Stem Cells to Cure Blindness?

People suffering from a form of incurable blindness could soon become the first patients in the world to benefit from a new and controversial transplant operation using stem cells derived from spare human embryos left over from IVF treatment. 

 Scientists working for an American biotechnology company yesterday applied for a licence to carry out a clinical trial on patients in the US suffering from a type of macular degeneration, which causes gradual loss of vision. They expect the transplant operations to begin early in the new year. 

The development is highly controversial because many “pro-life” groups are opposed to using human embryos in any kind of medical research but scientists believe that the benefits could revolutionise the treatment of many incurable disorders ranging from Parkinson’s to heart disease.

The company has applied for a licence from the US Food and Drug Administration (FDA) and is confident of its application being granted. 

“We’ve seen absolutely no adverse effects whatsoever in any of the preclinical experiments and our cells are more than 99.9 per cent pure,” said Dr Robert Lanza, the chief scientific officer of Advanced Cell Technology (ACT) in Worcester, Massachusetts. 

“We certainly expect them [the FDA] to come back with comments and questions but our hope is that we will start sometime early next year. We’re optimistic and certainly confident in our own data. We’ve been in dialogue [with the FDA] and we know what was on their mind and what they wanted us to do,” he said. “We’re hoping, assuming no hitches, to begin early next year, perhaps March.” 

Stem cells derived from human embryos that are only a few days old have the ability to develop into any of the scores of specialised tissues of the body. The hope is that they could be used to repair the damaged organs and tissues of patients with a relatively simple transplant procedure. 

ACT has filed an “investigational new drug” application with the FDA to treat a form of progressive damage to the retina of the eye called Stargardt’s macular degeneration, which destroys the central part of the retina involved in recognising faces and reading words on a page. They also intend to follow this with an application to treat age-related macular degeneration, which affects more than 500,000 people in Britain and is the most common cause of blindness. 

“We hope to file a second application for age-related macular degeneration very soon within the next few months,” said Dr Lanza. “I think we’ve put together a pretty convincing case but the FDA has to be pretty careful. I’m sure they will come back to us in the next 30 days with more questions.” 

The treatment for eye disease uses stem cells to recreate a type of cell in the retina that supports the photoreceptors needed for vision. These cells form the retinal pigment epithelium – which keep the light-sensing cells of the retina alive – which are often the first to die off in macular degeneration, which in turn leads to loss of vision, he said. 

A single cell from a human embryo left over from IVF treatment was used in the creation of the stem cell “line” that Dr Lanza and his colleagues cultivated in the laboratory. By bathing the stem cells in a suite of chemical messengers, they were able to stimulate them to develop into fully mature retinal pigment epithelium cells. 

Tests on animals found that transplants of the human cells into rats with macular degeneration resulted in a “100 per cent improvement” in vision with no side-effects, Dr Lanza said. Transplants into the 12 human volunteers chosen as guinea pigs for the first clinical trial will involve giving them mild immuno-suppressant drugs to prevent tissue rejection. 

“We’re going to take a precautionary approach and use low-dose immuno-suppression after the operation and after six weeks we’ll taper it off. We don’t know whether we will really need it,” Dr Lanza said. 

He said the clinical trial could well be the first in the world because the only other company that had received a licence from the FDA had had to delay the start of its own clinical trial until the end of next year. 

Geron, which received its FDA licence earlier this year, has run into safety problems with experiments on animals involving the growth of cysts. It has had to provide further information to the FDA in order to satisfy nervous regulators that the new technique is as safe as possible. 

Meanwhile, ACT believes it has stolen a march on Geron because its own pre-clinical studies on animals have shown that its embryonic stem cells are extremely pure and safe with no signs of the cysts seen in the animals injected with the embryonic stem cells that Geron was hoping to use in patients suffering from spinal cord injuries. “They’ve been through this with Geron and the company has put out an announcement that they won’t start until the third quarter of next year, so ours may well be the first trial,” Dr Lanza said.

