Compounds in blackcurrants could prevent Alzheimer's disease

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New research led by Dilip Ghosh of the Horticulture and Food Research Institute in New Zealand, shows that compounds in blackcurrants have a potent protective effect in cultured neuronal cells against the types of stress caused by dopamine and amyloid-ß, a peptide associated with Alzheimer's disease.

'These compounds also work in hippocampal cells taken straight from the brain,' researcher James Joseph of Tufts University told Chemistry & Industry. James says that the effect will likely be reproduced in the human body and that blackcurrants could help prevent or significantly delay the onset of Alzheimer's.

Blackcurrants and boysenberries, more common in the US, both contain anthocyanins and polyphenolics. British blackcurrants are bred to be darker, which means they have more anthocyanins and are likely to be more potent. Compounds from these berries are already known to act as antioxidants, but a role in neuroprotection has not been demonstrated previously, according to the researchers.

The mechanism of action is unclear. But James said: 'We have evidence that the compounds protect against Alzheimer's by influencing the early gene expression in learning and memory, which influences cell signaling pathways that help neuronal cells communicate with each other.' Dilip's team recently demonstrated the potent protective effect of blackcurrant compounds on cultured human promyeloyte and neuroblastoma cells assaulted by hydrogen peroxide

For People With Dementia

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A groundbreaking home that uses the latest smart technology to give people with dementia and other serious long-term health conditions greater independence has been showcased for the first time in Bristol.

The technology, which has been developed by the Bath Institute of Medical Engineering (BIME) in the School for Health at the University of Bath, has been designed to help people readjust to living on their own after a stay in hospital, and aims to reduce the risk of users being readmitted to hospital or going into long term care. It uses special sensors that can wirelessly 'talk' to devices, such as the cooker, taps and light switches, in response to the behaviour of the resident. By monitoring movement within the home, the system is able to respond to many different situations without having to contact care staff, often just using simple voice prompts, which could be recorded by family members.

For example, if the occupant was detected opening the main door at inappropriate times they would be given a prompt to let them know the time and encourage them to go back to bed. Similarly, if the occupant got out of bed at night, the bedroom lights would be gently faded up. The system provides a very quick response and gives residents a greater feeling of control and independence as it doesn't rely on people coming in from outside to resolve problems, with outside help only called in for real emergencies.

The technology in the 'enabling smart home' at the Hillside Court 'very sheltered' housing scheme in St George, Bristol, has been developed over several years in consultation with people with dementia and their carers. It is a joint project between BIME, Bristol City Council's Adult Community Care service, Bristol PCT's Intermediate Care Service, Dementia Voice (dementia services development centre for the south west) and Housing 21 (a national provider of housing with care and support for older people).

"The really smart thing about the wireless technology we have used in this flat is that we can take the elements that clients find particularly useful in the smart home and install them in their own home," said Professor Roger Orpwood, Director of BIME. "The whole installation is quite unique because it is designed to empower the resident rather than relying on outside help to deal with problems. "The idea is that residents will stay in the smart home for a short period of around three months, before returning to their own home."

The flat has been set up as a two year pilot to assess how the technology helps give people more independence and control, reducing the risk of users being readmitted to hospital or going into long term care. Individual components of the system have been tested by people with dementia, but the complete installation has previously only been used at one other Housing 21 property in Lewisham, south London. David Self, Dementia Services Advisor at Dementia Voice, said: "The work we have already done in Lewisham has shown that by using technology we can improve independence and quality of life for people with dementia and reduce anxieties for relatives, without increasing the burden on care staff. "We hope this latest project will take things a step further with the opportunity to install the successful 'smart' elements of the flat in people's own homes."

Anesthetics In Alzheimer's

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Inhaled anesthetics commonly used in surgery are more likely to cause the aggregation of Alzheimer's disease-related plaques in the brain than intravenous anesthetics say University of Pittsburgh School of Medicine researchers in a journal article published in Biochemistry. This is the first report using state-of-the-art nuclear magnetic resonance (NMR) spectroscopic technique to explain the detailed molecular mechanism behind the aggregation of amyloid B (AB) peptide due to various anesthetics.
Previous studies by the Pittsburgh researchers found that the inhaled anesthetics halothane and isoflurane and the intravenous anesthetic propofol encouraged the growth and clumping of AB in a test tube experiment.

"Our prior research had shown in molecular models that anesthetics may play a role by causing amyloid peptides to clump together - something that is thought to signal the advancement of Alzheimer's disease. In this study, we set out to see why this was happening and to determine if any one form of anesthesia might be a safer option than another," said Dr. Mandal.

In this study the researchers used NMR spectroscopy to determine how the inhaled anesthetics halothane and isoflurane and the intravenous anesthetics propofol and thiopental interact with AB influencing the aggregation of AB in forms commonly found in the brains of people with Alzheimer's disease. The results were strikingly different between the inhaled and injected anesthetics. The inhaled halothane and isoflurane had the most potent interaction with AB peptides causing the highest levels of AB aggregation. The injected anesthetic propofol only interacted and caused aggregation at high concentrations - interaction was not evident at lower concentrations. The intravenous thiopental did not cause the clustering of AB peptides even at high concentrations. Additionally, the molecular details for the interaction of these anesthetics with AB peptide were revealed.

