It means patients will no longer be diagnosed with the debilitating condition only to be sent away to wait for their symptoms to worsen before they can be treated.

A fourth drug which was restricted to those with severe symptoms will also be made available to a wider group of patients.

The draft guidance overturns a decision made in 2007 to restrict the drugs because of uncertainty over their cost effectiveness.

New research and calculations have now been conducted by independent teams showing that the drugs work in patients with mild symptoms and offer a large enough benefit to justify the cost of around £2.80 per patient per day.

Final guidance on the drugs called donepezil or Aricept, made by Eisai and Pfizer, galantamine or Reminyl, made by Shire and rivastigmine or Exelon, made by Novartis is due in March this year.

The guidance also allows memantine or Ebixa, made by Lundbeck to be used for those with for severe disease and for some patients with moderate disease, after previously having been restricted to research trials.

Chief Executive, Sir Andrew Dillon said: “We are pleased to now be able to recommend these three drugs for both mild and moderate Alzheimer’s disease and another for moderate or severe Alzheimer’s, extending recommendations made in 2007.

“Since 2007 clinical trials have continued to show the positive effects of these drugs and, in the case of memantine, have reduced the uncertainty about its clinical effectiveness. In addition, we now have more information about the costs of living with and treating this very distressing disease, as it progresses through its mild, moderate and severe stages.”

If ratified in March, doctors will have three months before they have to start prescribing the drugs.

A survey has shown that around half of GPs plan to recall patients diagnosed with early Alzheimer’s to offer them the drugs.

The new calculations, conducted by a team at the Peninsula Medical School, took into account the delay in admission to care homes which the drugs can offer of between one and two months and was better able to judge how many patients stopped taking the medicines which was skewing the costs.

It was concluded that giving patients the drugs in the early stages saved £500 out of the £70,000 total cost of caring for them after diagnosis.

Andrew Chidgey, Head of Policy and Public Affairs at Alzheimer’s Society, said: “This is a victory for people with Alzheimer’s and their carers, many of whom have been campaigning for this day for years.

“These drugs don’t work for everyone, but for some people they can radically improve their quality of life. We now need more people to be diagnosed early and for them to receive the treatment, support and advice that they desperately need.”

There are currently 465,000 people living with Alzheimer’s in the UK and a further 62,000 people are developing Alzheimer’s each year.

Only around one in ten are currently receiving medication.

Around 80,000 people are in the early or mild stages of the disease.

Professor Roy Jones from The Research Institute for the Care of Older People at the Royal United Hospital, in Bath, said: “This is great news for people with Alzheimer’s disease and their families because we will now be able to offer effective drug treatment in mild, moderate and severe Alzheimer’s disease.

“For example, patients with mild disease will at last be able to get access to early, cost-effective treatment at the point of diagnosis – treatment that can potentially help to relieve the symptoms in these patients.

“Previously it was difficult to see patients with mild disease and ask them to come back when their condition worsened before we were able to prescribe drugs that could improve their symptoms. This new ruling will help keep patients as independent as possible for as long as possible.

Professor June Andrews, Director of the Dementia Services Development Centre at the University of Stirling said: “People with dementia and their carers have a lot to contend with, so it’s a relief that at last those in the early stages of Alzheimer’s disease will have access to medication. Then they can get on with taking the other steps they need to keep well, and enjoy life as much as possible.”

Rebecca Wood, Chief Executive of the Alzheimer’s Research Trust, said: “This welcome decision gives everyone living with Alzheimer’s the best possible chance of benefiting from the treatments we have available. These drugs hold the promise of relief from the symptoms of Alzheimer’s for thousands of people and, while not the cure we desperately need, they can still help.

“It’s an irony that clinical research of the kind that has helped realise the benefits of drugs like these remains sorely underfunded in the UK. If we are to produce treatments that can alter the course Alzheimer’s disease itself, rather than just temporary relief from symptoms, then research is our only answer.”