A similar proposal to treat age-related macular degeneration with embryonic stem cells is being developed by scientists in Britain led by Professor Pete Coffey of University College London, but this clinical trial is unlikely to start until early 2011. “It’s such a complex, wholly new process that nobody had done before and it has to be done properly,” he said. 

“It hasn’t been done before in humans and that is affecting the last stages of the plan to get into the clinic so it’s obvious that we don’t want anything to go wrong. But someone has to be the first take that step.” 

Dr Lanza said that extensive work had been done to ensure that the cells derived from embryonic stem cells were of high enough quality to be considered clinical grade. His company has submitted nine volumes of safety data to the FDA to address concerns over purity and the possibility that the stem cells may trigger the formation of cancerous tumours. 

“What we definitely have going for us is that the cells are so well purified, well characterised and there are no adverse effects. So there is nothing here to send up a flag of concern,” Dr Lanza said. “It has been over a decade since human embryonic stem cells were first discovered. The field desperately needs a big clinical success.”

“After years of research and political debate, we’re finally on the verge of showing the potential clinical value of embryonic stem cells. Our research clearly shows that stem cell-derived retinal cells can rescue visual function in animals that otherwise would have gone blind.

 “We are hopeful that the cells will be similarly efficacious in patients,” Dr Lanza added.

Dog Hair May Provide Insight on Cancer

Scientists have located the genes that make a poodle’s hair curly, and a collie’s hair long and straight.

No, this wasn’t just a way to ease the boredom of laboratory work, but part of a long-term project to figure out how genes cause disease.

The coats of domestic dogs vary widely — they can be long, short, straight, wavy, curly, wiry, smooth or a combination of different varieties. And that difference is exactly why cancer geneticist Elaine Ostrander decided to study dog hair.

Ostrander, who works at the National Human Genome Research Institute, wanted to know how genes create all this variety. So she studied about 1,000 dogs from about 90 different breeds.

She searched dog DNA the way a chef might compare recipes for souffle. What changed ingredient makes one different from the next? What mutation gives an Airedale terrier his curls and a golden retriever her tresses?

A Three-Gene Recipe

What Ostrander and her team discovered was that only three genes control all the different kinds of dog hair.

“You can go to the dog park, and every breed of dog looks different from every other breed, it seems,” says Ostrander. “Yet, you know, when we get down to the molecular biology, we really find that it’s a combination of three different genes that accounts for all that variation.”

This also has value in studying disease. Human and dog cancers are similar, so the fact that only three genes can create so much variation in hair might provide clues to how genes cause so many cancers in dogs and humans.

“Whether or not the exact same gene is mutated in humans doesn’t really matter,” says Ostrander. “It’s telling us the pathways that are involved, the kinds of genes that are involved, and the kinds of changes in those genes that lead to those diseases.”

The research appears online Thursday in Science Express.

Source: NPR

How Fast Can a Human Possibly Run?

Amazing as Usain Bolt’s new world record 100-meter victory was, his time of 9.58 seconds is nowhere near what biostatisticians such as Peter Weyand of SMU thinks is the natural limit for the human body. Experts studying the steady progression of records over the past 50 years, see the limit of the world record, with a probable error of 0.17 seconds, namely, to lie between 9.26 to 9.60 seconds. Some see 5.0 seconds a possibility.

Because 6′ 5″ Usian Bolt broke the mathematical model that had fit 100-meter record data for almost a century, his incredible performance has reset the bar for how fast researchers believe humans ultimately can run. Will it be done by a 6′ 9″  or 7′ future version of Bolt?

 

How fast will man eventually run? Will he ever run the 100 meters in five seconds flat?

“Not impossible,” says one of the world’s best known authorities on physiology and biomechanics. Professor Peter Weyand, of Southern Methodist University, known for his expertise in terrestrial locomotion and human and animal performance. Weyand said that humans would soon have the ”ability to modify and greatly enhance muscle fibre strength.” This is would actually reduce the difference between the muscle properties of humans and the world’s fastest animal, the cheetah, to almost zero.

Usain Bolt has now brought up the question — will man get faster and faster? And based on what Weyand says, will he one day outrun the cheetah?

