Toronto scientists test whether noodle-thin metal rods buried beneath the cortex can jolt memories and repair faulty nerve circuits

Carolyn Abraham

A team of Toronto scientists is pushing Alzheimer’s research in a radical new direction – testing whether electrodes implanted in patients’ brains can jolt their memories into good working order.

The procedure, known as Deep Brain Stimulation, aims to repair faulty nerve circuits with steady electrical pulses from two noodle-thin metal rods buried beneath the cortex. It is most often used to treat chronic pain, Parkinson’s disease and in research against intractable depression.

But at the University Health Network – after an intense 18-month ethics review – researchers have performed DBS as an experimental brain surgery on six men and women in the early stages of Alzheimer’s disease.

The small, world-first trial – published Wednesday in the Annals of Neurology – found DBS is a relatively safe procedure for people with Alzheimer’s, which affects about 500,000 Canadians. But no one knows yet if it will also prove to be an effective one. After a year of stimulation, two patients deteriorated, two showed no change, while two improved.

Exactly how or why electricity might bolster a brain struck with Alzheimer’s, however, is as mysterious as the disease itself – which after more than 100 years of study, still defies explanation. But the Toronto research team feels the phase-one results are promising enough to pursue a phase-two study, and now hopes to find funding to test DBS in another 50 early Alzheimer’s patients.

“This has to be pursued to find out if it is valuable or not,” said Dr. Andres Lozano, the neurosurgeon and senior scientist who led the study at Toronto Western Hospital. “It’s not more of the same, it’s a very bold, aggressive approach that seems reasonably safe.”

SOURCE: www.theglobeandmail.com

Scientists at the University of Lethbridge say they have successfully regrown adult brain cells in tests on mice, a breakthrough that could lead to treatment of neural diseases such as Alzheimer’s.

“We’re pretty excited by it,” said Dr. Robert Sutherland, who led the five-year project at the Canadian Centre for Behavioural Neuroscience.

“In just the same way as people have been able to regenerate pieces of skin that have been damaged, we’ve been able to do that in a part of the brain,” Sutherland told CBC News.

In the study, brain cells were destroyed in mice, which were then treated with a naturally occurring growth factor and behavioural and memory exercises.

According to Sutherland, the three-part treatment allowed the cells to regrow, and after six weeks of treatment, those rats fared just as well as those in a control group.

“We discovered the memory disorder [in the mice] was reversed,” Sutherland said. “It was gone. The memory was as good as normal.”

Dr. Simon Spanswick, one of the primary researchers involved in the project, said the implications of the cell regrowth research are vast.

“Things like Alzheimer’s disease, a number of memory diseases … dementia for example, Parkinson’s disease, what we’ve discovered will be part of a treatment process for these disorders,” he said.

Researchers couldn’t say when their research can start to be applied to humans. However, the Canadian Institute for Health Research has renewed funding for the research for another five years.

Read more: http://www.cbc.ca/health/story/2010/07/31/cgy-alzheimers-breakthrough.html

SOURCE: www.cbc.ca

Alzheimer patients have high accumulations of the beta-amyloid – appearing in the form of plaques – in their brain. The precursors of these plaques are thought to be the underlying cause of the nerve cell loss that leads to Alzheimer’s. Now scientists have identified an enzyme, alpha secretase, which cleaves the amyloid precursor protein (APP) without forming beta-amyloid.

The work, by researchers at the German Centre for Neurodegenerative Diseases (DZNE) and Ludwig Maximilian University of Munich (LMU), appears in EMBO Journal.

The research team has now been able to show that the enzyme ADAM10 alone is responsible for the specific cleavage. Dr. Stefan Lichtenthaler and his team developed highly specific antibodies that can identify the different cleavage products of the precursor protein in the brain cells of mice and in human cell cultures.

Using a special technique called RNA interference, the researchers managed to block each of the three genes that code for the three ADAM enzymes under suspicion. An analysis of the cleavage products revealed that the ADAM10 gene was the only one able to prevent the formation of beta-amyloids. They confirmed their results using mass spectrometry.

