Can human lifespan be extended by 45%?

Madrid: The human lifespan could be extended by up to 45 per cent if tests on mice can be replicated in people.

As well as a longer life the dicovery could also mean one where people suffer less serious diseases.

Scientists have made a genetic breakthrough which they claim could extend human life and and left them free from tumours.

The researchers, at the Spanish National Cancer Research Centre (CNIO), carried out an experiment in which they inserted three genes, known for their longevity benefits into the stem cells of mice.

The extra copies of the genes – telomerase, P53 and p16, improves the body’s function and immunity to disease, including cell mutation which occurs more frequently in ageing adults.

The technique is a new breakthrough because the scientists managed to extra copies of both p53 and p16 into the mice, which has never been achieved before. It is also the first time that scientists have been able to extend the life of mice in this way while protecting them against cancer.

The modified mice were allowed to breed to strengthen their new DNA pattern, which created a group of ‘supermice’ with longer lifespans and in-built cancer protection.

It is thought the researchers managed to create mice which lived to around four-and-a-half years. Normally, they live for an average of three years – the equivlent of a human living to 125.

Chief researcher Maria Blasco, one of Spain’s leading scientists, said that the elixir of eternal youth is now a Utopian dream.

“The discovery opens the door to the possibility that humans could live 125 years and without cancer.’

US scientists on track of elixir of youth


Los Angeles: Scientists in California have used biochemical signals to rejuvenate elderly bodily tissues in mice.

Research by Dr Morgan Carlson, published in the journal Nature, was overseen by Irina Conboy, associate professor at UC Berkeley.

Professor Conboy said: “We don’t realize it, but as we grow our bodies are constantly being remodeled. We are constantly falling apart, but we don’t notice it much when we’re young because we’re always being restored. As we age, our stem cells are prevented, through chemical signals, from doing their jobs.”

“When old tissue is placed in an environment of young blood, the stem cells behave as if they are young again,” according to the Berkeley press release.

Essentially, the Californian researchers were able to persuade muscle tissues in some mice that they were young again.

“Interestingly, activated Notch competes with activated pSmad3 for binding to the regulatory regions of the same CDK inhibitors in the stem cell,” said Professor Conboy.

“We found that Notch is capable of physically kicking off pSmad3 from the promoters for the CDK inhibitors within the stem cell’s nucleus, which” – as any fool would realise – “tells us that a precise manipulation of the balance of these pathways would allow the ability to control stem cell responses.”

Altering the Notch and pSmad3 levels using “an established method of RNA interference” allowed Conboy and Carlson to manipulate TGF-beta proteins and fire up the dormant stem cells of a group of elderly mice.

“When we are young, there is an optimal balance between Notch and TGF-beta,” according to Conboy. “We need to find out what the levels of these chemicals are in the young so we can calibrate the system when we’re older. If we can do that, we could rejuvenate tissue repair for a very long time.”

Read more at Pathways to the Fountain of Youth

Scientists develop nasal spray for Alzheimer’s


Tel Aviv: Israeli scientists have developed a nasal spray that zaps the brain plaque doctors believe is the cause of Alzheimer’s disease.

The spray which contains bacteriophages, a virus which scientists call “phages” has only been used to treat mice with a disease similar to Alzheimer’s. But it is hoped a version for humans will go on sale within seven years.

The spray attacks beta amyloid, a sticky protein that destroying connections between brain cells in Alzheimer’s sufferers.

In tests on mice, regular treatment for a year with the spray reduced the amount of amyloid in their brains by 80 per cent. The drug also improved the mice’s memory and learning, and restored their sense of smell, which is often lost early in the onset of Alzheimer’s.

Experts are predicting an Alzheimer’s epidemic by 2050 as life expectancies increase.

Stem cell experiment may help lung disease sufferers

Stockholm: Lung cells grown from mouse embryo stem cells have been successfully implanted into the lungs of mice, a breakthrough that could one day help humans with sick lungs, say researchers.

The experiment was conducted by a team of scientists from London’s Imperial College and is a “global breakthrough” that “opens up exciting new horizons for the treatment of lung disease,” a statement from the European Respiratory Society’s (ERS) annual congress in Stockholm said.