The gene, Sox9, plays a critical role in how stem cells behave and is crucial to developing the central nervous system, reports express.co.uk.

“We are one step closer to correcting damaged nerve cells which would be a huge leap forward for the millions with Alzheimer’s, stem cell-related brain tumours or who have suffered from a stroke,” said James Briscoe, of the Medical Research Council(MRC) who headed the study.

A disorder of the immune system. Another hypothesis is that an immune system “error” may be partly to blame. In 1987 researchers at Rockefeller University reported finding abnormal antibodies in patients with Alzheimer’s disease; they speculate that these antibodies, instead of functioning normally to destroy outside invaders such as viruses, may attack the blood/brain barrier, the vital chemical sheath that keeps injurious substances from gaining access to the brain. Once the integrity of the blood/brain barrier is breached, a virus or other harmful substance might gain access to the brain and set off the disease.
Aluminum. Besides a virus, a strong candidate for instigating Alzheimer’s disease is aluminum, because a striking feature of the brains of Alzheimer’s victims is an abnormal concentration of this particular element. Does absorbing too much aluminum over a lifetime play any part in producing the disease? So far, laboratory studies of this hypothesis have been negative; but because high aluminum levels are such an important feature of the illness, many scientists think this substance is likely to play some role in the puzzle of Alzheimer’s disease.

A genetic defect. Without doubt, the most exciting new research lead involves genetics. In 1987 scientists at Massachusetts General Hospital reported identifying a genetic defect in people with a strong family history of Alzheimer’s disease.
The Alzheimer’s-related genetic marker is found on chromosome number 21, the very chromosome that is duplicated in people suffering from the birth defect Down’s syndrome. For several years researchers had been tantalized by what they knew was an important connection between these two illnesses, because victims of Down’s syndrome (mongolism) universally develop Alzheimer’s disease if they live to age forty. Now the mystery is solved. Having an extra chromosome 21 may be giving people victimized by Down’s syndrome the Alzheimer’s-related genetic program in spades.

Other research reported in the February 1987 issue of Science suggests that the illness may be set off by abnormal deposits of a protein called amyloid accumulating in the brain. Amyloid is a major component of senile plaques and neurofibrillary tangles – the abnormal structures that replace the normal neurons. Do the genetic instructions “produce amyloid” trigger Alzheimer’s disease directly by causing this toxic protein to build up? Does an Alzheimer’s gene (or set of genes) act in concert with a chemical such as aluminum or with a virus to produce these harmful deposits? Whatever the answer, some scientists now believe amyloid is central to the mystery of this devastating disease.

The action is part of a plan to improve the care of those with dementia, by improving the training of nurses and doctors, and closely monitoring the quality of services provided by care homes and hospitals.

Care homes will be told to review the use of all medications given to people with dementia, to reduce the numbers of people prescribed antipsychotic drugs which should only be used as a last resort.

Last year a major report found that 180,000 patients are prescribed the treatments each year, despite the fact they do not benefit three quarters of those given them, and can cause death, or major side effects, such as strokes.

Care Minister Paul Burstow has been campaigning for years against the misuse of such drugs.

He told The Sunday Telegraph: “Far too many prescriptions of antipsychotics are not clinically justified and can lead to premature death. We want to dramatically cut the use of these drugs among elderly people.

http://www.telegraph.co.uk/health/healthnews/8024972/Government-orders-action-on-chemical-cosh-which-kills-thousands.html

The target called neutral sphingomyelinase (N-SMase) is a protein that when activated, can cause a chain of reactions in the cell leading to neuronal death and memory loss.

“There are multiple, neurotoxic, disease-causing pathways that converge on the neutral sphingomyelinase that can cause neuronal loss in the brain of an Alzheimer”s patient,” said Kalipada Pahan, PhD, neurological researcher and lead investigator at Rush.

“If we can stop the activation of the neutral sphingomylinase, we may be able to stop memory loss and the progression of Alzheimer”s disease,” he said.

