Public release date: 29-Mar-2012 [ | E-mail | Share ]

Contact: Samantha Martin 44-015-179-42248 University of Liverpool

Scientists at the University of Liverpool have developed a new method to detect proteins associated with longevity, which helps further our understanding into why some animals live longer than others.

The team looked at the genome of more than 30 mammalian species to identify proteins that evolve in connection with the longevity of a species. They found that a protein, important in responding to DNA damage, evolves and mutates in a non-random way in species that are longer-lived, suggesting that it is changing for a specific purpose. They found a similar pattern in proteins associated with metabolism, cholesterol and pathways involved in the recycling of proteins.

Findings show that if certain proteins are being selected by evolution to change in long-lived mammals like humans and elephants, then it is possible that these species have optimised pathways that repair molecular damage, compared to shorter-lived animals, such as mice.

The study, led by Dr Joao Pedro Magalhaes and postgraduate student, Yang Li, is the first to show evolutionary patterns in biological repair systems in long-lived animals and could, in the future, be used to help develop anti-ageing interventions by identifying proteins in long-lived species that better respond to, for example, DNA damage. Proteins associated with the degradation of damaged proteins, a process that has been connected to ageing, were also linked with the evolution of longevity in mammals.

Dr Magalhaes, from the University's Institute of Integrative Biology, said: "The genetic basis for longevity differences between species remains a major puzzle of biology. A mouse lives less than five years and yet humans can live to over 100 for example. If we can identify the proteins that allow some species to live longer than others we could use this knowledge to improve human health and slow the ageing process.

"We developed a method to detect proteins whose molecular evolution correlates with longevity of a species. The proteins we detected changed in a particular pattern, suggesting that evolution of these proteins was not by accident, but rather by design to cope with the biological processes impacted by ageing, such as DNA damage. The results suggest that long-lived animals were able to optimise bodily repair which will help them fend off the ageing process."

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The research is published in the American Aging Association's journal, AGE.

Originally posted here:
Study suggests why some animals live longer

ScienceDaily (Mar. 29, 2012) Scientists at the University of Liverpool have developed a new method to detect proteins associated with longevity, which helps further our understanding into why some animals live longer than others.

The team looked at the genome of more than 30 mammalian species to identify proteins that evolve in connection with the longevity of a species. They found that a protein, important in responding to DNA damage, evolves and mutates in a non-random way in species that are longer-lived, suggesting that it is changing for a specific purpose. They found a similar pattern in proteins associated with metabolism, cholesterol and pathways involved in the recycling of proteins.

Findings show that if certain proteins are being selected by evolution to change in long-lived mammals like humans and elephants, then it is possible that these species have optimized pathways that repair molecular damage, compared to shorter-lived animals, such as mice.

The study, led by Dr Joao Pedro Magalhaes and postgraduate student, Yang Li, is the first to show evolutionary patterns in biological repair systems in long-lived animals and could, in the future, be used to help develop anti-aging interventions by identifying proteins in long-lived species that better respond to, for example, DNA damage. Proteins associated with the degradation of damaged proteins, a process that has been connected to aging, were also linked with the evolution of longevity in mammals.

Dr Magalhaes, from the University's Institute of Integrative Biology, said: "The genetic basis for longevity differences between species remains a major puzzle of biology. A mouse lives less than five years and yet humans can live to over 100 for example. If we can identify the proteins that allow some species to live longer than others we could use this knowledge to improve human health and slow the aging process.

"We developed a method to detect proteins whose molecular evolution correlates with longevity of a species. The proteins we detected changed in a particular pattern, suggesting that evolution of these proteins was not by accident, but rather by design to cope with the biological processes impacted by aging, such as DNA damage. The results suggest that long-lived animals were able to optimise bodily repair which will help them fend off the aging process."

The research is published in the American Aging Association's journal, Age.

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Why some animals live longer than others

Those looking for a magic elixir to keep them healthy and happy need look no further than their bank account. Wealth and, more broadly, socioeconomic status play powerful roles in determining how long we live.

"It's clear that those who have less wealth will have fewer years to live than those with more wealth," says James Smith, senior economist at the research group Rand. The connection is so widely accepted that researchers have given it a name: "the wealth gradient in mortality." What's far more complicated to understand is why the connection exists, and whether wealth causes better health, or vice versa.

The longest-running longitudinal study of health, run by George Vaillant, a professor of psychiatry at Harvard Medical School, found education to be one of the biggest determinants of longevity, along with behavioral factors -- excessive drinkers were more likely to die young, for example. Out of the 500-plus Harvard students and inner-city Boston men the study has followed since 1937, the Harvard students have lived an average of 10 years longer than the inner-city men, says Vaillant. In fact, three in 10 of the Harvard students reached age 90, compared with the 3% to 5% one would expect.

Among the inner-city men who attended college, health was just as good as that of Harvard students who attended college but not graduate school, says Vaillant. "(The Boston men) went to terrible colleges by Harvard standards, but they did get 16 years of education, and that absolutely evened the playing field," says Vaillant. People who go to college tend to drink less, smoke less, and are less likely to be obese, he adds, all factors that contribute to longevity. In fact, after controlling for education and other factors, Vaillant found that income alone had little effect on longevity.

People who pursue higher education, explains Vaillant, tend be more focused on the future, which probably also helps them make healthier choices. "In order to get an education, especially if you're poor, you have to think you have a future," he says.