In the experiment, the researchers injected lung cells cultivated from embryonic stem cells into the mice’s lungs.

Two days later, they killed the rodents and found that the lung cells had lodged themselves in the animals’ lungs, demonstrating the “high degree of specialisation of these cells, which attach only to their target organ, ie. the lungs,” the statement said.

Embryonic stem cell therapy has given rise to hopes for the treatment of many conditions and could one day help repair organs, such as a heart damaged by a heart attack.

Experiments suggest stem cells could also yield effective treatments for Parkinson’s and Alzheimer’s disease, spinal cord injury, diabetes, osteoarthritis, and numerous other illnesses.

But lung diseases have not yet benefited from stem cell research.

One of the great challenges of cell biology is figuring out how stem cells remain unspecialised or “pluripotent,” maintaining the capacity to become virtually any type of cell found in blood, nerves and individual organs.

“The lung is a very difficult target for tissue engineering researchers … especially since it is an extremely complex organ and contains a large variety of cells, some of which have a very slow renewal rate,” researcher Sile Lane of Imperial College said in the statement.

The ERS said the capacity to “regenerate lungs damaged by disease or accident would help tens of millions of patients.”

While the study sparked “great hopes”, the British researchers noted that human medical applications were “still a long way off.”

According to the ERS, respiratory diseases are the main cause of death in the world. In Europe, respiratory diseases cost society more than 100 billion euros (140 billion dollars) a year.

A total of 15,000 clinical doctors, researchers, physiotherapists and medical and pharmaceutical industry workers from more than 100 countries are attending the congress in Stockholm, which concludes on Wednesday.

Scientists prolong the life of mice

Madrid: Researchers in Spain discovered a way to make mice live up to 16% longer – equivalent to an extra 12 years on the average human lifespan.

Mice with elevated levels of a protein called p53 appeared younger, healthier and were more resistant to the development of cancers, according to a study by scientists at the Spanish National Cancer Research Centre.

Their discovery will accelerate the development of new drugs that fight cancer while extending healthy youth and lifespan. The protein p53 is known as “the guardian of the genome” because it makes sure that damaged cells destroy themselves and do not divide uncontrollably to cause tumours.

Scientists have long speculated that boosting our body’s levels of p53 could help us live longer, but early studies found it actually accelerated ageing.

But not according to the findings of Dr Manuel Serrano, of the Spanish National Cancer Research Centre. His team genetically engineered mice to have an extra copy of p53 and a related gene – ARF.

They showed that mice with an increased dose of the two proteins were more resistant to the development of cancers. It came as no surprise, therefore, that these animals had an extended lifespan compared with normal mice.

But remarkably, the animals outlived their normal counterparts even after the impact of having less cancer was removed from the equation, according to the study which is published in the magazine Nature.

Moreover, various biological and molecular markers of ageing indicated that these mice stay younger for longer. The researchers conclude that boosting the body’s ARF/p53 activity provides an anti-oxidant effect, which not only suppresses cancers, but also delays ageing.

Dr Serrano said: “The mice lived 16% longer in their average lifespan,” said Dr Serrano.

“Everyone agrees that ageing is produced by the accumulation of damaged cells. If p53 is the main quality control that eliminates such cells, then the expectation is that having more p53 mice will have a more strict quality control for cells, hence less cancer and less ageing.”

The study opens up possibilities for new drugs that delay ageing by boosting the body’s production of p53.

“There are a number of chemical compounds that have been developed by the big pharmaceutical companies and these compounds are able to boost p53 in the organism,” said Dr Serrano.

“These compounds are being tested now for their possible anti-cancer activity and hopefully in the light of our study also for their possible anti-ageing activity.”

Cool mice live longer!

La Jolla: Mice cooled by half a degree below normal had a life expectancy 20% longer, or the equivalent of 7-8 additional human years.

The result implies that chilling human blood could also stretch out our lifespan, if a safe way can be found to do it. “Maybe from the point of view of survival, 37 is not exactly optimal,” says lead researcher Bruno Conti of the Scripps Research Institute in La Jolla, California.

