker Magazine's list of "Top Doctors" in New York. A specialist in high-risk pregnancy issues, Dr. Lederman has authored a number of scientific papers and is a highly regarded public speaker. He adds a very important dimension to the Biostem Scientific and Medical Board of Advisors by bringing specialized knowledge regarding the potential use of stem cell applications for the health of women and children.

Biostem President Dwight Brunoehler said, "Dr. Lederman is one of the most highly respected Obstetric and Gynecological physicians in the country. Sandy and I have worked together very actively on stem cell projects for over 18 years, including setting up a cord blood stem cell national donation system where all expectant moms have a chance to donate their baby's cord blood to benefit others."

Dr. Lederman stated, "Biostem's expansion plans mesh well with my personal interest in developing and advancing the use of non-controversial stem cells to improve the health of women and children. I have a particular interest in increasing the use of cord blood stem cells for in-utero transplant procedures, where stem cells are used to cure a potential life threatening disease such as sickle cell or thalassemia and other selective genetic disorders in a baby before it is even born."

Prior to accepting his current position with New York Methodist Hospital, Dr. Lederman was Residency Program Director and Vice Chairman of the Department of Obstetrics and gynecology at Long Island College Hospital in Brooklyn. At various times, he has served as a partner at Brooklyn Women's Health Care, President at Genetics East and Clinical Associate Professor at the State University of New York. He has served on the medical advisory board of several companies. He previously was Medical Director of Women's Health USA and was a founding member of the Roger Freeman Perinatal Society.

A graduate of Hunter College in New York, he received his initial medical training at Universidad Autonoma de Guadalajara School of Medicine. His initial internship was at New York Medical College in the Bronx. During the course of his career, Dr. Lederman has served and studied in various capacities at Long Island College Hospital in the Bronx, North Shore University Hospital in New York, Kings County Medical Center in Brooklyn, Long Beach Memorial Medical Center in California and the University of California at Irvine.

About Biostem U.S., CorporationBiostem U.S., Corporation (OTCQB: BOSM.PK - News) is a fully reporting Nevada corporation with offices in Clearwater, Florida. Biostem is a technology licensing company with proprietary technology centered around providing hair re-growth using human stem cells. The company also intends to train and license selected physicians to provide Regenerative Cellular Therapy treatments to assist the body's natural approach to healing tendons, ligaments, joints and muscle injuries by using the patient's own stem cells. Biostem U.S. is seeking to expand its operations worldwide through licensing of its proprietary technology and acquisition of existing stem cell related facilities. The company's goal is to operate in the international biotech market, focusing on the rapidly growing regenerative medicine field, using ethically sourced adult stem cells to improve the quality and longevity of life for all mankind.

More information on Biostem U.S., Corporation can be obtained through http://www.biostemus.com, or by calling Kerry D'Amato, Marketing Director at 727-446-5000.

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Biostem U.S., Corporation Continues Building Its Scientific and Medical Board of Advisors With Appointment of Leading ...

PARIS--(BUSINESS WIRE)--

In the mid 1980s, Stanley Prusiner startled the scientific world by claiming that transmissible neurodegenerative diseases such as Creutzfeldt-Jakob in humans and Bovine Spongiform Encephalopathy (BSE; mad cow disease) were caused by self-replicating protein molecules, which he named prions. Painstaking work to establish that prion proteins could replicate without the need for genetic material won him the Nobel prize in 1997. What at first seemed an unusual mechanism restricted to a rather rare group of diseases has now become central to the study of all neurodegenerative conditions: the pathogenic proteins that characterise these diseases all seem to behave like prions. The implications for understanding how these diseases are transmitted through the nervous system and the possibility that environmental contamination may account for the sporadic forms of these diseases, as well as therapeutic possibilities, were among the topics discussed by the thirteen international experts, including two Nobel Prize winners, at the 27th annual colloquium on Alzheimers disease, hosted by the Fondation IPSEN. The meeting, hold in Paris on February 27, 2012, has been organized by Mathias Jucker (University of Tbingen, Germany) and Yves Christen (Fondation IPSEN, Paris).