Researchers at Rush were able to determine that the neutral sphingomyelinase is triggered by the activated brain cells and beta-amyloid.

However, when the neutral sphingomyelinase was inhibited by using a small molecule inhibitor and a chemical inhibitor, the activated brain cells and beta amyloid were unable to kill neurons.

Experts tested the two inhibitors using human brain cells in a mouse model and a cell culture model.

“Understanding how the disease process works is important in identifying effective approaches to protect the brain and stop the progression of Alzheimer”s disease.

“The results of this study are very promising and our next step is to translate these findings to the clinic.

“If we can develop and test a clinical medication that can target the neutral sphingomyelinase, we may be able to halt memory loss in Alzheimer”s disease patients,” said Pahan.

Results from the study were published in the September 22 issue of the Journal of Neuroscience.

“The nice thing about this is we may be able to predict Alzheimer’s very early,” said Craig Stark, UCI associate professor of neurobiology and behavior.

That’s what prompted Diana Burns of Anaheim to participate in the study.

In late 2008, when she forgot yet again where she’d put her purse, and then couldn’t remember why she was in the laundry room, Burns decided she had to know: Was she, like her aging mother, going to be a victim of the debilitating loss of brain function known as Alzheimer’s disease?

“When you’re a caregiver for somebody with Alzheimer’s, you always wonder if it’s going to happen to you,” said Burns, who had quit her job to stay home the day her mother was found unconscious and bleeding half a mile from their house, with no idea how she got there. “I was becoming concerned because I myself was forgetting things, so I thought, ‘Now is the time to find out.’

Burns, 64, searched online for human clinical trials and found UCI’s Center for the Neurobiology of Learning and Memory. Soon Stark, the center’s interim director, and his staff had her ensconced in their big MRI machine.

The UCI researchers developed and used a new ultrahigh-resolution technique to electronically peer through dense matter near the brain’s hippocampus in search of the perforant path.

The passageway is basically a bundle of nerve fibers, lined up like straws, connecting a region called the entorhinal cortex to the seahorse-shaped hippocampus.

By monitoring the brains of Burns and others via their ultrahigh-resolution technique – know as diffusion tensor imaging – the UCI team was able to detect water molecules moving in the exact area where they knew the passage had to be.

The scientists then painstakingly tracked the progress of the molecules along the length of the fiber bundle, thereby identifying the perforant path.

The UCI team is now examining people with mild cognitive impairment – often the first stage of Alzheimer’s. They expect to see far faster deterioration of the perforant path. Such a finding could aid the testing of new medicines.

The study has been published June 28 in the Proceedings of the National Academy of Sciences.

It is known that memantine (marketed in the United States as Namenda), which is currently FDA-approved can treat moderate-to-severe Alzheimer”s disease.

Developed, in part by Dr. Stuart A. Lipton, Director of the Del E. Web Center for Neuroscience, Aging and Stem Cell Research at Sanford-Burnham Medical Research Institute (Sanford-Burnham), memantine improves symptoms by blocking abnormal activity of glutamate, a chemical that transmits messages between nerve cells.

In the new study, researchers at Sanford-Burnham led by Dr. Lipton unravel exactly how the drug helps Alzheimer”s patients without causing serious side effects.

“While memantine is partially effective in treating Alzheimer”s disease, one of its major advantages is how safe and well-tolerated it is clinically,” said Lipton

Memantine is a particularly safe treatment for Alzheimer”s disease because it dampens excessive glutamate signaling that occurs away from synapses without blocking glutamate activity at the synapses.

This is important because interfering with synaptic glutamate signaling would disrupt normal brain activity.

“We showed definitively for the first time that memantine, the drug our group developed for Alzheimer”s disease, works in a unique way. It inhibits a protein that binds glutamate called the NMDA receptor, but predominantly blocks NMDA receptors that signal molecularly to cause neuronal injury and death. It spares the synaptic receptors that mediate normal communication between nerve cells in the brain,” said Lipton.

