Dr Dougal claims that only ten minutes under the hat a day is enough to have an effect.

"Currently all you can do with dementia is to slow down the rate of decay - this new process will not only stop that rate of decay but partially reverse it," he said.

Low level infra-red red is thought to stimulate the growth of cells of all types of tissue and encourage their repair. It is able to penetrate the skin and even get through the skull.

"The implications of this research at Sunderland are enormous - so much so that in the future we could be able to affect and change the rate at which our bodies age," he said.

"We age because our cells lose the desire to regenerate and repair themselves. This ultimately results in cell death and decline of the organ functions - for the brain resulting in memory decay and deterioration in general intellectual performance.

The drug, called Enbrel, is injected into the spine where it blocks a chemical responsible for damaging the brain and other organs.

A pilot study carried out by U.S. researchers found one patient had his symptoms reversed "in minutes".

Other patients have shown some improvements in symptoms such as forgetfulness and confusion after weekly injections over six months.

The study of 15 patients with moderate to severe Alzheimer's has just been published in the Journal of Neuroinflammation by online publishers Biomed Central.

The experiment showed that Enbrel can deactivate TNF (tumour necrosis factor) - a chemical in the fluid surrounding the brain that is found in Alzheimer's sufferers.

The test identifies changes in a handful of proteins that cells use to convey messages to one another.

The US researchers found it could indicate who had Alzheimer's, as well as who was likely to develop the condition, with 90% accuracy.

The work, led by Stanford University, features in Nature Medicine.

One of the most distressing aspects of Alzheimer's disease is the difficulty in determining whether mild memory problems are the beginning of an inevitable mental decline.

Those chips are now being implanted in some people, especially Alzheimer's patients, and encoded with their medical records. The Food and Drug Administration called the microchip one of 2005's top innovative technologies.

The microchips have been implanted in hundreds of people like Ida Frankel, who has Alzheimer's disease. If she gets lost and ends up in a hospital, doctors can scan her arm and get all of her medical records.

But when the government approved these chips for use in humans three years ago, it didn't mention that there were studies showing that similar chips caused malignant tumors in lab rats and mice.

Cancer doctors who spoke to The Associated Press, which broke this story, say you can't make the leap between cancer in mice and cancer in humans.

More than 5 million Americans are living with Alzheimer's disease, a 10 percent increase since the last Alzheimer's Association estimate five years ago and a count that supports the long-forecast dementia epidemic as the population grays.

Age is the biggest risk factor, and the report to be released Tuesday shows the nation is on track for skyrocketing Alzheimer's once the baby boomers start turning 65 in 2011. Already, one in eight people 65 and older have the mind-destroying illness, and nearly one in two people over 85.

Unless scientists discover a way to delay Alzheimer's brain attack, some 7.7 million people are expected to have the disease by 2030, the report says. By 2050, that toll could reach 16 million.

Why? Ironically, in fighting heart disease, cancer and other diseases, "we're keeping people alive so they can live long enough to get Alzheimer's disease," explains association vice president Steve McConnell.

The test zeroes in on two forms of an enzyme involved in the degradation of amyloid, the protein that accumulates in the brain of someone with Alzheimer's, said Alkon, scientific director of the Blanchette Rockefeller Neurosciences Institute at the West Virginia University Health Sciences Center.

The presence of Alzheimer's disease is indicated by a steep imbalance in the ratio of the two forms of the enzyme, MAP kinase Erk, in skin cells that are exposed to bradykinin, an inflammation-related molecule, Alkon said. That imbalance is not seen in cells of people without dementia or those with other forms of dementia, he said.

The test produced good results when run on 60 tissue samples: 30 from a tissue bank, 30 from autopsy samples of people diagnosed with Alzheimer's disease, Alkon said.

"We have seen a correlation with the duration of the disease," he said. "The earlier it is done in the course of the disease, the larger is the abnormality."

During the trial, a brief pulse of infrared light into the eyes of four mice with Alzheimer's and four without accurately identified which had the condition.