“Probably not,” said Weyand. “The same laws of physics apply to all runners. However, biologically speaking, speed is conferred by an ability of the limbs to hit the ground forcefully in relation to the body’s weight, an attribute conferred largely by the properties of the muscles of the runner. The fast four-legged runners or quadrupeds do seem to be advantaged versus bipeds in terms of the mechanics allowed by their anatomy. These mechanics help quadrupeds to get the most out of the muscles that they have in a way that bipedal runners probably cannot.

Scientists believe man can’t run faster than 30 mph, with the best at about 27mph. A cheetah, on the other hand, reaches speeds triple that. Weyand said he expected speed to continue to improve and faster runners to emerge.

Reza Noubary, a mathematician at Bloomsburg University of Pennsylvania and author of a textbook on statistics and sports, had previously calculated an “ultimate record” of 9.44 seconds for the 100 meter.

Mathematicians don’t use the body’s physiology to assess human physical limits. They were merely working with data that suggested that human speed increases were decelerating and would eventually stop completely. Indeed, in some events, like the long jump, the pace of record-setting has slowed nearly to a stop. That record has only been broken twice since 1968.

Despite the success of Mureika’s model, Weyand, said that mathematical models could never predict how fast humans might eventually run.

“Predicting it is fine for the sake of kicks, but it’s not a scientifically valid approach,” Weyand said. “You have to assume that everything that has happened in the past will continue in the future.”

He suggested that it’s impossible for mathematicians to predict the magnitude of the “freakiness of athletic talent at the extreme margins of humanity. Bolt, it turns out, is a perfect example.”

Weyand, who has conducted research on the body types of the top 45 100-meter sprinters in the last 15 years, said that almost all elite runners conform to the body norms for their race length, except for the most-recent Olympic champion.

“Bolt is an outlier. He’s enormous,” Weyand said. “Typically when you get someone that big, they can’t start.”

That’s because muscle speed in animals is generally tied to their size. For example, rodents, being much smaller than elephants, can move their muscles much faster. The same holds true for human beings. Sprinters are short and have more fast-twitch muscle fibers, allowing them to accelerate quickly, but compromising their ability to run longer distances. Four hundred-meter runners, almost always taller, have the reverse composition of muscle fibers.

Bolt, though, combines the mechanical advantages of taller men’s bodies with the fast-twitch fibers of smaller men.

“We don’t really know what the best form is and maybe Bolt is redefining that and showing us we missed something,” said biomechanicist John Hutchinson of the Royal Veterinary College at the University of London, who studies how animals move.

Hutchinson also agreed with Weyand that the human speed limit will remain impossible to predict with any confidence.

For him, it’s the International Olympic Committee and other regulatory authorities that will determine how fast athletes will be able to run by limiting the amount of advanced biotechnologies sprinters can use.

“The limits will be largely set by the rules of the IOC,” Hutchinson said. “It’s kind of an arms race with the regulators of the sport and the people trying to push the technology to the limits. At some point here there must be a détente where technology can’t push us any further and the rules will restrict it.”

With techniques for gene therapy likely to become available at some point in the not-too-distant future, Weyand said that its use by athletes was “inevitable.”

“You could see really freakish things and we probably will,” he warned.

Source: Daily Galaxy

10 Years Away From Artificial Human Brain?

“It’s a new brain. The mammals needed it because they had to cope with parenthood, social interactions, complex cognitive functions. It was so successful an evolution from mouse to man it expanded about a thousand fold in terms of the numbers of units to produce this almost frightening organ. It is evolving at an enormous speed.”

Henry Markram, Director, Project Blue Brain. 

Excellent news for fans of computer technology, neuroscience, and people who think that humans telling the machines what to do is totally backwards.  Henry Markram, director of the Blue Brain Project, says we are ten years away from a functional artificial human brain. The Blue Brain project was launched in 2005 and aims to reverse engineer the mammalian brain from laboratory data.