Prions are Janus-like proteins synthesised by neurons: in their normal, globular conformation they participate in cellular functions but in certain circumstances they adopt a pleated -sheet configuration, which forms insoluble fibrous aggregates that disrupt cell function. This aggregated form is found in neurons in a group of neurodegenerative diseases known as the transmissible spongiform encephalopathies, which include Kuru, Creutzfeldt-Jakob disease (CJD) in humans, BSE in cattle and scrapie in sheep. All of these diseases can be transmitted by contact with brain material from affected individuals the cause of great concern in the late 1980s and early 1990s when people developed a form of CJD after eating products from cows with BSE.

By the 1980s, a long hunt had failed to find either a bacterial or viral agent causing these diseases. Stanley Prusiner and his colleagues proposed instead that the infectious agent was the -sheet form of the prion protein, which was able to replicate using itself as a template. As the first claim for replication without the need for nucleic acids, this was to say the least controversial. Now it is well accepted that rogue molecules in the -sheet conformation, now known as prions, can act as a seed, converting normal prion proteins into -sheet type molecules. These adopt a fibrillar configuration and aggregate into an amyloid-like deposit that disrupts the neurons function. Prions released from cells are taken up by neighbours and trigger the same cascade of transformation and aggregation. Genetics still plays a part, because various mutations in the prion protein gene promote this transformation, while some polymorphisms (substitution of one base in the gene sequence for another) make individuals more susceptible to developing a prion disease.

The parallels with Alzheimers disease (AD) were soon noted: a cellular protein, in this case the amyloid- peptide, adopts a -sheet, fibrillar conformation that aggregates in the brain as amyloid plaques; again genetics plays a part, at least in early-onset, familial AD, which is associated with mutations in amyloid-s parent protein, the amyloid precursor protein. More recently, it has become clear that this prion-like pattern is common to all the neurodegenerative diseases, including Parkinsons, Huntingtons and motor neuron disease (Stanley Prusiner, University of California San Francisco, San Francisco, USA): each is characterised by a disease-specific cellular protein that transforms into a -sheet configuration that subsequently aggregates. Moreover, mutations associated with familial forms of the diseases have now been identified for all these signature proteins. As a consequence these conditions are now being designated as protein misfolding disorders (Claudio Soto, University of Texas Houston Medical School, Houston, USA) and the proteins responsible could be considered as mammalian prions (Prusiner).

If the misfolded proteins associated with the various neurodegenerative diseases do behave like prions, they should be capable of triggering the transformation of the cellular protein in unaffected cells. Transfer of a systemic (non-neural) amyloidosis between mice was first demonstrated over 40 years ago (Per Westermark, Uppsala University, Uppsala, Sweden). Several speakers at the meeting have presented data supporting this hypothesis for various neurodegenerative diseases, either by injecting a brain homogenate from mice genetically engineered to develop the disease into the brains of susceptible but disease-free animals (Prusiner; Mathias Jucker, Hertie-Institute for Clinical Brain Research and German Center for Neurodegenerative Diseases, Tbingen, Germany; Soto; Michel Goedert, MRC Laboratory of Molecular Biology, Cambridge, UK; Patrik Brundin, Lund University, Lund, Sweden; Virginia Lee, University of Pennsylvania School of Medicine, Philadelphia, USA); by injecting synthetic protein fibrils into brains (Lee); or by testing purified protein extracts on neuron cultures (Anne Bertolotti, MRC Laboratory of Molecular Biology, Cambridge, UK; Ron Kopito, Stanford University, Stanford, USA). Another clear indication of transcellular induction comes from Parkinsons disease patients who have had stem-cell transplants: -sheet proteins have been found in the neurons derived from the stem cells (Brundin).

