Brain pacemaker delivers constant Deep-Brain Stimulation (DBS) for Alzheimer’s patients

Credit Image: Functional Neuromodulation

Once implanted into the brain, a pacemaker-like device delivering electrical stimulation could help improve the memory of Alzheimer’s patients. Technology Review reports.

Using electrodes, Deep-Brain Stimulation (DBS) is already used to treat patients with Parkinson’s, epilepsy, and obsessive-compulsive disorder.

In this Alzheimer’s trial, co-chaired by Constantine Lyketsos of Johns Hopkins, the device was placed into a region of the brain involved in learning and memory.

In Alzheimer’s patients, brain tissue atrophies and the reduction of memory and thinking skills increase over time.

According to the Johns Hopkins team, electrical shocks could stimulate critical neural networks disrupted by Alzheimer’s.

Recent trials for potential Alzheimer’s drugs have failed to halt or stave off cognitive decline.

Now, in a pilot study with these deep brain stimulators, after one year of constant stimulation, brain scans of six Alzheimer’s patients showed signs of increased neuron activity in areas involving learning and memory, although, it could be unlikely to actually reverse the effects or damage to the brain caused by Alzheimer’s disease.

The researchers are recruiting patients into the new trial initiated by Toronto-based Functional Neuromodulation. The trial will track patients who have the device for a year using doctor observations and brain scans.

[Via Technology Review]

Alzheimer's Disease: Damage Starts earlier than first thought

The first changes in the brain of a person with Alzheimer’s disease can be observed as much as ten years in advance – ten years before the person in question has become so ill that he or she can be diagnosed with the disease.

This is what a new study from Lund University in Sweden has found.

Physician Oskar Hansson and his research group are studying biomarkers – substances present in spinal fluid and linked to Alzheimer’s disease.

The group has studied close to 140 people with mild memory impairment, showing that a certain combination of markers (low levels of the substance beta-amyloid and high levels of the substance tau) indicate a high risk of developing Alzheimer’s disease in the future.

As many as 91 per cent of the patients with mild memory impairment who had these risk markers went on to develop Alzheimer’s within a ten-year period.

In contrast, those who had memory impairment but normal values for the markers did not run a higher risk of getting Alzheimer’s than healthy individuals. Oskar Hansson previously carried out a study showing that pathological changes can be seen in the brain of an Alzheimer’s patient five years before the diagnosis.

The new study has thus doubled this time span to ten years.

“This is a very important finding with regard to the development of new therapies against the disease.

All prospective therapies have so far shown to be ineffective in stopping the disease, and many people are concerned that the pharmaceutical companies will give up their efforts in this field.

But these failures may depend on the fact that the new therapies were initiated too late. When a patient receives a diagnosis today, the damage has already gone too far,” says Oskar Hansson.

With the help of the biomarkers studied by the group, pharmaceutical companies will now be able to identify the people with mild symptoms who run the highest risk of developing Alzheimer’s within a ten-year period.

These individuals can then be offered the opportunity of taking part in trials for new medicines, while those who run a low risk of developing the disease do not need to be involved. A new trial of this kind is already underway, on the basis of the earlier study by the Hansson group.

The 90 per cent accuracy of the risk markers means that they are not sufficient as the only method for early diagnosis of Alzheimer’s. But if they can be combined with a clinical assessment and, for example, imaging of the blood flow in the brain, it should be possible to increase the level of accuracy, according to Oskar Hansson.

However, this will only be relevant once drugs that are effective in slowing down the disease have been developed. Only then will it really be meaningful to identify patients earlier than is currently possible.

By observing how the levels of the biomarkers develop over the ten years before the patient’s diagnosis, the research group has also been able to map the progression of the disease in the brain.

The results indicate that it starts with a modified turnover of beta-amyloid. Only later is this followed by changes in the tau protein and damage to nerve cells. This can be important information for those developing new therapies for Alzheimer’s.