We reported on the attempts of the Swiss Mind Brain Institute to simulate the neocortical column of the rat last year using an IBM Blue Gene machine with 10,000 processors, and they’ve announced success of the first phase of their project.

“We cannot keep on doing animal experiments forever,” Markram told the audience at the TED Global Conference at Oxford, England. “There are two billion people on the planet affected by mental disorder,” he told the audience. The project may give insights into new treatments.”

They’ve successfully simulated the neocortical column of a rat – only a fraction of a full brain, but they proved that you don’t get to do world-shattering research when you settle for second-best by choosing one of the most complicated and vital pieces of any mammalian cortex.

They also proved that even world-class scientists still have to compete for funding, following up this amazing achievement with bold claims that the same process could simulate an entire rat brain within three years, and a human brain within ten.  Obviously a team that sat down one day and said “We’re going to build a mind from scratch using better parts than nature did” is ambitious, but projecting an upgrade to human consciousness  from a 2 mm chunk of grey matter designed purely to think “eat garbage” and “carry Plague” within ten years?  That’s enough to make Alexander the Great wave his hands and say “Hang on guys, aren’t you setting your sights a little high?”

To anyone who’s worked in science the reasons for these assertions are obvious: attention and funding.  And it’s a travesty that they have to do so – they’ve achieved one of the most incredible advances in the last decade of neuroscience and the idea that they have to make that sound even cooler is insane: it’s like inventing a perpetual motion machine and having to offer it in designer colours to get people interested.  Assuming they continue to get support for this little “One of the Greatest Achievements ever to be conceived of by Man” project, it will raise a number of critical questions:

1.  Are we going to need a court order to reboot this thing?

Considering that most scientists don’t subscribe to the “magic invisible soul dust” theory of what creates human consciousness, a simulation that recreates the activity of a human brain may produce ethical concerns.  Technically a computer that recreates a rat brain would raise similar issues but, as you’re about to see, these guys don’t have any sympathy for rats.

2.  How do they plan to get a human model?

The existing rat neocortical model is based on a huge amount of data from real working rat brains – or at least, brains that were working until the scientists got a hold of them.  Where the team ran into gaps in the existing data they cracked open rat skulls, extracted the brains, sliced them into wafers while keeping them alive and recorded their responses.  It isn’t known whether they cackled maniacally while screaming “They said we were fools, but we’ll show them, we’ll show them ALL!” during this procedure, because  anybody who can slice a brain into strips while keeping it alive isn’t someone you want to annoy with questions.

Suffice to say when one third of your research staff are on the “Knifing things in the head” payroll:

a) You’re already two steps into a horror movie script
b) You aren’t just assuming there are no such thing as ghosts, you’re betting the survival of everyone in the building on the fact
c) This is NOT a method that can be scaled up to humans without a rogue agent with nothing to lose being sent to kill you in a highly ironic manner.

3.  Can we make improvements?

Those involved in the project sing its praises in work to understand the human brain, but it’s only a matter of time until somebody thinks about making improvements – minus an hour at most, actually, because that’s the first thing I thought of when I read about it. 

With the ability to simulate the effects of rewiring, drugs or external electric fields at an individual neuron level we can investigate enhancements (such as new senses, new cognitive modes or neuroelectric interfaces) without all the inconvenient “human rights violations” and “Crimes against humanity” such research normally entails.  We could improve our own minds – and since we’ll have just invented a silicon model operating at computer speeds in a bulletproof shell, we’ll have to.

Source: Daily Galaxy

Ever Heard of: The Fermi Paradox

The Fermi paradox is the apparent contradiction between high estimates of the probability of the existence of extraterrestrial civilizations and the lack of evidence for, or contact with, such civilizations.

The extreme age of the universe and its vast number of stars suggest that if the Earth is typical, extraterrestrial life should be common. In an informal discussion in 1950, the physicist Enrico Fermi questioned why, if a multitude of advanced extraterrestrial civilizations exist in the Milky Way galaxy, evidence such as spacecraft or probes are not seen. A more detailed examination of the implications of the topic began with a paper by Michael H. Hart in 1975, and it is sometimes referred to as the Fermi-Hart paradox. Another closely related question is the Great Silence—even if travel is hard, if life is common, why don’t we detect their radio transmissions?