This triggering ability of the aberrant proteins, which has gained them the label of proteopathic seeds, also seems to be responsible for the temporal spread of degeneration through the brain that is typical of the neurodegenerative diseases (Jucker; Brundin; Lee). Perhaps more significant, the aberrant proteins have been found in the brain after intra-peritoneal injection or blood transfusion (Soto); as with prions, transport along the vagal nerve seems to be the most likely route into the brain (Prusiner; Brundin). This opens up the possibility of an environmental causation for the many patients with a neurodegenerative disease who do not have hereditary links (Jucker; Soto; Westermark).

The mechanisms underlying proteopathic seeding are still unclear. The spread of the -sheet transformation seems to depend on both the configuration of the seed itself and the genetic constitution of the animal again very like the prion diseases (Jucker; Goedert). The uptake of the seed proteins into neurons is being examined in culture (Bertolotti; Kopito) and model systems (Brundin). The key seems to be in the interaction between the seed protein and cell membranes and, in some cases at least, helper proteins are required (Brundin).

To understand how seeding works, it is essential to know the structure of the -sheet proteins. Taking amyloid- as an example, the conditions that determine what type of fibril and aggregates will form, and how this relates to the mutations in the amyloid precursor protein will be discussed (Robert Tycko, National Institutes of Health, NIDDK, Bethesda, USA). Cooperativity between -sheet molecules may also be important in aggregation (Roland Riek, ETH Zrich, Zrich, Switzerland). Helpful insights can also come from systemic diseases in which amyloid accumulates, such as AA amyloidosis. Amyloid, a generic term for protein aggregates, is in this case produced by the inflammatory protein serum amyloid A (Westermark). There is evidence that AA amyloid formation can be triggered by other types of amyloid molecule, leading to speculation that amyloid fibrils found in the environment and food could cross-seed amyloid formation in the body or brain.

As knowledge about proteopathic seeding accumulates, new prospects for therapeutic intervention open up (Peter Lansbury, Brigham and Womens Hospital, Boston, USA). The initial conversion of functional globular protein into potentially pathogenic -sheet form, the seeding cascade that coverts further globular protein to -sheet, and the mechanisms by which neurons take up prion-like -sheet molecules are all potential targets. The discovery that amyloid- seeds are partly soluble and may be present in body fluids offers a possible alternative strategy for an early diagnostic (Jucker).

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The 27th Colloque Médecine et Recherche of the Fondation Ipsen in the Alzheimer Disease series: “Proteopathic Seeds ...

ScienceDaily (Feb. 27, 2012) — Researchers from The University of Nottingham have demonstrated how a species of flatworm overcomes the aging process to be potentially immortal.

The discovery, published in the Proceedings of the National Academy of Sciences, is part of a project funded by the Biotechnology and Biological Sciences Research Council (BBSRC) and Medical Research Council (MRC) and may shed light on the possibilities of alleviating aging and age-related characteristics in human cells. Planarian worms have amazed scientists with their apparently limitless ability to regenerate. Researchers have been studying their ability to replace aged or damaged tissues and cells in a bid to understand the mechanisms underlying their longevity.

Dr Aziz Aboobaker from the University's School of Biology, said: "We've been studying two types of planarian worms; those that reproduce sexually, like us, and those that reproduce asexually, simply dividing in two. Both appear to regenerate indefinitely by growing new muscles, skin, guts and even entire brains over and over again.

"Usually when stem cells divide -- to heal wounds, or during reproduction or for growth -- they start to show signs of aging. This means that the stem cells are no longer able to divide and so become less able to replace exhausted specialised cells in the tissues of our bodies. Our aging skin is perhaps the most visible example of this effect. Planarian worms and their stem cells are somehow able to avoid the aging process and to keep their cells dividing."

One of the events associated with aging cells is related to telomere length. In order to grow and function normally, cells in our bodies must keep dividing to replace cells that are worn out or damaged. During this division process, copies of the genetic material must pass on to the next generation of cells. The genetic information inside cells is arranged in twisted strands of DNA called chromosomes. At the end of these strands is a protective 'cap' called a telomere. Telomeres have been likened to the protective end of a shoelace which stops strands from fraying or sticking to other strands.