“In ADAM10 we have identified a target molecule that plays a central role in the development of the molecular processes in Alzheimer’s disease. We know that ADAM10 is less active in Alzheimer patients,” said Dr. Lichtenthaler. When ADAM10 is less active, the precursor protein is more likely to be cleaved in a way that promotes the formation of beta-amyloids.

“It is possible that less ADAM10 activity could increase susceptibility to Alzheimer’s disease. If that is the case, stimulating ADAM10 could be an important mechanism for therapy. But our antibodies also open up new possibilities for diagnosing and preventing the disease,” said Lichtenthaler.

The antibodies could be used to measure ADAM10 activity in spinal fluid and, by extension, identify persons who may have an increased risk of developing Alzheimer’s disease. A series of experiments to examine this possibility is already underway. (ANI)

SOURCE: http://sify.com

Over the past 20 years, scientists have learned that proteins called sirtuins play a vital role in longevity and stress response in organisms as diverse as humans, yeast and mice. A new paper from MIT biologists now reveals a surprising additional role for sirtuins: They appear to suppress the production of amyloid beta proteins, which form plaques in the brains of Alzheimer’s patients.

The finding, reported in the July 23 issue of Cell, suggests that targeting sirtuins could offer a promising new approach to treating Alzheimer’s, says Professor Leonard Guarente, leader of the research team.

Guarente and his colleagues showed that boosting the activity of a sirtuin called SIRT1 stifled the production of amyloid beta proteins and enhanced brain function in mice engineered to express Alzheimer’s symptoms. This marks the first time sirtuins have been linked to those proteins.
Several drug companies are now developing and testing compounds that enhance sirtuin activity. Guarente, who consults for one of those companies, Sirtris (a unit of GlaxoSmithKline), believes that sirtuin activators may eventually prove useful against Alzheimer’s, which affects up to one-third of people who reach age 80.

Protein clumping

Though amyloid plaques are a defining feature of Alzheimer’s disease, many researchers now believe that the symptoms are caused by smaller clumps of two or three amyloid beta (A-beta) fragments, not the larger plaques.

A-beta peptides form when proteins called amyloid precursor proteins (APPs) are broken into smaller pieces. However, APPs can also be cleaved at other sites, producing harmless protein fragments. APP’s normal function is unknown, but it has been established that people with a gene mutation that stimulates overproduction of APP are more likely to develop Alzheimer’s at an early age (before age 65).

Another mutation that stimulates early-onset Alzheimer’s (which accounts for 5 to 10 percent of cases) occurs in the gene for the enzyme that cleaves APP into A-beta peptides. Although those genes for early-onset Alzheimer’s have been identified, “with late-onset Alzheimer’s, we still don’t know why some people get it and other people don’t,” says Guarente.

Guarente, who first discovered the life-extending ability of sirtuins 20 years ago, started studying their role in Alzheimer’s after some recent studies showed that the gene that produces sirtuins, SIRT1, appears to protect mice from the effects of Alzheimer’s disease. When those studies came out, “I thought that the mice with extra SIRT1 probably had just as much A-beta, but that SIRT1 was protecting them against it,” Guarente recalls. “It turns out that they were actually making less A-beta peptide.”

In the Cell paper, Guarente and his colleagues showed that SIRT1 activates the production of an enzyme (alpha-secretase) that carves APPs into harmless fragments, preventing the formation of Alzheimer’s-associated amyloid peptides. Mice engineered to produce excess sirtuins had reduced peptide levels, while mice with SIRT1 knocked out showed elevated peptide levels.

Furthermore, learning and memory deficits in the Alzheimer’s mice were improved when SIRT1 was overproduced and worsened when the gene was deleted. The researchers also found that SIRT1 activates the so-called notch-signaling pathway via the elevated levels of alpha-secretase, which protects neurons and helps maintain brain function.