Alzheimer's patch is effective

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University of South Florida researchers have reported that a new treatment for Alzheimer's disease, in the form of a patch, has demonstrated its effectiveness in clearing brain-damaging plaques from a mouse model. The Alzheimer's vaccine works by triggering the immune system to recognize the beta amyloid protein that abnormally builds up in the brains of Alzheimer's patients as a foreign invader and attack it.

This study is the first to demonstrate that immunization using the skin may be an effective way to reduce the beta amyloid protein. It may offer a simpler way of preventing or treating the neurodegenerative disease with less likelihood of adverse immune reactions. Previous research on an injectable Alzheimer's vaccine was suspended indefinitely when the initial clinical trial caused brain inflammation and death in a small percentage of patients. Patients also experienced an autoimmune reaction, which occurred when immune cells aggressively attacked the body's own proteins produced by the vaccine.

The USF researchers targeted the skin as the route of vaccine delivery in mice bred to develop age-related brain degeneration mimicking Alzheimer's. They found that transdermal immunization did not appear to trigger specific toxicities associated with past immunization strategies. The scientists plan to further test whether the transdermal vaccine can curb memory loss in Alzheimer's mice. If the studies show clear cognitive benefits, clinical trials to evaluate a beta amyloid skin patch or topical cream in patients with Alzheimer's would be warranted.

New Class Of Drugs That Can Impact Alzheimer's Disease

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The Roskamp Institute announced today the discovery of a new class of drugs that lower the production of the main pathological protein that causes Alzheimer's disease. The discovery is detailed in an article co-authored by Drs. Daniel Paris and Michael Mullan and currently appears in Neuroscience Letters.

The Roskamp Institute, which is devoted to finding treatments for Alzheimer's disease, has been researching drugs that have the potential to stop the production of B-amyloid.

"When B-amyloid builds up in humans, patients develop Alzheimer's disease," said Dr. Michael Mullan, Director of the Roskamp Institute. "By stopping its production we can potentially stop the disease. We have found a whole family of drugs that can stop the production of B-amyloid, giving many companies working on NF-kB inhibitors the opportunity to test these types of drugs in Alzheimer's."

NF-kB (a protein that occurs in all cells in the body) activity results in inflammatory responses due to the switching on of genes that encode proteins that are key in inflammation. NF-kB inhibitors are being developed widely in the pharmaceutical industry primarily for its use in inflammatory conditions such as Arthritis and, until now, have not been thought of as a potential treatment for Alzheimer's.

At the same time, many drug companies are searching for compounds that can lower or stop the production of B-amyloid. The finding that NF-kB controls B- amyloid production means that NF-kB inhibitors might be developed as anti- Alzheimer drugs. One such example is Celastrol, which is researched in the Roskamp Institute's publication, and is available as a food supplement but has never been formally tested in Alzheimer's.

"Although we have known about the important inflammatory role of NF-kB for a long time, we did not know that it controls B-amyloid production," said Dr. Daniel Paris, Senior Scientist of the Roskamp Institute. "This may be one way that the inflammation caused by B-amyloid leads to more B-amyloid being produced -- a positive feedback loop with awful consequences for the sufferer."

The publication details the NF-kB findings and explains why this family of drugs should be tested for their use in treating Alzheimer's disease patients.

For more information on the Roskamp Institute and to view the journal article in Neuroscience Letters, please visit us online at http://www.RoskampInstitute.com.

Reduction in blood flow declines Alzheimer's

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The research, putting proteins often linked to heart disease front and center in a brain disease whose causes remain a mystery, hark back to what German physician Alois Alzheimer noted when he first recognized the disease 100 years ago. Though Alzheimer noted changes in both the brain's cells and in the small arteries and capillaries that supply and drain blood to and from the brain, over the decades doctors separated the two concepts and have come to focus mainly on the toxic effects of the disease on cells. The changes to blood vessels have been pushed to the background.

The latest findings from the University of Rochester Medical Center mesh not only with Dr. Azheimer's initial observations but also with new findings from today's best imaging technologies. While the first visible symptom of Alzheimer's may be a person forgetting names or faces, the very first physical change is actually a decline in the amount of blood that flows in the brain. Doctors have found that not only is blood flow within the brain reduced, but that the body's capacity to allocate blood to different areas of the brain on demand is blunted in people with the disease. "A reduction in blood flow precedes the decline in cognitive function in Alzheimer's patients," said Berislav Zlokovic, M.D., Ph.D., professor in the Department of Neurological Surgery and a neurovascular expert whose research is causing scientists to consider the role of reduced blood flow in Alzheimer's disease.