Adiponectin: Hormone affects Dementia in Woman

Women with an abnormal number of a certain hormone are more likely to develop dementia, as suggested by latest study conducted in cooperation with the Framingham Heart Study (FHS).

Participants from the Boston University cardiovascular research initiatives provided frozen blood samples that allowed scientists to isolate a hormone known as adiponectin, which the new research findings said appear to be connected with dementia.

According to a report by U.S. network ABC, the study drew its conclusion on the analysis of 840 participants, which were monitored for 13 years, with 159 of them suffering brain degeneration with one common denominator - high presence of adiponectin.

The results, according to Dr Ernst Schaefer of Tufts University, were somewhat perplexing as the pursued links between dementia and diabetes were further complicated by what the researchers have so far appreciated from the decade-old study.

While science generally regards adiponectin as an important agent in preventing the onset of diabetes, its purportedly dementia-inducing function, at least in the context of the FHS experiment, had caught the researchers by surprise.

Trackers: GPS shoes for Alzheimer's patients

The first shoes with built-in GPS devices, to help track down dementia-suffering seniors who wander off and get lost, are set to hit the US market this month, the manufacturer says.

GTX Corp said the first batch of 3,000 pairs of shoes has been shipped to the footwear firm Aetrex Worldwide, two years after plans were announced to develop the product.

The shoes will sell at around $300 a pair and buyers will be able to set up a monitoring service to locate "wandering" seniors suffering from Alzheimer's Disease.

Andrew Carle, a professor at George Mason University's College of Health and Human Services who was an adviser on the project, said the shoes are likely to save lives and avoid embarrassing and costly incidents with the elderly.

"It's especially important for people in the earliest stages of Alzheimer's who are at the highest risk," Carle told AFP.

"They might be living in their home but they're confused. They go for a walk and they can get lost for days."

Carle said studies indicate more than five million Americans suffer from Alzheimer's, a number expected to quadruple in the coming years. He said 60 percent of sufferers will wander and become lost and up to half of those lost who are not found within 24 hours may die, from dehydration, exposure or injury.

Other devices such as bracelets or pendants can provide similar protection but seniors often reject these.

"The primary reason is that paranoia is a manifestation of the disease," Carle said. "If you put something on someone with Alzeheimer's that they don't recognize, they remove it. If it's a wristwatch and it's not their wristwatch, they will take it off. So you have to hide it."

The GPS system, which is implanted in the heel of what appears to be a normal walking shoe, allows family members or carers to monitor the wearer and to set up a "geofence" that would trigger an alert if the person strays beyond a certain area.

The shoes are being developed by GTX Corp., which makes miniaturized Global Positioning Satellite tracking and location-transmitting technology, and Aetrex. They received certification from the Federal Communications Commission this year for the system.

The makers say the market for such shoes is growing, given the soaring costs of Alzheimer's.

"This is a significant milestone for both companies and while the $604 billion worldwide cost of dementia has become and will continue to be a significant fiscal challenge, the under $300 GPS enabled shoes will ease the enormous physical and emotional burden borne by Alzheimer's victims, caregivers and their geographically distant family members," said Patrick Bertagna, chief executive of GTX Corp.

Professor Carle said the original idea was to develop the shoes for children and long-distance runners but the makers changed the plan when he offered his advice, noting that the devices can also help ease a lot of anxiety about seniors who want to remain active.

"They feel a need to walk and it is good for them," he said. "They should take a walk. It's good for them."

Gantenerumab: New Alzheimer's drug shows early promise

An experimental Alzheimer's disease drug, Gantenerumab, may help lower levels of amyloid plaque in the brains of people with the disease, an early clinical trial indicates.

The new study, which appears online Oct. 10 in the Archives of Neurology, is among the first to show the effects of an anti-amyloid drug in humans with Alzheimer's disease, but experts caution that while promising, more research is needed before this drug can be deemed safe or effective.

And, in what may turn out to be an equally important caveat, experts also say that it's by no means certain that reducing levels of amyloid plaque would stave off memory loss and the other mental declines associated with the disease because the role of the plaque in Alzheimer's isn't fully understood.