There have been attempts to resolve the Fermi Paradox by locating evidence of extraterrestrial civilizations, along with proposals that such life could exist without human knowledge. Counterarguments suggest that intelligent extraterrestrial life does not exist or occurs so rarely that humans will never make contact with it.

Starting with Hart, a great deal of effort has gone into developing scientific theories about, and possible models of, extraterrestrial life, and the Fermi paradox has become a theoretical reference point in much of this work. The problem has spawned numerous scholarly works addressing it directly, while various questions that relate to it have been addressed in fields as diverse as astronomy, biology, ecology, and philosophy. The emerging field of astrobiology has brought an interdisciplinary approach to the Fermi paradox and the question of extraterrestrial life.

Should alien artifacts be discovered, even here on Earth, they may not be recognizable as such. The products of an alien mind and an advanced alien technology might not be perceptible or recognizable as artificial constructs. Exploratory devices in the form of bio-engineered life forms created through synthetic biology would presumably disintegrate after a point, leaving no evidence; an alien information gathering system based on molecular nanotechnology could be all around us at this very moment, completely undetected. Clarke’s third law suggests that an alien civilization well in advance of humanity’s might have means of investigation that are not yet conceivable to human beings.

Certain theoreticians accept that the apparent absence of evidence proves the absence of extraterrestrials and attempt to explain why. Others offer possible frameworks in which the silence may be explained without ruling out the possibility of such life, including assumptions about extraterrestrial behaviour and technology. Each of these hypothesized explanations is essentially an argument for decreasing the value of one or more of the terms in the Drake equation. The arguments are not, in general, mutually exclusive. For example, it could be that both life is rare, and technical civilizations tend to destroy themselves, or many other combinations of the explanations below. 

One explanation is that the human civilization is alone in the galaxy. Several theories along these lines have been proposed, explaining why intelligent life might be either very rare, or very short lived. Implications of these hypotheses are examined as The Great Filter.

Further reading:

The Fermi Paradox

Can Easter Island Compound Extend Life?

The giant monoliths of Easter Island are worn, but they have endured for centuries. New research suggests that a compound first discovered in the soil of the South Pacific island might help us stand the test of time, too.

Wednesday, July 8, in the journal Nature, The University of Texas Health Science Center at San Antonio and two collaborating centers reported that the Easter Island compound – called “rapamycin” after the island’s Polynesian name, Rapa Nui – extended the expected lifespan of middle-aged mice by 28 percent to 38 percent. In human terms, this would be greater than the predicted increase in extra years of life if cancer and heart disease were both cured and prevented.

The rapamycin was given to the mice at an age equivalent to 60 years old in humans.

The studies are part of the National Institute on Aging (NIA) Interventions Testing Program, which seeks compounds that might help people remain active and disease-free throughout their lives. The other two centers involved are the University of Michigan at Ann Arbor and Jackson Laboratory in Bar Harbor, Maine.

The Texas study was led by scientists at two institutes at the UT Health Science Center: the Institute of Biotechnology (IBT) and the Barshop Institute for Longevity and Aging Studies.

“I’ve been in aging research for 35 years and there have been many so-called ‘anti-aging’ interventions over those years that were never successful,” said Arlan G. Richardson, Ph.D., director of the Barshop Institute. “I never thought we would find an anti-aging pill for people in my lifetime; however, rapamycin shows a great deal of promise to do just that.”

Discovered in the 1970s, rapamycin was first noted for its anti-fungal properties and later was used to prevent organ rejection in transplant patients. It also is used in stents, which are implanted in patients during angioplasty to keep coronary arteries open. It is in clinical trials for the treatment of cancer.

The new aging experiments found that adding rapamycin to the diet of older mice increased their lifespan. The results were the same in Texas, Michigan and Maine.