A new target for Alzheimer’s

The research, funded by the American Parkinson Disease Association, National Institutes of Health and the Paul F. Glenn Foundation, demonstrates that drugs that activate SIRT1 in the brain may be a promising approach to treating Alzheimer’s, says Guarente. Any such drug would have to be able to cross the blood-brain barrier, which prevents large molecules from diffusing into the brain.

Sirtris, a company co-founded by Guarente and then bought by GlaxoSmithKline, is now testing SIRT1 activators in a clinical trial for diabetes. Guarente believes that related drugs could have an impact on a range of neurodegenerative diseases, as well as diabetes and other diseases of aging.

However, any potential drug for Alzheimer’s would likely take several years to reach clinical trials, because of the need to find a drug that crosses the blood-brain barrier, says Guarente.

Rudolph Tanzi, professor of neurology at Harvard Medical School, says the new findings also suggest another approach: targeting one specific aspect of SIRT1’s activity. Tanzi’s lab recently found that mutations in the gene that produces alpha-secretase (ADAM10) are associated with late-onset Alzheimer’s disease.

“If this is how SIRT1 protects against Alzheimer’s — by turning on ADAM10 — you could try finding a drug that specifically addresses that mechanism,” instead of globally activating SIRT1, says Tanzi.
Provided by Massachusetts Institute of Technology (news : web)

SOURCE: www.physorg.com

By GAUTAM NAIK

Scientists have found a way to dramatically reduce the erosion of memory and learning ability in mice with a version of Alzheimer’s disease, potentially offering a new approach for tackling the illness in humans.

Mice with a model of Alzheimer’s disease that were genetically engineered to produce more sirtuin one retained both memory and learning ability as they aged; the loss of both are hallmarks of Alzheimer’s. Alzheimer’s mice without the extra sirtuin one capability, and those genetically engineered to produce no sirtuin one at all, showed steep declines in learning ability and memory as they aged.

Sometimes described as the “longevity gene,” SIRT1 has become the focus of intense research in recent years. Studies have shown that a highly calorie-restricted diet can turn on the gene and thereby increase longevity in everything from yeast to mice.

Similarly, a compound called resveratrol, found in red wine, also might switch on the gene, and tap the brakes on aging, at least in animals.

The connection between SIRT1 and Alzheimer’s is important because the illness has proved to be extremely hard to treat, even as its burden grows among the population. While lab-dish experiments have suggested a link between SIRT1 and Alzheimer’s, the new study establishes that link more definitively. It also suggests an alternative drug-based approach for treating the disease.

“This is the first demonstration that the SIRT1 pathway can mitigate Alzheimer’s,” said Leonard Guarente, a biologist at MIT and the lead author of the study, which appears in the journal Cell.

Dr. Guarente is a consultant for GlaxoSmithKline PLC, which is conducting early-stage research based on his findings. He sits on the advisory board of Sirtris, a GlaxoSmithKline company that is conducting sirtuin research on the diseases of aging.

The study was funded by an American Parkinson Disease Association fellowship and grants from the National Institutes of Health and the Paul F. Glenn Foundation, which backs research on the biology of aging.

Alzheimer’s is a neurodegenerative disorder affecting up to one-third of people who reach the age of 80. Patients suffer from memory loss and impaired cognition, which are believed to be linked to amyloid plaques. These plaques form when certain proteins get broken up into smaller fragments known as amyloid peptides.

But the proteins can also be broken into harmless fragments. The MIT researchers showed that sirtuin one breaks up the protein into such fragments, rather than the toxic ones associated with Alzheimer’s disease.

In one group of mice, the biologists introduced a second SIRT1 gene. These animals had lower amounts of toxic peptides in their brains than the mice with just one SIRT1 gene.

When put through lab tests as they aged, the mice with the second SIRT1 gene retained their memory and learning ability, while the other group showed a steep decline. The brains of the first group also revealed less inflammation and fewer plaques.