Alzheimer's disease is the most common form of dementia. Symptoms including serious memory loss, confusion and mood changes develop gradually and worsen with time.

Recently, many strides have been made in diagnosing Alzheimer's disease earlier, but doctors have been stymied by a lack of effective treatments to stop or slow the course of the disease.

It's long been known that a protein fragment called beta-amyloid builds up in the spaces between nerve cells in the brains of people with Alzheimer's disease.

The new drug, Gantenerumab, targets these amyloid proteins by priming the body's immune system to recognize them as invaders.

Of 16 people with mild-to-moderate Alzheimer's disease, those who received two to seven infusions of the experimental drug every four weeks showed marked reductions in the amount of plaque in their brains via imaging tests that were conducted several months after their treatments.

By contrast, amyloid load increased among people who were randomized to receive the placebo. The new drug was given at either 60 or 200 milligrams (mg) doses.

The higher dose yielded greater reductions in amyloid levels, the study showed. People who were given the 60 mg doses saw a nearly 16 percent reduction in the amount of amyloid, and those given the 200 mg doses saw a 36 percent reduction.

The new study was conducted and funded by the drug's manufacturer, F. Hoffmann-LaRoche Ltd., in Basel, Switzerland.

The big question is whether or not reducing amyloid levels has any effect on the symptoms or progression of Alzheimer's disease, said Dr. Patrick Lyden, chief of neurology at Cedars-Sinai Medical Center in Los Angeles.

"There is a growing concern that amyloid is a guilty bystander, but not the actual culprit in the brains of people with Alzheimer's disease, and taking away the bystander may not help the patient," he said.

Alzheimer's might be transmissible in air

Light photomicrograph of brain tissue reveals the presence of typical amyloid plaques found in a case of variant Creutzfeldt-Jakob disease (vCJD), a prion disease.

(Credit: Sherif Zaki; MD; PhD; Wun-Ju Shieh; MD; PhD; MPH / via CDC Public Health Images Library)

The brain damage that characterizes Alzheimer's disease may originate in a form similar to that of infectious prion diseases such as bovine spongiform encephalopathy (mad cow) and Creutzfeldt-Jakob, according to newly published research by The University of Texas Health Science Center at Houston (UTHealth).

"Our findings open the possibility that some of the sporadic Alzheimer's cases may arise from an infectious process, which occurs with other neurological diseases such as mad cow and its human form, Creutzfeldt-Jakob disease," said Claudio Soto, Ph.D., professor of neurology at The University of Texas Medical School at Houston, part of UTHealth.

"The underlying mechanism of Alzheimer's disease is very similar to the prion diseases. It involves a normal protein that becomes misshapen and is able to spread by transforming good proteins to bad ones. The bad proteins accumulate in the brain, forming plaque deposits that are believed to kill neuron cells in Alzheimer's."

The results showing a potentially infectious spreading of Alzheimer's disease in animal models were published in the Oct. 4, 2011 online issue of Molecular Psychiatry, part of the Nature Publishing Group. The research was funded by The George P. and Cynthia W. Mitchell Center for Research in Alzheimer's Disease and Related Brain Disorders at UTHealth.

Alzheimer's disease is a form of progressive dementia that affects memory, thinking and behaviour. Of the estimated 5.4 million cases of Alzheimer's in the United States, 90 percent are sporadic.

The plaques caused by misshapen aggregates of beta amyloid protein, along with twisted fibers of the protein tau, are the two major hallmarks associated with the disease. Alzheimer's is the sixth leading cause of death in the United States, according to the Alzheimer's Association.

Researchers injected the brain tissue of a confirmed Alzheimer's patient into mice and compared the results to those from injected tissue of a control without the disease. None of the mice injected with the control showed signs of Alzheimer's, whereas all of those injected with Alzheimer's brain extracts developed plaques and other brain alterations typical of the disease.

"We took a normal mouse model that spontaneously does not develop any brain damage and injected a small amount of Alzheimer's human brain tissue into the animal's brain," said Soto, who is director of the Mitchell Center.