Each time a cell divides the protective telomere 'cap' gets shorter. When they get too short, the cell loses its ability to renew and divide. In an immortal animal we would therefore expect cells to be able to maintain telomere length indefinitely so that they can continue to replicate. Dr Aboobaker predicted that planarian worms actively maintain the ends of their chromosomes in adult stem cells, leading to theoretical immortality.

Dr Thomas Tan made some exciting discoveries for this paper as part of his PhD. He performed a series of challenging experiments to explain the worm's immortality. In collaboration with the rest of the team, he also went some way to understanding the clever molecular trick that enabled cells to go on dividing indefinitely without suffering from shortened chromosome ends.

Previous work, leading to the award of the 2009 Nobel Prize for Physiology or Medicine, had shown that telomeres could be maintained by the activity of an enzyme called telomerase. In most sexually reproducing organisms the enzyme is most active only during early development. So as we age, telomeres start to reduce in length.

This project identified a possible planarian version of the gene coding for this enzyme and turned down its activity. This resulted in reduced telomere length and proved it was the right gene. They were then able to confidently measure its activity and resulting telomere length and found that asexual worms dramatically increase the activity of this gene when they regenerate, allowing stem cells to maintain their telomeres as they divide to replace missing tissues.

Dr Tan pointed out the importance of the interdisciplinary expertise: "It was serendipitous to be sandwiched between Professor Edward Louis's yeast genetics lab and the Children's Brain Tumour Research Centre, both University of Nottingham research centres with expertise in telomere biology. Aziz and Ed kept demanding clearer proof and I feel we have been able to give a very satisfying answer."

However, what puzzled the team is that sexually reproducing planarian worms do not appear to maintain telomere length in the same way. The difference they observed between asexual and sexual animals was surprising, given that they both appear to have an indefinite regenerative capacity. The team believe that sexually reproductive worms will eventually show effects of telomere shortening, or that they are able to use another mechanism to maintain telomeres that would not involve the telomerase enzyme.

Dr Aboobaker concluded: "Asexual planarian worms demonstrate the potential to maintain telomere length during regeneration. Our data satisfy one of the predictions about what it would take for an animal to be potentially immortal and that it is possible for this scenario to evolve. The next goals for us are to understand the mechanisms in more detail and to understand more about how you evolve an immortal animal."

Professor Douglas Kell, BBSRC Chief Executive, said: "This exciting research contributes significantly to our fundamental understanding of some of the processes involved in aging, and builds strong foundations for improving health and potentially longevity in other organisms, including humans."

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The above story is reprinted from materials provided by University of Nottingham, via AlphaGalileo.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Thomas C. J. Tan, Ruman Rahman, Farah Jaber-Hijazi, Daniel A. Felix, Chen Chen, Edward J. Louis, and Aziz Aboobaker. Telomere maintenance and telomerase activity are differentially regulated in asexual and sexual worms. Proceedings of the National Academy of Sciences, February 27, 2012 DOI: 10.1073/pnas.1118885109

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

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Immortal worms defy ageing

Public release date: 27-Feb-2012
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Contact: Emma Thorne
emma.thorne@nottingham.ac.uk
44-115-951-5793
University of Nottingham

Researchers from The University of Nottingham have demonstrated how a species of flatworm overcomes the ageing process to be potentially immortal.

The discovery, published in the Proceedings of the National Academy of Sciences, is part of a project funded by the Biotechnology and Biological Sciences Research Council (BBSRC) and Medical Research Council (MRC) and may shed light on the possibilities of alleviating ageing and age-related characteristics in human cells.

Planarian worms have amazed scientists with their apparently limitless ability to regenerate. Researchers have been studying their ability to replace aged or damaged tissues and cells in a bid to understand the mechanisms underlying their longevity.

Dr Aziz Aboobaker from the University's School of Biology, said: "We've been studying two types of planarian worms; those that reproduce sexually, like us, and those that reproduce asexually, simply dividing in two. Both appear to regenerate indefinitely by growing new muscles, skin, guts and even entire brains over and over again.