Still another group of mice, engineered without any SIRT1 at all, showed an earlier and steeper decline in memory and learning than the “normal” mice.

“SIRT1 is protecting the mice against memory loss,” Dr. Guarente concludes.

Scientists induced Alzheimer’s in mice by inserting in the animals two human genes associated with inheritable Alzheimer’s disease.

Translating the intriguing new findings into humans won’t be easy. Nobody knows whether mice are a good model for Alzheimer’s disease. And any future drug that can boost SIRT1 levels will need to reach a patient’s brain cells. That requires breaching the blood-brain barrier, not an easy hurdle to overcome, but one that Dr. Guarente says Glaxo is working on.

The Alzheimer’s Society, based in the U.K., said in a statement, “Much more research is now needed before we can find out if drugs that activate SIRT1 could be used to fight dementia.”

“The instant that GSK says they have a brain-permeable compound, I’ll try it in mice,” Dr. Guarente said.

Write to Gautam Naik at gautam.naik@wsj.com

SOURCE: online.wsj.com

A Cambridgeshire charity has funded research into Alzheimer’s disease, using fruit flies.

The Shelford-based Alzheimer’s Research Trust has given The University of Cambridge £30,000 to investigate the link between this combination.

The insects share many of the same genes as humans, and scientists hope knowledge of the flies’ ageing process will help them understand the disease.

The Trust says with an aging population research has never been more crucial.

Age and Alzheimer’s

Age is the biggest factor in Alzheimer’s with the risk doubling every five years after the age of 65. Alzheimer’s is the most common cause of dementia with 465,000 people suffering from it in the UK.

Dr Maria Giannakou is using fruit flies to understand Alzheimer’s disease

Dr Maria Giannakou is leading the research at The University of Cambridge. She says scientists are beginning to understand what is causing the disease.

They are looking into how ageing affects a protein called amyloid that builds up to form plaques in the brain causing brain cells to die.

Fruit flies

Fruit flies are commonly used in all sorts of laboratory research because their life cycle is so short, which means the ageing process can be tracked relatively quickly.

Dr Giannakou explained that a fruit fly has a lot of the same genes as humans, and similar brain processes, making them a good comparison for study purposes.

The protein amyloid which builds up causing Alzheimer’s

A cure in Cambridge

Dr Simon Ridley, head of research at The Alzheimer’s Research Trust said that £1.8m is being spent on various studies in Cambridge. The studies are looking at the causes, diagnosis, prevention, treatment and cure of the condition.

When this fruit fly project is complete, the trust will decide whether to continue along similar lines or send their research in a different direction.

He said: “We need to tackle this disease as soon as we can because it is likely to increase as our population ages. Really, there is an urgency to tackle this.”

‘Frighteningly rapid’

Kenny Fryde from Chesterton, in Cambridge, is looking after his mother who has Alzheimer’s.
Although only recently diagnosed, he said they saw symptoms years ago.

Kenny described how his mother would suffer memory lapses and was convinced she was living abroad.

He described her as “a highly intelligent professional woman” but her mental deterioration was “frighteningly rapid”.

He went on: “She’s disappearing bit by bit.”

SOURCE: news.bbc.co.uk

Marilyn Maldonado is not quite sure why she is at the Memory Enhancement Center in the seaside town of Oakhurst, N.J.

“What are we waiting for?” she asks. About 10 minutes later, she asks again. Then she asks again.

She is waiting to enter a new type of Alzheimer’s drug study that will, in the boldest effort yet, test the leading hypothesis about how to slow or stop this terrifying brain disease.

The disease is defined by freckles of barnacle-like piles of a protein fragment, amyloid beta, in the brain. So, the current thinking goes, if you block amyloid formation or get rid of amyloid accumulations — plaque — and if you start treatment before the disease is well under way, you might have a chance to alter its course.

On Tuesday, that plan got a new push. The National Institute on Aging and the Alzheimer’s Association proposed new guidelines for diagnosis to find signs of Alzheimer’s in people who do not yet have severe symptoms, or even any symptoms at all.