"The mouse developed Alzheimer's over time and it spread to other portions of the brain. We are currently working on whether disease transmission can happen in real life under more natural routes of exposure."

Repeated Head Blows may cause Premature Dementia disease in athlete brain

Professional athletes who suffer repeated blows to the head are at risk for developing a brain disease that years later manifests as memory loss, mood disorders, and even early dementia.

The pattern of protein tangles and plaques associated with the disease, known as chronic traumatic encephalopathy (CTE), is distinct from those in Alzheimer’s patients, according to new research reported in the journal Neurosurgery.

“The first thing is to identify the disease, give it a name, and identify its pathology. We’ve done that,” says Bennet Omalu, associate clinical professor of pathology at University of California, Davis. Omalu was the first to describe CTE in 2002, after examining the brain of former Pittsburgh Steelers football player Mike Webster
“We’re seeing CTE in any activity that subjects your brain to repeated acceleration and deceleration.”

In the current study, Omalu and colleagues detailed histological examinations of the brains of 17 athletes who played contact sports, including eight professional football players, four professional wrestlers, and three high school football players. All had died suddenly from suicide, drug abuse, or in accidents.

The researchers diagnosed CTE in 10 of the 14 professional athletes, and one high school football player.

Important differences exist between CTE and Alzheimer’s disease, Omalu says.

Subjects with CTE have tangles of tau proteins in their brains that were similar to those seen in later-stage Alzheimer’s patients, but they occurred in a very different pattern. While the tangles in Alzheimer’s patients are scattered throughout the brain, those in the athletes exhibited a “skip phenomenon.”

The tangles occurred in some areas of the cerebral cortex but were absent in others within the same lobe. In addition, the brains of the athletes did not show the classic neuritic amyloid plaques or the widespread cerebral atrophy characteristic of Alzheimer’s disease.

Finally, the subjects diagnosed with CTE ranged from 18 to 52 years old, whereas Alzheimer’s disease typically does not occur until after age 60.

The study also questions the connection between CTE and a variant of the apolipoprotein E gene. Previous researchers have linked the ApoE4 allele to a predisposition for Alzheimer’s disease and the behaviour changes of CTE, but the CTE-positive subjects in this study were more likely to have the ApoE3 genotype, which is associated with tangle-only dementia. The CTE also produces tangle-only brain abnormalities.

Identifying the genotypes associated with CTE could help patients evaluate the risks they face when playing high contact sports.

“Although we do not have the capability now, it may one day be possible to develop a battery of genetic tests to identify individuals at high, medium or low risk for CTE. Knowing whether you had these certain types of genes, you may be advised not to play football,” Omalu says.

Currently, CTE can only be diagnosed during autopsy. Omalu and his colleagues are now focusing their research on ways to identify the disease in the living and to develop potential drug treatments.

In the meantime, “parents need to be aware of the dangers of repeated blows to the head sustained by children in football, wrestling, and hockey. The younger you are when you start playing, the greater risk you have of permanent brain damage,” says Omalu.

“We need to embark on an aggressive education of physicians and parents, so people are able to make informed judgments before they decide to play or not to play.”

The research received funding from the West Virginia University Foundation, the Hazel Ruby McQuain Charitable Trust, and Robert Fitzsimmons.

More news from UC Davis: http://www.news.ucdavis.edu/

Hopes for new Alzheimer's and Parkinson's treatments

Diseases such as Alzheimer's and Parkinson's could be caused by just a handful of genetic "repeat offenders" in the brain, Scottish scientists have revealed.

Researchers have identified a small set of proteins responsible for more than 130 brain diseases, the biggest cause of disability in the world.

The scientists, led by Professor Seth Grant at the Wellcome Trust Sanger Institute and Edinburgh University, hope that the identification of such a relatively small number of damaging genetic triggers could lead to new treatments for brain disease.