"Usually when stem cells divide ? to heal wounds, or during reproduction or for growth ? they start to show signs of ageing. This means that the stem cells are no longer able to divide and so become less able to replace exhausted specialised cells in the tissues of our bodies. Our ageing skin is perhaps the most visible example of this effect. Planarian worms and their stem cells are somehow able to avoid the ageing process and to keep their cells dividing."

One of the events associated with ageing cells is related to telomere length. In order to grow and function normally, cells in our bodies must keep dividing to replace cells that are worn out or damaged. During this division process, copies of the genetic material must pass on to the next generation of cells. The genetic information inside cells is arranged in twisted strands of DNA called chromosomes. At the end of these strands is a protective 'cap' called a telomere. Telomeres have been likened to the protective end of a shoelace which stops strands from fraying or sticking to other strands.

Each time a cell divides the protective telomere 'cap' gets shorter. When they get too short, the cell loses its ability to renew and divide. In an immortal animal we would therefore expect cells to be able to maintain telomere length indefinitely so that they can continue to replicate. Dr Aboobaker predicted that planarian worms actively maintain the ends of their chromosomes in adult stem cells, leading to theoretical immortality.

Dr Thomas Tan made some exciting discoveries for this paper as part of his PhD. He performed a series of challenging experiments to explain the worm's immortality. In collaboration with the rest of the team, he also went some way to understanding the clever molecular trick that enabled cells to go on dividing indefinitely without suffering from shortened chromosome ends.

Previous work, leading to the award of the 2009 Nobel Prize for Physiology or Medicine, had shown that telomeres could be maintained by the activity of an enzyme called telomerase. In most sexually reproducing organisms the enzyme is most active only during early development. So as we age, telomeres start to reduce in length.

This project identified a possible planarian version of the gene coding for this enzyme and turned down its activity. This resulted in reduced telomere length and proved it was the right gene. They were then able to confidently measure its activity and resulting telomere length and found that asexual worms dramatically increase the activity of this gene when they regenerate, allowing stem cells to maintain their telomeres as they divide to replace missing tissues.

Dr Tan pointed out the importance of the interdisciplinary expertise: "It was serendipitous to be sandwiched between Professor Edward Louis's yeast genetics lab and the Children's Brain Tumour Research Centre, both University of Nottingham research centres with expertise in telomere biology. Aziz and Ed kept demanding clearer proof and I feel we have been able to give a very satisfying answer."

However, what puzzled the team is that sexually reproducing planarian worms do not appear to maintain telomere length in the same way. The difference they observed between asexual and sexual animals was surprising, given that they both appear to have an indefinite regenerative capacity. The team believe that sexually reproductive worms will eventually show effects of telomere shortening, or that they are able to use another mechanism to maintain telomeres that would not involve the telomerase enzyme.

Dr Aboobaker concluded: "Asexual planarian worms demonstrate the potential to maintain telomere length during regeneration. Our data satisfy one of the predictions about what it would take for an animal to be potentially immortal and that it is possible for this scenario to evolve. The next goals for us are to understand the mechanisms in more detail and to understand more about how you evolve an immortal animal."

Professor Douglas Kell, BBSRC Chief Executive, said: "This exciting research contributes significantly to our fundamental understanding of some of the processes involved in ageing, and builds strong foundations for improving health and potentially longevity in other organisms, including humans."