Indeed, says Smith, one hypothesis is that "more-educated people are more forward-looking, and when they make decisions, they take into account the future more than uneducated people. A lot of things you might do don't have an immediate negative impact -- excessive drinking, smoking and doing drugs can (feel good in the short-term) -- but the fact is, it's going to kill you in the future." Another possibility is that people with higher levels of education are more likely to maintain their health, have better access to health care, and follow doctors' directions when it comes to taking pills or other instructions.

Smith's research also suggests that causality doesn't just run one way; health contributes to wealth, as well. "Because you are healthy and able to work, you are wealthier," he explains. At the same time, poor health often takes a toll on a person's wealth, either because it prevents one from working or because of expensive medical treatments. Taken together, researchers at the University of Chicago estimate that the gains in life expectancy between 1970 and 2000 resulted in an additional $3.2 trillion a year in national wealth.

Meanwhile, as income disparities continue to grow in this country, so do life expectancy disparities. According to an analysis by the Social Security Administration, life expectancy for 65-year-old men in the top half of the earnings distribution has increased by five years, to 21.5 more years. For those in the bottom half of the earnings distribution, life expectancy has increased just over one year, to 16.1 more years.

More:
Do rich people live longer?

Rapamycin-induced longevity in mice can be uncoupled from diabetes-inducing side effects

Newswise PHILADELPHIA A Penn- and MIT-led team explained how rapamycin, a drug that extends mouse lifespan, also causes insulin resistance. The researchers showed in an animal model that they could, in principle, separate the effects, which depend on inhibiting two protein complexes, mTORC1 and mTORC2, respectively.

The study suggests that molecules that specifically inhibit mTORC1 may combat age-related diseases without the insulin-resistance side effect, which can predispose people to diabetes.

Senior author Joseph A. Baur, PhD, assistant professor of Physiology, Perelman School of Medicine, University of Pennsylvania, and colleagues at the Whitehead Institute for Biomedical Research and Broad Institute, Massachusetts Institute of Technology, in Cambridge, MA, describe their work in this weeks issue of Science. Baur is also a member of Penns Institute for Diabetes, Obesity, and Metabolism.

The hope is that in the future, we will be able to develop molecules that target mTORC1 specifically, separating out the beneficial effects of rapamycin on aging and disease, and leaving behind the insulin-resistance side effect, says Baur.

Our results demonstrate that reduced mTORC1 signaling is sufficient to extend lifespan and mTORC2 signaling has profound effects on metabolism, says co-first author Lan Ye, PhD, postdoctoral fellow in the Baur lab. Our findings indicate that mTORC2 may be an important player in the pathogenesis of type 2 diabetes and metabolic syndrome."

One Compound, Many Effects Rapamycin extends the lifespan of yeast, flies, and mice and is also an immunosuppressant drug for organ transplants and an anti-cancer drug. It was first discovered as a byproduct of Streptomycin hygroscopicus, a bacterium found in a soil sample from Easter Island, an island also known as Rapa Nui, hence the name. Rapamycin was originally developed as an antifungal agent, but that use was abandoned when it was discovered to have immunosuppressive properties.

The mTOR complexes, for mammalian (or mechanistic) target of rapamycin, are proteins that regulate cell growth, movement, and survival, as well as protein synthesis and transcription. Specifically, there are two mTOR complexes and one mTOR protein. The mTOR protein is the core of both complexes (mTORC1 and mTORC2), which behave differently based on their associated proteins. One or both of the mTOR complexes can be inappropriately activated in certain cancers, and dual-specific inhibitors are being developed as chemotherapeutic agents.

Several theories have been put forward by researchers to explain the observations that patients receiving rapamycin are more prone to developing glucose intolerance, which can lead to diabetes. Chronic treatment with rapamycin impairs glucose metabolism and the correct functioning of insulin in mice, despite extending lifespan. The research team demonstrated that rapamycin disrupts mTORC2 in the mice, and that mTORC2 is required for the insulin-mediated suppression of glucose metabolism in the liver.

On the other hand, they also demonstrated that decreasing mTORC1 signaling was sufficient to extend lifespan independently from changes in glucose metabolism. They used a mouse strain in which mTORC1 activity was decreased and saw that lifespan was extended by 14 percent, yet the animals had normal glucose metabolism and insulin sensitivity.

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Duality of Longevity Drug Explained

Published: March. 29, 2012 at 7:36 PM

LIVERPOOL, England, March 29 (UPI) -- British scientists say their genetic studies have helped detect proteins associated with longevity, helping explain why some animals live longer than others.

The researchers examined the genome of more than 30 mammalian species to identify proteins that evolve in connection with the longevity of a species, the University of Liverpool reported Thursday.

A particular protein -- involved in responding to DNA damage -- evolves and mutates in a non-random way in species that are longer-lived, the researchers found, suggesting it is changing for a specific purpose.

The study is the first to show evolutionary patterns in biological repair systems in long-lived animals, they said.

The findings may help develop anti-aging interventions by identifying proteins in long-lived species that better respond to DNA damage, they said.

"The genetic basis for longevity differences between species remains a major puzzle of biology," researcher Joao Pedro Magalhaes said. "A mouse lives less than five years and yet humans can live to over 100, for example.

"If we can identify the proteins that allow some species to live longer than others we could use this knowledge to improve human health and slow the aging process."

More here:
Genetic study yields longevity clue