The finding helps explain why the drug is so well tolerated by Alzheimer”s patients and might provide hints for the development of future therapies targeting the NMDA receptor and similar cellular machinery in other diseases.

The study is appearing in The Journal of Neuroscience.

An imbalance in the metals needed for healthy brain function has been found at the root of the degenerative disease, which afflicts 10 per cent of people, aged over 60.

University of Melbourne Professor of Pathology Ashley Bush and his research colleagues have traced the imbalance to the brain”s improper and related processing of zinc and iron.

The research focused on the complex relationship between amyloid precursor protein (APP) and its breakdown product amyloid, along with the zinc and iron.

Professor Bush said as zinc was seen to accumulate in amyloid it blocked the APP from performing its critical, and previously unknown, job of exporting iron out of the brain”s neurons.

This led to a build-up of iron “in the grey matter”, he said, resulting in oxidative stresses that could kill off neurons.

So the loss of mental function in an Alzheimer”s patient is caused by rust in their brain

“That”s the kind of chemistry that is going on in the brain and, similar to actual rust, it involves an abnormal combustion of oxygen with iron,” the Courier Mail quoted Bush as saying.

“The brain is an unusual organ in that it has very high concentrations of metals which it uses for its electrical chemistry,” he added.

The research will be published in the international journal Cell.

The study by researchers in Australia also reveals the role of beta-amyloid precursor protein (APP), which forms plaques in affected brains.

To each the conclusion, Jack Rogers at the University of Melbourne and colleagues, used mouse studies, healthy human brain cells and post-mortems to show that APP”s role is probably to flush toxic iron from neurons.

However, in Alzheimer”s, the APP”s function is sabotaged by zinc, which accumulates in the disease”s trademark plaques, reports New Scientist.

Normally, zinc aids neuronal signalling, but as it becomes trapped in plaques, it both disrupts APP”s iron-clearing role and denies neurons the zinc they need for signalling.

The outcome is a double-whammy, which sees iron continuing to accumulate and neurons losing their ability to signal appropriately.

As the disease progresses, the above communication problems steadily worsen. As the word finding deteriorates other words (paraphasias) are added in to fill the gaps so that the true sense of the communication may be lost or the wrong thing asked for. Comprehension similarly gets worse and questions may not get answered or the person may withdraw from talking altogether. Keeping a sentence going often proves too hard for the sufferer and the increasingly frequent change of subject means that the outcome becomes babbling or gibberish.

In advanced disease, communication may prove impossible and the sufferer is often unable to let even their basic needs be known. In a few people there may be an automatic verbal response occasionally, but at this stage the brunt of communicating falls on carers who will need to approach the sufferer with non-verbal means (expression, touch, etc.) Massage and stroking can convey caring probably better than the spoken word.

Proteins called amyloid plaques which build up in the brain of dementia sufferers are thought to be linked to the onset of symptoms such as memory loss and mental impairment.

Now scientists claim to have established a link between the production of the plaques and a separate process through which the brain converts sugar into energy, known as aerobic glycolysis.

Scans of a group of young adults, whose average age was 25, showed that aerobic glycolysis was especially high in the same areas of the brain where amyloid plaques build up in older patients, including Alzheimer’s sufferers.

http://www.telegraph.co.uk/health/8000396/Adults-as-young-as-25-could-be-screened-for-dementia.html

A gene variation associated with aggressive progression of Alzheimer’s was identified in patients with high levels of a protein linked to the disease.

The findings could help predict how quickly patients move from their initial diagnosis to full-blown dementia, researchers said.

Knowing that certain patients are going to develop the disease very quickly could also help experts better analyse the effectiveness of trial drugs designed to slow its development.

http://www.telegraph.co.uk/health/elderhealth/8006969/Gene-predicts-speed-of-Alzheimers-development.html

Scientists studied more than 2,000 people aged 70 to 89 and found that rates of mild cognitive impairment (MCI) were 50 per cent higher in men than in women.