“We believe this is the first convincing evidence that the aging process can be slowed and lifespan can be extended by a drug therapy starting at an advanced age,” said Randy Strong, Ph.D., who directs the NIA-funded Aging Interventions Testing Center in San Antonio. He is a professor of pharmacology at the UT Health Science Center and a senior research career scientist with the South Texas Veterans Health Care System.

The findings have “interesting implications for our understanding of the aging process,” said Z. Dave Sharp, Ph.D., director of the Institute of Biotechnology and professor and chairman of the Health Science Center’s Department of Molecular Medicine.

“In addition,” Dr. Sharp said, “the findings have immediate implications for preventive medicine and human health, in that rapamycin is already in clinical usage.”

Source: PhysOrg.com

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Because it’s the universe’s most abundant element, hydrogen is a good candidate for a renewable energy source. But there’s a problem: the finicky element is difficult to manage. Storing it in its pure form is a hassle that requires high pressure and low temperature, and unbinding it from paired elements used to stabilize it comes with significant secondary energy costs.

Fortunately, though, there’s urine to the rescue.

Gerardine Botte, an Ohio University professor, sees the liquid as a solution thanks to the particular composition of its major component, urea. Its make-up, a 2-to-1 ratio of hydrogen and nitrogen, is convenient because hydrogen can be extracted from nitrogen using much less electricity than that needed to, say, pull apart hydrogen and oxygen. (It’s a matter of 0.037 Volts versus 1.23 Volts, if you really need to know.)

Botte has recently come up with a nickel-based electrode that can do just that: dip the electrode into urine, apply electrical current, and voila, hydrogen is released. While the research is still in an initial phase, it’s possible that urine could power cars, homes, and various devices in as near of a future as six months from now.

Source: Discovery.com

Photographic Memory in Pill Form?

The most interesting upgrades aren’t for your computer, your car, or even the internet – they’re for you.  We’ve always tinkered with our own thought processes (using crude equipment like “alcohol” and “regular exercise”) but now mankind has the tools and time to tune the system directly, and one team of scientists may make yellow sticky notes obsolete: they’ve found a way to boost visual memory.

A team of scientists at the Spanish University of Malaga were working with rat brains, because of the combination of ethics and wimpiness that prevents human trials.  They found that a particular protein (RGS-14) boosted a region of the brain known as the “V2 secondary visual cortex”, which makes rats sound significantly more like Terminators than you previously thought.  (Nightmares resulting from that image are not our responsibility).

Increasing the levels of this protein upgraded the rats visual memory allowing them to remember things for fifteen hundred times longer than normal (two months instead of an hour).  The interesting aspect is that this upgrade isn’t a new property, but a re-routing of existing processes – the protein seems to cause the formation of long term memories instead of short term, gifting the rat with what could be a photographic visual memory.  Which, considering that these are actual lab rats with needles being jabbed into their brains, probably sucks quite a lot.  The team also found that destruction of the V2 region utterly eliminated all visual memory of the past – which you can view as research, cruel, or gifting the the rats with a Zen state that takes decades of meditation to achieve.

The potential applications are obvious, and enormous, but beware the hidden downsides – the human brain is the most incredibly sophisticated system ever even conceived of and any tinkering can have huge side effects.  This doesn’t mean don’t do anything (we’d still be in caves otherwise), but be aware that you can’t say “IF this THEN that” where neural networks are concerned.  Intelligence-upgrades are an inevitable field, already in progress with prototype products like piracetam and caffeine, so it’s time to make up your mind if you’re going to make your own mind.

Source: Daily Galaxy

Global Warming Shrinking Sheep

Changing winter conditions are causing Scotland’s wild Soay sheep to get smaller, according to a study that suggests climate change can trump natural selection.

The authors of the study published in “Science” believe that it highlights how wide-ranging the effects of global climate change can be, adding further complexity to the changes we might expect to see in animal populations in future.

“It’s only in the last few years that we’ve realized that evolution can influence species’ physical traits as quickly as ecological changes can. This study addresses one of the major goals of population biology, namely to untangle the ways in which evolutionary and environmental changes influence a species’ traits,” said Andrew Sugden, deputy and international managing editor at Science.