The guidelines are needed for the new approach to Alzheimer’s drug development. Just about every pharmaceutical company and many biotechnology companies have experimental drugs to block amyloid — there are more than 100 in the pipeline. And the companies would like to show that if they give their drugs early, they can slow or stop the disease.

That is the ultimate goal for the drug in the study Mrs. Maldonado wants to enter, sponsored by Bristol-Myers Squibb. The company is, for the first time, testing such a drug in patients who, on evaluation with memory tests and new brain scans and tests for amyloid in cerebrospinal fluid, seem to be in a very early stage of Alzheimer’s. The idea is to attack the disease when there may still be time to stop the worst brain cell death.

But there is a problem. The Food and Drug Administration says it needs to know not just that plaque was reduced or even that it disappeared, but that those who took a drug ended up with better memory and better ability to think and reason as compared with those who did not take the drug.

Alzheimer’s, though, progresses so slowly that showing that a drug, started early, affects symptoms can take far longer than companies can afford to wait.

There is reason not to accept other forms of proof, like scans or cerebrospinal fluid that show changes in amyloid in the brain, the F.D.A. says. The agency has approved drugs for diseases, including sudden death from heart arrhythmias, on the basis of tests that showed symptoms, like heart rhythms, improved. Then it turned out the drugs did not affect the course of the disease and, in the case of the heart drugs, actually hastened death.

So the Alzheimer’s field is poised at an agonizing point — ready to move forward with new methods of diagnosis and drugs that might modify the course of the disease, but without proof that blocking amyloid actually makes a difference.

In the meantime. Bristol-Myers is trying a two-pronged strategy to gain faster approval. It is starting treatment early, but not so early that patients are a decade or more away from Alzheimer’s. And as it looks for effects on symptoms like memory and reasoning, the company will be tracking what happens to amyloid in the brain, hoping to show symptoms improve or no longer worsen as plaque formation slows or stops.

It is a gamble for the company, because even people with fairly mild symptoms may have too much brain damage to be helped. But it is a strategy that makes sense, said Dr. Dennis J. Selkoe, a Harvard researcher who is not affiliated with the study.

“In my view, the sweet spot for amyloid-lowering trials is mild Alzheimer’s disease,” Dr. Selkoe said. “As soon as one of those trials shows benefit, everyone will move to prevention trials,” he said. “They will begin treating before there are symptoms.”

Mrs. Maldonado may be one of the pioneers.

The Amyloid Hypothesis

Considering how important a medical problem Alzheimer’s is — afflicting 5.3 million Americans, the seventh-leading cause of death, and devastating and bankrupting families — it took a surprisingly long time to be recognized as a disease at all. And it took longer still to reach any kind of agreement on its cause.

Dr. Paul Aisen, an Alzheimer’s expert at the University of California, San Diego, remembers well the old days, in the late 1970s. He was in medical school, studying to be a geriatrician. There was no discussion of Alzheimer’s disease.

Ever since it was described by Dr. Alois Alzheimer in 1906 as a “peculiar” disease in a 51-year-old woman, doctors had considered it an oddity, a rare illness of middle, not old, age. Old people who lost their memory and ability to reason and care for themselves were said to be “senile.” That word did not refer to any specific disease like Alzheimer’s. Senility, Dr. Aisen said, was “what might happen when you got old.” And “there was nothing you could do about it.”

Then, in 1976, doctors’ eyes were opened by an editorial in Archives of Neurology by Dr. Robert Katzman, a neurologist. Alzheimer’s, he wrote, is not rare — it is common. It can arise in old age. And it is a leading cause of death and, Dr. Katzman said, a disease whose origin could be determined and whose course might be stopped.

Neurologists took note. But it was 20 years before there were any drugs for Alzheimer’s, and the four approved so far treat only symptoms, modestly and temporarily improving memory, for example, and do not affect the relentless brain cell death.