Professor Grant said: "These diseases include common debilitating diseases such as Alzheimer's disease, Parkinson's disease and other neurodegenerative disorders as well as epilepsies and childhood developmental diseases including forms of autism and learning disability."

Neurology Professor Jeffrey L Noebels, of Baylor College of Medicine in Texas, said around half of the damaging proteins are "repeat offenders", giving researchers a strategic entry point to get to the bottom of brain diseases.

He added: "The rest of us have a front row seat to witness neuroscience unravel the complexity of human brain disorders."

The scientists say the findings open several new paths toward tackling these diseases.

"Since many different diseases involve the same set of proteins, we might be able to develop new treatments that could be used on many diseases", said Professor Grant.

"We also can see ways to develop new genetic diagnostic tests and ways to help doctors classify the brain diseases."

Neuroscientists discover connection between nicotine and Alzheimer’s disease

Hey-Kyoung Lee, associate professor in the University of Maryland Department of Biology, and her research team have shown that they may be able to eliminate debilitating side effects caused by a promising Alzheimer’s drug by stimulating the brain’s nicotine receptors.

Scientists believe that an over-production of a peptide called A-beta in the brain is the cause of Alzheimer’s and are developing drug treatments that prevent the action of the enzyme BACE1, which produces A-beta.

But Lee and her team, including University of Maryland and Johns Hopkins University researchers, previously demonstrated that eliminating — or “knocking out” — the BACE1 enzyme in laboratory mice caused some of the test animals to become confused and aggressive. “The mice exhibit signs of schizophrenia and memory loss when you block the enzyme,” says Lee.

“BACE1 is a very promising drug target, but you have to overcome these obviously debilitating side effects to effectively treat Alzheimer’s disease.”

Lee and her colleagues have been searching for a solution that could circumvent the abnormal brain function and behavioral side effects caused by BACE1 inhibition, and they think they may have found it.

They pinpointed the receptor that is targeted by nicotine, the Alpha7 nicotinic acetylcholine receptor, as a potential therapeutic target. A paper describing their breakthrough appears in the current issue of the Journal of Neuroscience.

“By stimulating the Alpha7 receptor with nicotine, we were able to recover normal brain function,” explains Lee. “We are very hopeful that this will be a way to overcome the deficits seen with the BACE-1 knockouts.”

The research group pinpointed the brain dysfunction to the regulation of calcium uptake by neurons. Calcium triggers the release of neurotransmitters, the chemicals which transmit signals from a neuron to a target cell across a synapse.

“The mice with BACE1 knockouts have less calcium signaling in the pre-synaptic neuron, and that is why they were releasing less neurotransmitters,” Lee says. “We looked at what receptors on the pre-synaptic terminal were linked to a calcium signaling pathway.

This Alpha7 receptor happens to be on one of the pre-synaptic receptors that is a calcium channel, and we thought we could use that to enhance the calcium signaling.”

The research team found that nicotine activated the uptake of calcium, and thus the neurotransmitter release mechanism.

“After treatment with nicotine,” says Lee, “the mice released normal amounts of the neurotransmitter as seen in brains of normal animals.”

Alzheimer’s: Experimental vaccine development

Researchers at UT Southwestern Medical Center have created an experimental vaccine against beta-amyloid, the small protein that forms plaques in the brain and is believed to contribute to the development of Alzheimer’s disease.

Compared with similar so-called DNA vaccines that the UT Southwestern researchers tested in an animal study, the new experimental vaccine stimulated more than 10 times as many antibodies that bind to and eliminate beta-amyloid. The results appeared in the journal Vaccine.

Future studies will focus on determining the safety of the vaccine and whether it protects mental function in animals, said Dr. Roger Rosenberg, director of the Alzheimer’s Disease Center at UT Southwestern and senior author of the study.

“The antibody is specific; it binds to plaque in the brain. It doesn’t bind to brain tissue that does not contain plaque,” Dr. Rosenberg said. “This approach shows promise in generating enough antibodies to be useful clinically in treating patients.”