Dr Goldstein and his team envisage the test could be used to detect the disease at its earliest stages as well as to track disease progression and monitor how people respond to Alzheimer's treatments.

Currently there is no simple test to make a diagnosis of dementia and it can only be confirmed with certainty by looking at someone's brain in a post-mortem examination.

The scientists believe the technology, known as quasi-elastic light scattering, may detect the very earliest stages of amyloid deposits in the lens, even when they appear completely clear to the naked eye.

The researchers identified 560 people who were diagnosed with dementia between 1990 and 1994. They then found a group of people of similar age who did not have dementia.

They looked back at the weight of all of the patients over the preceding 30 years.

Among the women in the study, those who later developed dementia started off at the same weight as those who did not develop dementia, but then their weight drifted downward by a few pounds 10 years before the developed any dementia symptoms.

The weight of these women also went downward a few more pounds when the memory loss first manifested.

Astrocytes produce fat-like lipid neurons used to create their outer membranes and they also produce glutamate, the most abundant neurotransmitter in the nervous system and one of the most important chemical messengers in the brain.

Recent experiments, however, revealed that astrocytes form connections with blood vessels and control the flow of nutrients, including oxygen, to neurons. When brain activity increases, neurons trigger astrocytes to release calcium, which in turn affects other chemical messengers that can cause blood vessels to either dilate or contract.

The classical symptoms of memory loss and dementia associated with Alzheimer's are the result of neurons dying over a period of years. Brain scans of Alzheimer's patients show decreased blood flow to critical parts of the brain, and doctors have always assumed that this was because there was less of a demand for blood because there were fewer neurons to feed.

The new result could mean that Alzheimer's affects mainly astrocytes and not neurons and that blood flow to the brain is not decreased because the neurons are dying, but that the neurons are dying because there is decreased blood flow.

"It may be that for whatever reason, astrocytes are not doing their job properly, and then blood flow decreases," Nedergaard said. "This could lead to the death of the neurons, which would starve from a lack of nutrients, since the neurons depend on the astrocytes for their survival."

The study, from 1994 to 2003, followed 1,740 people ages 65 and older who showed no signs of dementia at the outset. The participants' health was evaluated every two years for six years.

Out of the original pool, 1,185 people were later found to be free of dementia, 77 percent of whom reported exercising three or more times a week; 158 people showed signs of dementia, only 67 percent of whom said they exercised that much. The rest either died or withdrew from the study.

The study could not say if exercise helped prevented dementia altogether, because not all of the participants were followed up to their deaths.

The frequency of dementia was 13 per 1,000 person years for those who said they exercised three or more times a week, compared with 19.7 per 1,000 person years for those who reported exercising less.

Outward symptoms start with memory loss, which progresses to complete helplessness as brain cells are destroyed. In the brain, neurons die as messy plaques and tangles of protein form.

The two proteins involved are unhealthy forms of natural brain compounds called amyloid beta and tau protein.

Ashe's team worked with mice genetically engineered to develop the mutant tau, but this mutation could be stopped - or de-activated - with use of a drug called doxycycline.

As expected, the mice developed dementia and had brain atrophy similar to human Alzheimer’s disease.

And when the engineered gene was turned off, memory loss stopped, as expected. But the mice did not merely stop getting worse. They got better.

"Even mice that had lost half the neurons that are involved in forming memories, when we removed the molecule causing the memory loss from the remaining neurons by turning off the genes, the mice were able to learn and remember new information," Ashe said in a telephone interview.

"No one suspected so many neurons would still be able to function."

Still, the discovery may provide leads to scientists searching for therapies to at least delay the onset of the degenerative brain disease. It already affects 4.5 million people in the U.S. and is predicted to strike 14 million by 2050 as the population ages.

Moreover, researchers are honing in on lifestyle choices that may help protect the brain in the first place.

"It's exciting that we can even talk about prevention," said William Thies, scientific director of the Alzheimer's Association. He noted that just 10 years ago there was hardly any research into that possibility.