In the meantime, researchers came upon an exciting target for a drug. They discovered two enzymes that snip pieces from a large protein protruding from brain cells. The result is toxic fragments of a substance known as amyloid beta peptides. Those shards accumulate as plaques on the brain. One way to prevent plaques might be to block one of those crucial enzymes.

Just about every drug company got to work.

They had long suspected amyloid beta was a key player in the genesis of Alzheimer’s, but until they found the enzymes researchers had no way to block it. Amyloid beta itself might be injuring nerve cells or the plaques, made of accumulations of amyloid beta, could be the culprits. But whichever was true, three lines of evidence pointed to amyloid beta: rare gene mutations that lead to its overproduction cause Alzheimer’s in middle age. Down syndrome also causes overproduction of amyloid beta, and people with Down always get Alzheimer’s. And when scientists put the rare mutated genes that cause Alzheimer’s into mice, the mice developed plaques and memory problems.

The logic was not airtight. Scientists note that older people with typical Alzheimer’s often have something else wrong in their brain — damage from mini-strokes, for example. Perhaps some of these other conditions set off waves of cell death independent of amyloid beta.

But over the years, researchers say, what has become known as the amyloid hypothesis — the notion that overproduction or reduced clearance of amyloid beta is a cause of the disease and blocking amyloid beta could stop it — dominated their thinking.

“Ninety percent of us in the field believe it is correct,” Dr. Aisen said.

An Antibody Approach

Testing of the amyloid hypothesis began a few years ago with two experimental anti-amyloid drugs, homotaurine and tarenflurbil.

Patients who took them did not improve.

But, some researchers asked, was that a fair test? The first drug was not very potent, and little of the second reached the brain. And it was not clear whether either was really affecting amyloid because there were no direct measurements of plaques or amyloid beta protein.

The results, said Dr. Samuel E. Gandy, a professor of Alzheimer’s disease research at Mount Sinai School of Medicine, were “uninterpretable.”

Then there was the vaccine approach — immunize against amyloid beta and let the immune system clear plaque. It worked in mice and so, to great excitement, researchers tested it in patients. But a preliminary study was abruptly halted when 18 of 300 patients developed a brain inflammation. Two immunized patients who later died after reaching “severe end-stage dementia” had almost no plaque in their brains on autopsy — the vaccine had apparently cleared plaques but not noticeably affected their disease.

But that is not proof a vaccine would not work, said Dr. Selkoe, a founder of the company that did the study and a consultant to it. Two patients hardly constitutes a full analysis of the trial data, he says.

Now, the company, Elan, and its collaborators are trying a different tack. Instead of using a vaccine, they made an antibody to amyloid beta, a drug called bapineuzumab.

Some initial results were published in March. A new type of scan that can show plaques found the drug was removing them. But so far it is unclear whether patients are improving.

Johnson & Johnson, which partnered with Elan and its collaborator, Pfizer, says it will continue the study.

That makes sense, said Dr. Gandy, who is not part of the study.

“We have no idea how long we might need to treat,” he said.

Tough Road to Consensus

Dr. Russell Katz, director of the F.D.A.’s division of neurology products, is in a quandary about Alzheimer’s drugs. What, he must decide, should be the criteria for showing that a drug works?

The agency is not ready to do that, Dr. Katz said.

“You only care if down the road the patient gets better,” Dr. Katz said. “What we are concerned about is approving a drug based on a lab test and being wrong about what happens to the patient clinically.”

With Alzheimer’s, Dr. Katz said, “the great fear is that maybe amyloid has nothing to do with the disease.” If that were the case, and the agency approved a drug that blocked amyloid formation, millions of healthy people could end up taking something useless or even dangerous. And because it takes so long for Alzheimer’s to develop, it could be decades, if ever, before anyone knew the drug did not work.

“It is a conundrum,” Dr. Katz said. “We all hope to get to the point in our understanding of the disease process where everyone in the field says: ‘Look. We know it now. Amyloid causes Alzheimer’s, and we have drugs that decrease amyloid.’ But we are not there yet.”