MCI involves a level of mental decline beyond that which can be explained by normal ageing. It is often associated with Alzheimer’s disease.

The U.S. research has been hailed an ‘exciting’ development in the drive to find a cure for the disease.

Lead researcher Dr Ronald Petersen, from the Mayo Clinic in Rochester, Minnesota, said: ‘This is the first study conducted among community-dwelling persons to find a higher prevalence of MCI in men.

‘The finding that the frequency of mild cognitive impairment is greater in men was unexpected, since the frequency of Alzheimer’s disease is actually greater in women. It warrants further study.

http://www.dailymail.co.uk/health/article-1309657/Men-likely-lose-memory-Exciting-finding-hunt-Alzheimers-cure.html

A study of older people in their 70s and 80s has revealed that mild cognitive impairment marked by symptoms such as increasing forgetfulness was 50 per cent higher in men than in women.

Mild cognitive impairment (MCI) involves a level of mental decline beyond that which can be explained by normal ageing. It is often associated with dementia and Alzheimer’s disease later in life.

The onset of dementia is a slow process of mental derangement that strips sufferers of their memory, personality and, eventually, their humanity. It is a progressive, neuro-degenerative disorder that is incurable and irreversible. Some people subside gently into dementia without evident distress, but for others the experience of losing their mental faculties is confusing, distressing and – in some cases – frightening. In the case of Alzheimer’s, the condition is thought to be caused by the build-up of protein deposits in the brain – called “plaques and tangles” – whose first symptoms may be a difficulty in finding words.

Scientists from the Mayo Clinic in Rochester, Minnesota, one of the premier research institutes in the US, tested the memory and thinking skills of more than 2,000 people aged 70 to 89.

They found that more than one in six (16 per cent) had mild cognitive impairment, one in 10 was suffering from dementia, and three-quarters had normal mental faculties. A total of 19 per cent of men were affected with MCI, compared with 14 per cent of women.

Lead researcher Dr Ronald Petersen said: “This is the first study conducted… to find a higher prevalence of MCI in men. The finding that the frequency of mild cognitive impairment is greater in men was unexpected, since the frequency of Alzheimer’s disease is actually greater in women. It warrants further study.

http://www.independent.co.uk/life-style/health-and-families/health-news/men-twice-as-likely-as-women-to-be-forgetful-in-old-age-says-study-2072189.html

Tests carried out on mice have revealed changes in their brains, similar to those observed in humans with dementia, when the animals are operated on.

The researchers suspect the same effect could occur in humans after surgical procedures and are now to start a new study to further explore the theory.

Many doctors already suspect there may be a link between surgery and the onset of Alzheimer’s.

Previous studies have suggested that between 10 and 30 per cent of elderly people who undergo surgery suffer memory problems afterwards, but it has not been established whether these are a short-term response to physical trauma, or the beginnings of dementia.

Cognitive problems, ranging from memory loss to delirium, have been found most commonly when elderly people have undergone heart surgery, but also following other operations.

It is not known if the procedures themselves, or the body’s response to major trauma, spark changes in the brain.

http://www.telegraph.co.uk/science/science-news/7969549/Alzheimers-risk-could-be-increased-by-surgery.html

In tests on mice, the memory loss associated with Alzheimer’s was partially reversed by the protein, which can also lower the risk of catching the illness.

In some of the animals, memory impairment was completely undone after treatment with the protein.

Scientists hope it can soon be tested on humans.

While people with rheumatoid arthritis have to put up with swollen joints and decreased mobility, GM-CSF, the unique protein produced by the disease, stimulates scavenger cells.

These cells remove amyloid deposits left by Alzheimer’s in the brain, lowering the risk of catching the disease and helping to restore memory.

http://www.dailymail.co.uk/health/article-1305335/Arthritis-hold-key-beating-Alzheimers-protein-released-reverses-memory-loss.html

In the Journal of Alzheimer’s Research study, mice with memory loss given the protein fared better in tests.

