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Long-lived bats offer clues on diseases, cancer and aging

Long-lived bats offer clues on diseases, cancer and aging | AgingLab | Scoop.it

Studying the DNA of two distant bat species, the scientists discovered how genes dealing with the bats' immune system had undergone the most rapid change. This may explain why they are relatively free of disease and live exceptionally long lives compared with other mammals of similar size, such as the rat, said Professor Lin-Fa Wang, an infectious disease expert at the Duke-NUS Graduate Medical School in Singapore who led the multi-centre study.

 

"We are not saying bats never get sick or never get infections. What we are saying is they handle infections a lot better," Wang said. What was missing from both species of bats was a gene segment known to trigger extreme, and potentially fatal, immune reactions to infections, called the cytokine storm.

Cytokine storms end up killing not only offending viruses in the body, but the host's own cells and tissues too.

 

"Viruses rarely kill the host. The killing comes from the host's immune response. So it looks like what bats are doing is depress the inflammation (cytokine storm). If we can learn that, we can design drugs to minimize the inflammation damage and control viral infection," Wang said.

 

Compared with other mammals of similar size, bats live a long time, with lifespans of between 20 and 40 years. Rats live between 2 and 3 years, on average.

 

Interestingly, Wang and his colleagues found that the highly evolved genes that give bats their superior immune system also enable them to fly. Out of more than 5,000 types of mammals on the planet, bats are the only one capable of sustained flight and some species can fly more than 1,000 km in a single night.

 

Such intense physical exertion is known to produce toxic "free radicals" that cause tissue damage and it is these same genes that give the bat the ability to repair itself, Wang said. "What we found was the genes that evolved fastest were genes involved in repairing DNA damage. That makes sense ... because when you fly, metabolism goes up and it generates free radicals that are toxic to cells," Wang said.

 

"Because bats fly, they (would have had) to evolve and adapt ... to get genes that can repair DNA damage." Wang said we have much to learn from the bat, which has evolved to avoid disease and live exceptionally long lives. "Cancer, ageing and infectious disease, these are the three major areas of concern for people," he said.

 

"We have studied rats for 150 years to understand how to do better in these three areas. Now we have a system, the bat, that has done very well in evolution. We can learn from the bat. With modern techniques, we can design new drugs to slow down the ageing process, treat cancer, fight infections."


Via Dr. Stefan Gruenwald
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A new — and reversible — cause of aging | KurzweilAI

A new — and reversible — cause of aging | KurzweilAI | AgingLab | Scoop.it

Researchers have discovered a cause of aging in mammals that may be reversible: a series of molecular events that enable communication inside cells between the nucleus and mitochondria.

As communication breaks down, aging accelerates. By administering a molecule naturally produced by the human body, scientists restored the communication network in older mice. Subsequent tissue samples showed key biological hallmarks that were comparable to those of much younger animals.

“The aging process we discovered is like a married couple — when they are young, they communicate well, but over time, living in close quarters for many years, communication breaks down,” said Harvard Medical School Professor of Genetics David Sinclair, senior author on the study. “And just like with a couple, restoring communication solved the problem.”


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Delayed aging is better investment than cancer, heart disease research

Delayed aging is better investment than cancer, heart disease research | AgingLab | Scoop.it

Via Louie Helm
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Louie Helm's curator insight, December 16, 2013 2:05 AM

"Recent scientific advances suggest that slowing the aging process (senescence) is now a realistic goal. Yet most medical research remains focused on combating individual diseases."


"Using the Future Elderly Model—a microsimulation of the future health and spending of older Americans—we compared optimistic “disease specific” scenarios with a hypothetical “delayed aging” scenario in terms of the scenarios’ impact on longevity, disability, and major entitlement program costs. Delayed aging could increase life expectancy by an additional 2.2 years, most of which would be spent in good health."


"The economic value of delayed aging is estimated to be $7.1 trillion over fifty years."


"In contrast, addressing heart disease and cancer separately would yield diminishing improvements in health and longevity by 2060—mainly due to competing risks. Delayed aging would greatly increase entitlement outlays, especially for Social Security. However, these changes could be offset by increasing the Medicare eligibility age and the normal retirement age for Social Security. Overall, greater investment in research to delay aging appears to be a highly efficient way to forestall disease, extend healthy life, and improve public health."

Mark Waser's curator insight, December 23, 2013 6:09 PM

Simple economics . . . .

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Scientists Develop Initial Anti-Aging Formula: Progeria Mice live 30% longer

Scientists Develop Initial Anti-Aging Formula: Progeria Mice live 30% longer | AgingLab | Scoop.it

A new study indicates that scientists have found a new way of delaying the aging process in mice, and they hope to replicate the finding in people. The research was built upon an earlier study that shed light on progeria, a rare genetic disease that prematurely ages one in four million babies.

 

A mutation was found in the Lamin A protein, which lines the nucleus in human cells, disrupting the repair process and accelerating aging. They also found that normal and healthy Lamin A binds to and activates the gene SIRT1, which has been long associated with longevity. If scientists can develop drugs that mimic Lamin A or increase the binding between Lamin A and SIRT1, this may lead to anti-aging drugs.

 

The team also examined if the binding efficiency was boosted with resveratrol, a compound found in the skin of red grapes. Mice fed with concentrated resveratrol fared significantly better than healthy mice that weren’t given it and the onset of aging was delayed and the life expectancy was extended. Mice with progeria lived 30% longer when fed with resveratrol compared with progerial mice not given the compound.

 


Via Dr. Stefan Gruenwald
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NoAging's curator insight, July 7, 2013 5:29 AM

Extending lifespan of mutated mice is the first key to extending our healthspans!

Linda Holroyd's curator insight, November 12, 2014 12:01 PM

Let's fund research on Lamin A and SIRT1

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Scientists Reverse the Signs of Aging in Mice

Scientists Reverse the Signs of Aging in Mice | AgingLab | Scoop.it
By administering a molecule that is naturally produced by the human body scientists restored communication between the nucleus and mitochondria inside cells in older mice, reversing the signs of aging.

Via Allen Taylor
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Allen Taylor's curator insight, December 20, 2013 5:36 PM

Some aspects of aging may be reversible if humans respond the same way that mice did in a recent experiment.