Bristol-Myers Squibb, though, is betting amyloid beta is the culprit. And it is betting it can show an effect in people who are in the early stages of Alzheimer’s.

Still, Dr. Aisen is concerned that even those patients, people like Mrs. Maldonado, might be beyond help. Treatment may have to start much earlier. So he is planning a large federal study to test amyloid-blocking drugs in people over 70 with normal memories but evidence of some amyloid accumulation. His criteria for success will not be the F.D.A.’s current one. Instead, he will ask whether the drugs slow the brain atrophy that is characteristic of Alzheimer’s and prevent amyloid from accumulating in subjects’ brains.

“If you think Bristol-Myers Squibb is going out on a limb, this is going farther,” Dr. Aisen said. If blocking amyloid beta and slowing brain atrophy are not accepted as sufficient evidence that a drug works, a study with normal 70-year-olds could end up taking 10 to 15 years to show an effect on the actual symptoms of Alzheimer’s.

After her scan that recent day, Mrs. Maldonado was entered in the Bristol-Myers study.

She is 82, a former school bus driver living in nearby Jackson with a diagnosis of mild memory impairment. She came with her son-in-law to the Memory Center that day, in black slacks and a flowered blouse, wearing a gold bracelet and gold rings. Her short white hair was fluffy, freshly washed. And she had a way about her, a joking demeanor, intended to disguise her forgetfulness.

Her brain, the scan showed, was riddled with plaque.

Dr. Joel Ross, who runs the Memory Center, told her the results.

“We found you are producing a sticky material called plaque,” he told her.

“Yeah,” she said.

“It’s coating some of your brain.”

“Yeah,” she said again.

“If you stay this way there will be a lot of it.”

“Yeah.”

“So we’re going to give you a drug that may clear it up.”

“Yeah.”

SOURCE: www.nytimes.com

Results of a new interesting study suggest that the more weight a woman is carrying, the greater their risk is of developing memory loss.

For years researchers have been trying to find clues that would indicate memory loss which can lead to Alzheimer’s disease and now they have found what they say is a key contributor.

The study was carried out by researchers at Northwestern University in Chicago who analyzed data from the Women’s Health Initiative, comparing body mass index of 8,745 postmenopausal women to their mental compitence tests.

They found that the higher the BMIs of study participants, the lower they scored on an array of different mental tasks and according to Dr. Diana Kerwin this proves that obesity can mess with the mind.

“While the women’s scores were still in the normal range, the added weight definitely had a detrimental effect,” she said.

“Even if you do have normal blood pressure and you’re not diabetic, it still should be something that’s looked at as an independent risk factor for your brain health.”

SOURCE: www.dbtechno.com

Boston (SmartAboutHealth) – A new study has revealed that Alzheimer’s not only causes cognitive decline and memory loss, but also takes emotions out of those who suffer from the terrible disease.

Researchers from the University of Florida have been doing a great deal of work on Alzheimer’s disease and dementia to see the various ways in which it will impact its victims.

One interesting thing that they found is that Alzheimer’s can actually suck the emotions right out of people, to the point where they will respond differently to things once the disease has developed when compared to before the disease.

The study was carried out by having a group of patients with Alzheimer’s experience ten different negative pictures, and ten different positive pictures.

The idea was to see how they would react when it comes these pictures, and how Alzheimer’s would impact their reaction.

Researchers stated that the Alzheimer’s patients, within their brains, realized what their emotions were, but they were different when compared those who did not have Alzheimer’s.

Emotions could vary depending on the case and the patient, but from this study those who have Alzheimer’s are not able to actively display their emotions the same way healthy people can.

The study has been published in the Journal of Neuropsychiatry and Clinical Neurosciences.

SOURCE: http://smartabouthealth.net

By MARILYNN MARCHIONE, AP Medical Writer

Scientists are reporting advances in detecting and predicting Alzheimer’s disease at a conference in Honolulu this week, plus more proof that getting enough exercise and vitamin D may lower your risk.