A traditional vaccine – an injection of beta-amyloid protein itself into the arm – has been shown in other research to trigger an immune response, including the production of antibodies and other bodily defenses against beta-amyloid. However, the immune response to this type of vaccine sometimes caused significant brain swelling, so Dr. Rosenberg and his colleagues focused on developing a nontraditional DNA vaccine.

The DNA vaccine does not contain beta-amyloid itself but instead a piece of the beta-amyloid gene that codes for the protein. In the current study, the researchers coated tiny gold beads with the beta-amyloid DNA and injected them into the skin of the animals’ ears. Once in the body, the DNA stimulated an immune response, including antibodies to beta-amyloid.

The next step in the research is to test long-term safety in animals, Dr. Rosenberg said.

“After seven years developing this vaccine, we are hopeful it will not show any significant toxicity, and that we will be able to develop it for human use,” he said.

Spouses of dementia sufferers have a 6-fold increased risk of dementia onset | ScienceBlog.com

Spouses of dementia sufferers have a 6-fold increased risk of dementia onset ScienceBlog.com

Older married adults whose spouse has dementia are at significantly higher risk for developing dementia themselves, compared to similar older married adults whose spouse never develops dementia. This is the key finding of a study published today in the Journal of the American Geriatrics Society.

Informal dementia caregiving for a spouse is a natural marital obligation, and spousal caregivers often report positive feelings toward caregiving, yet it is difficult, requiring time, energy and usually physical exertion.

Dementia caregivers have been shown to provide more assistance, and to report more personal sacrifices and stress, than those who care for physically-impaired elderly without dementia.

While there are many published studies showing that dementia caregivers are at higher risk for health problems and depression, none have examined risk for dementia in the caregiver.

2,442 subjects (1,221 married couples) aged 65 and older from Northern Utah, USA, without dementia at onset were studied for up to 12 years to monitor for onset of dementia in husbands, wives or both. During this time, 125 cases of dementia only in the husband were diagnosed, 70 only in the wife, and 30 where both spouses were diagnosed (60 people).

The researchers, led by Dr. Maria Norton of Utah State University, USA, adjusted for socioeconomic status, a significant predictor of many health-related outcomes including dementia to control for shared environmental exposures that might influence risk for dementia in both spouses.

The results showed that incident dementia was significantly associated with older age, and having a spouse with dementia. Participants with a spouse who developed dementia were at a six times increased risk of developing dementia, net of the effect of age, gender, APOE genotype, and socioeconomic status, with higher risk in men (11.9) than women (3.7).

"Future studies are needed to determine how much of this association is due to caregiver stress compared to a shared environment," said Norton. "On the positive side, the majority of these individuals, with spouses who develop dementia, did not themselves develop dementia, therefore more research is needed to explore which factors distinguish those who are more vulnerable."

"Given the significant public health concern of Alzheimer's disease and other dementias, and the upcoming shift in population age composition, continued research into the causes of dementia is urgent," concluded Norton.

Link: http://www.wiley.com/wiley-blackwell

New Computerised Self test for Alzheimer's Disease

Rex Cannon, an adjunct research assistant professor of psychology at UT Knoxville, and Dr. John Dougherty, an associate professor in the UT Graduate School of Medicine, worked with a team of researchers to develop a Computerised Self Test (CST) for early detection of Alzheimer's disease.

The impetus for the test came from data showing that 60 percent of Alzheimer's cases are not diagnosed in the primary care setting, and that those delays lead to missed treatment opportunities.

"Early detection is at the forefront of the clinical effort in Alzheimer's research, and application of instruments like CST in the primary care setting is of extreme importance," said Cannon.

The CST is a brief, interactive online test that works to asses various impairments in functional cognitive domains -- in essence, it's a "fitness test" of sorts for the basic functions of thinking and processing information that are affected by Alzheimer's and milder forms of cognitive impairment.

Cannon and Dougherty's research, published in the April issue of the Journal of Alzheimer's Disease and in an early online edition of the journal, showed that the CST was substantially more effective and more accurate in detecting the presence of Alzheimer's and other forms of cognitive impairment in patients than other existing tests.