A synthetic version of GM-CSF protein is already used as a cancer treatment.

UK experts said the study was “an important first step” and tests were needed to see if the drug worked for people with Alzheimer’s.

In people with rheumatoid arthritis, the immune system goes into “overdrive” and produces attacking proteins – including GM-CSF.
Rubbish collectors

It had already been recognised that people with rheumatoid arthritis were less likely to develop Alzheimer’s, but the protective link had been thought to be due to non-steroidal anti-inflammatory drugs (NSAIDs) taken by people with the condition.

However tests showed this was not the case.

In this study, University of South Florida researchers genetically altered mice to have memory problems similar to those seen in Alzheimer’s disease, which is a form of dementia.

They then treated them – and some healthy mice – with the protein. Other mice – both healthy ones and those with Alzheimer’s symptoms – were given a dummy (placebo) treatment.

http://www.bbc.co.uk/news/health-11035500

Women who reported repeated episodes of stress and anxiety in middle age were up to twice as likely to develop dementia than those who did not, a team of Swedish scientists found.

The majority of those affected were diagnosed with Alzheimer’s, the most common form of dementia.

Researchers followed the progress of 1,415 women between 1968 and 2000.

Three surveys in 1968, 1974 and 1980 were carried out to assess levels of psychological stress experienced by the women, who were aged between 38 and 60 at the start of the study.

Stress was defined as a ‘sense of irritation, tension, nervousness, anxiety, fear or sleeping problems’ lasting a month or more.

During the course of the study, 161 of the women taking part developed dementia, mainly in the form of Alzheimer’s disease.

Dementia risk was 65% higher in women who suffered frequent stress in middle age.

The chances of developing dementia increased as women responded to more than one survey by saying they were frequently stressed.

The risk increased by 73% when women reported frequent or constant stress on two occasions, and more than doubled when all three surveys showed they were stressed.

http://www.dailymail.co.uk/health/article-1303588/Alzheimers-disease-risk-linked-mid-life-stress-women.html

Researchers in the US have discovered the presence of “biomarkers” in the cerebrospinal fluid – which surrounds the spinal cord – enabling them to predict with 90 per cent accuracy the presence of the disease.

Tests showed that a “signature” consisting of three biomarkers present in the fluid of 90 per cent of patients with Alzheimer’s disease was also found in more than a third of “normal” older adults, who showed no sign of mental deterioration. The finding suggests these adults were in the earliest stages of the disease, before clinical symptoms had appeared. In the future, if medicines are developed which can effectively slow its development, the test might be used to select patients for preventive treatment.

The findings are published in the journal Archives of Neurology. An editorial said there was now “ample evidence” that analyses of the cerebrospinal fluid had “value”.

Doctors said that eradicating diabetes and depression would also reduce the number of people plagued by the disease.

They added that public health initiatives aimed at these four major areas could help 40 per cent of prospective sufferers avoid the condition.

Dementia, which causes memory loss and confused thinking, affects more than 800,000 mostly older people in the UK. More than half have Alzheimer’s, the most common form of the disease and numbers are increasing due to our ageing population.

The latest study of almost 1,500 people found increasing education would lead to a reduction of about 18 per cent in new cases of dementia over the next seven years.

It is believed that studying makes the brain more flexible and improves its ability to offset the symptoms of conditions such as Alzheimer’s disease.

The results also showed that eliminating depression and diabetes and increasing fruit and vegetable consumption lead to an estimated 21 per cent fall in newly diagnosed dementia patients, with depression making the greatest contribution at just over 10 per cent.