###

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Immortal worms defy aging

12-11-2011 21:49 Mr. Stolyarov provides a layman-friendly discussion of two recent major scientific discoveries in the war on senescence by Darren Baker and Jan van Deursen at the Mayo Clinic in Minnesota and Jean-Marc Lemaitre at the Institute de Génomique Fonctionnelle (IGF) in France. The Baker/van Deursen study highlights the possibility of extending health by targeting senescent cells. The Lemaitre study shows the promising possibility of creating pluripotent stem cells from the cells of very old individuals - paving the way for future genetic engineering and revitalization of these individuals. Both advances are highly encouraging steps in understanding and reversing the ravages of aging and eventually greatly expanding the human lifespan. References: * "Purging Cells in Mice Is Found to Combat Aging Ills" by Nicholas Wade, The New York Times. November 3, 2011. http://www.nytimes.com * "Forever young? A way to counteract part of the process of growing old". The Economist. November 5, 2011. http://www.economist.com * "Scientists Successful in Rejuvenating Cells in Elderly Patients" by Tiffany Kaiser. Daily Tech. November 8, 2011. http://www.dailytech.com * "French Scientists Restored The Youth Of 100 Years Old Cells" by Andrei Riciuon. DoctorTipster.com. November 2, 2011. http://www.doctortipster.com

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Combating Aging's Ravages - Advances in Minnesota and France - Video

Maxwell Jones (credit: CBS 2)

NEW YORK (CBSNewYork) — People in the Tri-State Area are living longer than ever, and if scientists have their way, life expectancies will continue to rise. Technologies today could allow the next generation to live up to 150, but how far should scientists go to allow people to live this long?

Baby Maxwell Jones’ life is just getting started, but if he’s lucky, the hours-old infant could live well into the next century.

“A hundred years, seems a stretch but it’s obviously possible,” his mother told CBS 2?s Kristine Johnson.

More than just possible as some aging experts believe scientific breakthroughs will mean babies born today will live more than 100 years.

Geriatrician Dr. Joyce Fogel says medical advances have already made a huge difference.

“There was a time when people didn’t live to older age because they died from the flu. We’re doing much better. In 1900, when somebody was born, they were expected to live to the age of 50,” she said.

Scientists are making huge advances in the lab, growing new organs from adult human stem cells, creating body parts with 3D printers, and using gene therapy to successfully treat diseases like blindness and leukemia.

And that’s not all. Doctors have already doubled the lifespan of a worm.

“The hope is that we could make a drug that would replicate in humans so that it would allow humans to stay young longer as well,” Dr. Cynthia Kenyon said.

However, work like this isn’t considered mainstream.

“Sometimes technology exceeds common sense,” one woman said.

“As long as science will allow me to live I want to live as long as possible,” another woman said.

Sonia Arrison researched the science of aging for eight years.  She says longer lifespans will change everything about the way we live, from our families to our finances.  Some people will have second and even third careers.

“Some people are worried that we’re going to create designer humans or  something like that, but what I’m talking about is helping people who are already here live longer and healthier lives,” she said.

“You wouldn’t want to retire at 65. It gives people options and allows  them to create the life that they really want to live.  And I think that’s extremely exciting,” she added.

But for now, prevention goes on long way to improve quality of life later on.

“I would question if we’re really going to hit 150, but I think I would want people to live with good quality life. If at 150 we’re filling up nursing homes, I wonder,” said Fogel.

Aging experts say lifestyle changes can help you make it to your 80s. After that, it’s genetics that matter most.

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Seen At 11: Could The Next Generation Live To Be 150?

18-11-2011 17:40 Fruit fly intestine may hold secret to the fountain of youth Long-lived fruit flies offer Salk scientists clues to slowing human aging and fighting disease November 02, 2011 LA JOLLA, CA—One of the few reliable ways to extend an organism's lifespan, be it a fruit fly or a mouse, is to restrict calorie intake. Now, a new study in fruit flies is helping to explain why such minimal diets are linked to longevity and offering clues to the effects of aging on stem cell behavior. Scientists at the Salk Institute for Biological Studies and their collaborators found that tweaking a gene known as PGC-1, which is also found in human DNA, in the intestinal stem cells of fruit flies delayed the aging of their intestine and extended their lifespan by as much as 50 percent. "Fruit flies and humans have a lot more in common than most people think," says Leanne Jones, an associate professor in Salk's Laboratory of Genetics and a lead scientist on the project. "There is a tremendous amount of similarity between a human small intestine and the fruit fly intestine." Learn more at: salk.edu

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Salk News Clip - Long Lived Fruit Flies (KPBS) - Video