The researchers analyzed body-weight measurements and life-history data for the female members of a population of Soay sheep. The sheep live on the island of Hirta in the St. Kilda archipelago of Scotland and have been studied closely since 1985.

They selected body size because it is a heritable trait, and because the sheep have, on average, been decreasing in size for the last 25 years.

According to the findings lambs are not growing as quickly as they once did as winters have become shorter so do not need to put on as much as weight in the first months of life to survive.

The results suggest that the decrease is primarily an ecological response to environmental variation over the last 25 years. Evolutionary change, the report says, has contributed relatively little.

“Sheep are getting smaller. Well, at least the wild Soay sheep living on a remote Scottish island are. But according to classic evolutionary theory, they should have been getting bigger, because larger sheep tend to be more likely to survive and reproduce than smaller ones, and offspring tend to resemble their parents,” said study author Tim Coulson of Imperial College London.

“Our findings have solved a paradox that has tormented biologists for years — why predictions did not match observation. Biologists have realized that ecological and evolutionary processes are intricately intertwined, and they now have a way of dissecting out the contribution of each. Unfortunately it is too early to tell whether a warming world will lead to pocket-sized sheep,” said Coulson.

Coffee May Reverse Alzheimer’s

Drinking five cups of coffee a day could reverse memory problems seen in Alzheimer’s disease, US scientists say.

The Florida research, carried out on mice, also suggested caffeine hampered the production of the protein plaques which are the hallmark of the disease.

Previous research has also suggested a protective effect from caffeine.

But British experts said the Journal of Alzheimer’s disease study did not mean that dementia patients should start using caffeine supplements.

The 55 mice used in the University of Florida study had been bred to develop symptoms of Alzheimer’s disease.

First the researchers used behavioural tests to confirm the mice were exhibiting signs of memory impairment when they were aged 18 to 19 months, the equivalent to humans being about 70.

Then they gave half the mice caffeine in their drinking water. The rest were given plain water.

The mice were given the equivalent of five 8 oz (227 grams) cups of coffee a day – about 500 milligrams of caffeine.

The researchers say this is the same as is found in two cups of “specialty” coffees such as lattes or cappuccinos from coffee shops, 14 cups of tea, or 20 soft drinks.

When the mice were tested again after two months, those who were given the caffeine performed much better on tests measuring their memory and thinking skills and performed as well as mice of the same age without dementia.

Those drinking plain water continued to do poorly on the tests.

In addition, the brains of the mice given caffeine showed nearly a 50% reduction in levels of the beta amyloid protein, which forms destructive clumps in the brains of dementia patients.

Further tests suggested caffeine affects the production of both the enzymes needed to produce beta amyloid.

The researchers also suggest that caffeine suppresses inflammatory changes in the brain that lead to an overabundance of the protein.

Earlier research by the same team had shown younger mice, who had also been bred to develop Alzheimer’s but who were given caffeine in their early adulthood, were protected against the onset of memory problems.

‘Safe drug’

Dr Gary Arendash, who led the latest study, told the BBC: “The results are particularly exciting in that a reversal of pre-existing memory impairment is more difficult to achieve.

“They provide evidence that caffeine could be a viable ‘treatment’ for established Alzheimer’s disease and not simply a protective strategy.

“That’s important because caffeine is a safe drug for most people, it easily enters the brain, and it appears to directly affect the disease process.”

The team now hope to begin human trials of caffeine to see if the mouse findings are replicated in people.

They do not know if a lower amount of caffeine would be as effective, but said most people could safely consume the 500 milligrams per day.

However they said people with high blood pressure, and pregnant women, should limit their daily caffeine intake.

Rebecca Wood, chief executive of the Alzheimer’s Research Trust, said: “In this study on mice with symptoms of Alzheimer’s, researchers found that caffeine boosted their memory. We need to do more research to find out whether this effect will be seen in people.

“It is too early to say whether drinking coffee or taking caffeine supplements will help people with Alzheimer’s.