The researchers, whose findings are published online in the British Medical Journal, point out that the direct causal relationship between depression and dementia remains unclear.

http://www.dailymail.co.uk/health/article-1300789/Four-10-dementia-cases-avoided.html

The story is based on a study in 8,745 postmenopausal women aimed at determining if body mass index (BMI) and hip-waist ratio (HWR), were associated with cognitive function. It found that in women with a higher BMI, those who were ‘pear-shaped’ (low HWR) tended to have slightly lower scores of cognitive function than their ‘apple shaped’ (high HWR) counterparts.

These findings do not mean that pear-shaped women are at risk of cognitive problems in later life. This type of study cannot show cause and effect as both body measurements and cognitive function were assessed at the same time. It is also important to note that all the women in this study had good cognitive function and none had dementia or cognitive impairment.

http://www.nhs.uk/news/2010/July07/Pages/memory-problems-and-pear-shape.aspx

A UK and Finnish team found those with more education were as likely to show the signs of dementia in their brains at death as those with less.

But they were less likely to have displayed symptoms during their lifetime, the study in Brain said.

Experts said scientists now had to find out why the effect occurred.

Over the past decade, studies on dementia have consistently shown that the more time you spend in education, the lower the risk of dementia.

But studies have been unable to show whether or not education – which is linked to higher socio-economic status and healthier lifestyles – protects the brain against dementia.

http://www.bbc.co.uk/news/health-10741274

A study has credited vitamin E – found in nuts, seeds and olive oil – with warding off Alzheimer’s.

Pensioners with the highest amounts of the ‘anti-ageing’ vitamin in their blood were around half as likely to develop the devastating disease as those with the least vitamin E in their bodies.

The finding suggests that nuts and oils could provide a cheap and tasty way of keeping the mind healthy as the years advance.

Alzheimer’s affects some 400,000 Britons and around 500 new cases are diagnosed every day.

The Swedish researchers measured vitamin E in samples of blood taken from 232 men and women. All were aged 80 or older at the start of the study and free of dementia.

After six years, 57 had developed Alzheimer’s, the Journal of Alzheimer’s Disease reports.

However, the disease was around half as common in those boasting the most vitamin E at the start of the study.

Previous research into the subject has produced conflicting results but the researchers believe this could be because it mainly focused on one sub-type of vitamin E, rather than looking at it as a whole.

Lead researcher Dr Francesca Mangialasche, of Stockholm’s Karolinska Institute, said: ‘Vitamin E is a family of eight natural components, but most studies related to Alzheimer’s disease investigate only one of these components.

http://www.dailymail.co.uk/health/article-1292181/Snacking-nuts-seeds-Alzheimers-bay.html

In a new trial, people with mild to moderate forms of the condition will be given the drug for six months to assess its impact on mental functioning.

This follows small laboratory studies which have suggested that the drug may have beneficial anti-inflammatory effects.

Alzheimer’s occurs when parts of the brain waste away, damaging the organ’s structure and how it works.

This may be partly due to a protein called TNTNF (Tumor Necrosis Factor-Alpha); A Alzheimer sufferers have high levels of this in their cerebral spinal fluid.

It’s thought thalidomide may block this protein.

In the U.S. trial, patients will have a lumbar puncture before and after treatment to collect cerebral spinal fluid.

This will then be tested to see if the drug is having an effect.

It follows the discovery that a toxic protein that builds up in the brains of dementia patients – triggering loss of memory and confusion – also accumulates in their eyes.

Although the test is several years away, it could eventually allow doctors to give drugs that slow down the onset of the disease.

Around 800,000 people in Britain suffer from Alzheimer’s and other forms of dementia. The number of cases is expected to double within a generation.

There is no cure and existing drugs can only ease symptoms.

The condition is diagnosed by memory tests and occasionally brain scans. However, the disease can only be confirmed by a post mortem which reveals the presence of a harmful protein called amyloid beta in the brain.

The new five year study, published in the journal PLoS One, looked at links between dementia and cataracts in people with Down’s Syndrome

http://www.dailymail.co.uk/health/article-1280049/Eye-test-hope-detect-Alzheimers-years-symptoms.html