The new CST claims to have a 96 percent accuracy rate, compared to 71 percent and 69 percent for the tests currently in use.

Early signs of Alzheimer's are in the eye - New Scientist

Early signs of Alzheimer's are in the eye - New Scientist

Your eyes reveal a lot about you, and now that includes the health of your brain. A new way of counting dying eye cells could allow Alzheimer's disease to be diagnosed and treated in its early stages.

Many neurological diseases – including Alzheimer's, Parkinson's and Huntington's – involve the death of neurons in the brain, but these events are extremely hard to detect.

"It's difficult to diagnose these conditions before considerable damage has taken place, because the symptoms don't show up straight away," says Francesca Cordeiro at University College London.

However, this cell death also tends to extend to cells at the back of the eye, where it is much easier to detect abnormalities. So Cordeiro and her colleagues set about creating a way of detecting these eye neuron deaths.

Ginko Biloba does not help Alzheimer's Disease

The popular botanical ginkgo biloba does not improve memory nor does it prevent cognitive decline in older people, according to the largest and longest scientific study ever undertaken to look at the supplement.

An extract derived from the ginkgo tree, ginkgo biloba has been touted since the 1970s by the supplement industry and others as an aid to improving memory, cognitive impairment, dementia and Alzheimer's disease. Gingko extract has been used in traditional Chinese medicine for more than 500 years, according to the American Botanical Council.

The study finding is "disappointing news," says Steven DeKosky, dean of the University of Virginia School of Medicine and the study's senior author. The only positive thing the researchers found is that ginkgo appears to be safe, he says.

The results are from the Ginkgo Evaluation of Memory study, funded by the National Center for Complementary and Alternative Medicine, a center of the National Institutes of Health. The randomized, double-blind and placebo-controlled study was conducted at six medical centers and involved more than 3,000 people between ages 72 and 96 for seven years. The report is in today's Journal of the American Medical Association.

The first set of results from the study, published last year, found that a twice-daily dose of 120 milligrams of ginkgo biloba extract was not effective in reducing the incidence of Alzheimer's dementia or dementia overall.

This new paper looked at the same results to see if ginkgo biloba extract had any effect on cognitive decline in older adults, specifically memory, visual-spatial construction, language, attention, psychomotor speed and executive function. It found no effect.

"It just continues to show that in properly designed, placebo-controlled studies, we can't seem to find an effect for ginkgo biloba," says Lon Schneider, an Alzheimer's and gerontology expert at the University of Southern California. The size of this study is larger than all previous ginkgo biloba studies combined, he says.

Douglas MacKay, vice president for scientific and regulatory affairs at the Council for Responsible Nutrition, a supplement industry trade group, disputes the study's findings.

"There is a large body of previously published evidence, as well as ongoing trials, which suggest that ginkgo biloba is effective for helping to improve cognitive impairment in older adults," he says.

U.S. sales for ginkgo biloba were $99 million in 2008, down 8% from 2007 but still placing it among the most popular supplements in the country, according to the Nutrition Business Journal

The Warning Signs of Alzheimer's disease

10 warning signs of Alzheimer's

1.Memory loss that affects day-to-day function, especially things that have happened more recently.
2.Difficulty performing familiar tasks such as preparing a meal.
3.May forget simple words or substitute words, making sentences difficult to understand.
4.Disorientation of time and place such as forgetting how to get home.
5.Poor or decreased judgment such as not recognising a medical problem that needs attention or wearing heavy clothing on a hot day.
6.Problems with abstract thinking such as not recognising what the numbers in a chequebook mean.
7.Putting things in inappropriate places such as an iron in the freezer or a wristwatch in the sugar bowl.
8.Having varied mood swings — from calm, to tears, to anger — for no apparent reason.
9.Becoming uncharacteristically confused, suspicious or withdrawn. Changes may also include apathy, fearfulness or acting out of character.
10.May become very passive, and require cues and prompting to become involved.

Source: Alzheimer Society of Canada

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