There are better brain scans to spot Alzheimer’s disease. More genes that affect risk. Blood and spinal fluid tests that may help tell who will develop the mind-robbing illness and when.

But what is needed most — a treatment that does more than just ease symptoms — is not at hand.

“We don’t have anything that slows or stops the course,” said William Thies, the Alzheimer’s Association scientific director. “We’re really in a silent window right now” with new drugs, he said.

Several promising ones flopped in late-stage tests — most recently, Pfizer Inc.’s Dimebon. Results on several others won’t be ready until next year.

Still, there is some progress against Alzheimer’s, a dementia that afflicts more than 5 million Americans and more than 26 million people worldwide. Highlights of the research being reported this week:

_Prevention. Moderate to heavy exercisers had half the risk of developing dementia compared with less active people, researchers from the long-running Framingham Heart Study reported Sunday. Earlier studies also found exercise helps.

“That seems to be as good as anything” for preventing dementia, said Dr. Richard Mayeux, a Columbia University neurologist and conference leader.

Another big government-funded study found that vitamin D deficiency can raise the risk of mental impairment up to fourfold. This doesn’t mean taking supplements is a good idea, doctors warn. A large study is testing whether that is safe and helps prevent a variety of diseases.

_Novel treatments. Tests of an insulin nose spray to improve cognition gave encouraging results, but “it’s still a pilot trial” and larger studies are needed to see if this works and is safe, said Laurie Ryan. She oversees Alzheimer’s study grants for the National Institute on Aging, which funded the work.

It’s based on the theory that Alzheimer’s and diabetes are related. Diabetics seem to have a higher risk of developing Alzheimer’s, and Alzheimer’s patients tend to have insulin resistance, Ryan said. Giving insulin as a nose spray sends it straight to the brain without affecting blood-sugar levels, she explained.

“If it works, it would certainly be an easy thing to administer. It’s not like taking a shot each day,” and likely would be cheap, she said.

_Improved detection. Many types of imaging can document dementia, which usually is diagnosed through cognition tests. For several years, scientists have used one such method — a radioactive dye and PET scans — to see the sticky brain plaque that is a key feature of Alzheimer’s. But the dye is tough to use, and at least four companies are developing better ones.

Philadelphia-based Avid Radiopharmaceuticals Inc. reports success with one such dye, and says it may offer an early warning for those on their way to developing Alzheimer’s. The claim has led to some media buzz.

“I don’t want to downgrade — it’s a significant accomplishment,” Thies said, but it mostly improves on the existing test.

A PET scan costs $3,000 to $5,000 plus whatever Avid would charge for the dye, if it wins federal approval. It may require special training to give the test and interpret it, so it likely will remain mostly a research tool to pick the right patients for clinical trials and monitor a drug’s effects, Thies said.

Mayeux, the Alzheimer’s conference leader, agreed.

“It’s not going to be helpful in diagnosis,” because a lot of people without Alzheimer’s have plaque that can be seen on scans, he said. These people may go on to develop Alzheimer’s someday, but more study would have to establish that for it to become a definitive diagnostic test, rather than a tool to monitor plaque levels in research, he said.

Until there are better treatments, there will be little demand for tests that show you have or are destined to get the disease, several experts said. There’s little testing now for the first gene strongly tied to Alzheimer’s risk, ApoE-4.

“It’s kind of like finding high cholesterol” but not having drugs that can lower it, said Dr. Mark Sager, director of the Wisconsin Alzheimer’s Institute at the University of Wisconsin-Madison. He was involved in a study of a different Alzheimer’s-linked gene that will be reported this week.

Scientists also don’t know if the plaque is a cause, an effect, or just a sign of Alzheimer’s. Two experimental drugs seemed to clear plaque but did not lead to clinical improvement.

“We’ve still got a long way to go,” Sager said.

SOURCE: Associated Press