It has long been held that the ideal human body temperature is 37 degrees Celsius. But this new study suggests that 36.5 °C might be even better.

Researchers have known for decades that a diet containing a third less calories than usual extends the lifetime of mice and other mammals by up to 40% and drops their body temperature by half a degree or more.

It was not known whether the cooler temperature helps stave off ageing or is simply a by-product of the low-calorie diet. And this is virtually impossible to test, because mammals maintain the same temperature regardless of the surrounding clime.

Conti’s team managed to cool down mice using genetic engineering. They used a gene called uncoupling protein 2, which diverts the cells’ mitochondria from their usual task of making chemical energy, and instead prompts them to release energy as heat.

They inserted this gene into a group of brain cells in the animals’ hypothalamus and near to the region that senses and controls body temperature, much like a thermostat. The gene effectively heated up the thermostat and, as a result, tricked the rest of the body into cooling down by 0.3 to 0.5 °C.

Cooled female mice had a life expectancy 20% longer and males 12% longer. The mice appeared to live typically healthy lives up to the point that they died; they were not simply stretching out their frail, elderly days. The results are published in Science1.

The study suggests that the lower body temperature accounts for some of the age-fighting effects of calorie restriction. It may be that the cooler temperature slows down metabolism and the manufacture of by-products such as free radicals that damage and age cells.

“You don’t necessarily have to eat less to have the beneficial effects,” Conti says.

“Not many people are willing to spend their lives starving themselves,” says Cliff Saper who studies sleep and feeding at Harvard Medical School in Boston, Massachusetts. If, on the other hand, researchers can find a way to carry out the same brain-warming gene therapy in people, “You could get people to sign up for that.”

Nobody knows why 37 °C is, on average, the temperature that evolution favoured for humans and most other mammals, but it is generally assumed to be optimal for biochemical reactions.

So if 36.5 °C helps animals to live longer, why wasn’t it selected for through evolution? The cooler temperature probably has no selective advantage because it stretches out life after reproduction, and does not affect the ability of animals to have children and pass on their genes. And although Conti’s mice appeared normal, it’s possible that the lower body temperature actually causes subtle health problems.

“If there is a selective advantage to being cooler, evolution would have pushed us in that direction,” Saper says.

Conti suspects that some people may have small differences in their core body temperature that might alter their rate of aging, perhaps making some longer-living than others. This would only be possible to test using small, swallowed or implanted thermometers such as those carried by the experimental mice.
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Exercise may help fight cancer

New Jersey:A study of mice has shown that exercise helps fight cancer.

Researchers at Rutgers University found that female mice exposed to a form of ultraviolet light took longer to develop skin tumours if they had access to a running wheel.

However, experts warned the study, published in the journal Carcinogenesis, was not an excuse to go out in the sun unprotected.

In the first part of the study mice were exposed to ultraviolet B (UVB) three times a week for 16 weeks. Then for the next 14 weeks, in the absence of further UVB treatment, half the mice had access to running wheels in their cages, while the other half did not.

In the second part mice were exposed to UVB light twice a week for 33 weeks, and, from the beginning, half had access to a running wheel and half did not.

All the mice in the high risk part of the study developed skin tumours. But exercising mice took an average of seven weeks to show signs of cancer, compared to an average of just 3.5 weeks in the mice which took no exercise.

The tumours in the exercising mice were also less numerous and smaller.

Non-malignant tumour size per mouse was decreased by 54% and malignant tumour size per mouse by 73%.

The second part of the study produced similar results. Again the exercising mice were slower to develop tumours, developed fewer tumours and those that they did develop were smaller.

This time non-malignant tumour size per mouse was decreased by 75% and malignant tumour size per mouse by 69%.

Analysis of samples found that exercise appeared to enhance programmed cell death (apoptosis) – a process that removes sun-damaged cells – both in the skin, and in tumours.

Lead researcher Dr Allan Conney said: “While UVB is triggering the development of tumours, exercise is counteracting the effect by stimulating the death of the developing cancer cells.”

Dr Conney said the results also showed that animals with less fat developed less tumours. He said this might be a significant factor – particularly as obesity rates were rising throughout the Western world.