"People used to say, well, the brain is atrophying because of the disease, so not as much blood as usual is needed. But perhaps it's the opposite, that the brain is dying because of the reduced blood flow," he adde

The two dominant proteins that determine how much blood flows through the body's arteries have been implicated in Alzheimer's disease, in a new study in the Jan. 16 issue of the Proceedings of the National Academy of Sciences. They offer new, surprising targets against Alzheimer's disease just as scientists are getting back in touch with the vascular roots of the disease that were first recognized early last century. Now the group is looking for ways to stop the two proteins from working together to constrict the blood vessels, so that blood flow in the brains of people with Alzheimer's disease would return to normal, much as the team achieved in mice. "More and more, people are paying attention to the role of the vascular system in Alzheimer's disease," said Zlokovic, director of the Frank P. Smith Laboratories for Neurosurgical Research, who has made several findings that implicate blood flow and the blood-brain barrier transport mechanism as key components of the Alzheimer's disease process.

Dementia Significantly Reduced By Regular Acupressure

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Acupressure can significantly reduce agitated behaviour in older patients with dementia, according to a study published in the February issue of the UK-based Journal of Clinical Nursing.

Researchers at the National Yang-Ming University in Taiwan found that providing 15-minute treatment sessions twice a day for five days a week yielded considerable benefits, including reductions in verbal and physical attacks and wandering.

But once the four-week treatment period ended, agitation levels started to rise again, suggesting that acupressure needs to be provided on an ongoing basis.

20 patients were studied over six weeks, including one week before the treatment started and one week after it finished. All lived in dementia special care units at a long-term care facility.

70 per cent of the patients suffered from severe behavioural disturbances, with a further five per cent suffering from extremely severe impairment. The remaining 25 per cent were classed as medium.

An average pre-treatment score of just over 79 was recorded on a specialist scale developed to measure agitation levels. After four weeks' treatment this had fallen to just under 60.

Pre-treatment agitation was highest in the 65-59 and 80 plus age groups (82 and 97 respectively) and in males (83).

"Agitated behaviour in people with dementia is a major concern for caregivers" says co-author Professor Li-Chan Lin from the Institute of Clinical Nursing at National Yang-Ming University, Taiwan. "It can endanger patients and others, make it necessary for them to be moved from familiar surroundings and demoralise and psychologically distress caregivers.

"People are living longer and, as a result, we face increased numbers of people with dementia. It is very important that we find interventions that enable us to provide more effective care for them, both in their own home and in long-term care facilities."

During the study, carried out with colleagues from the University, different types of agitation were measured on a specialist scale.

In week one, before the acupressure treatment began, physical attacks were given an average score of 5.53. These included pushing, beating, scratching and pinching.

Agitation levels were measured daily and by week two, when the treatment began, the physical attack score had fallen to 1.46. By week five, the last week of treatment, the score had fallen to 0.53. In week six, when the treatment had stopped, the figure rose to 2.17.

Verbal attacks, which included repeated questioning and shouting, showed a pre-treatment score of 2.81 in week one, 0.54 in week two and 0.29 in week five. By week six it had risen to 1.36.

Similar patterns were recorded for non-physical and non-verbal agitation, which included wandering, stealing, undressing and tearing things.

Wandering aimlessly was measured using pedometers. This reduced from an average of 5,368 steps a day in week one to 2,611 in week five. By week six it had risen again to 3,374.

Patients received acupressure based on five key pressure points - Fengchi (GB 20), Baihui (Du 20), Shenmen (He 7), Niguan (Pe 6) and Sanyinjiao (Sp 6) - after a short warm-up session which consisted of holding, rubbing and pressing the palms and finger joints on both hands.

Each acupressure point was pressed for two minutes using three to five kilograms of pressure.

"Our study showed that providing patients with acupressure twice-daily for five days a week significantly reduced agitated behaviour and wandering" says Professor Lin.

"This has important implications for the future care of dementia patients as it provides an effective option that, following training, can be carried out at home or in long-term care facilities."

Mental stimulation warding off Alzheimer's

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There is no known cure for Alzheimer's, which gradually destroys a person's memory and ability to learn, reason, make judgments, communicate and carry out daily activities.
Researchers at the University of California-Irvine studied hundreds of mice altered to make them develop abnormalities known as plaques and tangles in brain tissue that are considered hallmarks of Alzheimer's disease in people.

Writing in the Journal of Neuroscience, they said periodic learning sessions - swimming in a tub of water until finding a submerged platform to stand on - slowed the development in the mice of those two abnormalities.
The findings are in line with other research, which shows that exercising the mind is important in staving off the degenerative brain disorder, which is the most common form of dementia among the elderly.

Green said the mice in the study were given "a very mild learning experience" - essentially figuring out a maze but in the water - for a week at a time every three months. The sessions were performed four times daily for a week at a time when the mice were aged two, six, nine, 12, 15 and 18 months. The mice performing the task experienced slower development of the protein beta amyloid, which clumps in the brain forming plaque buildup that accumulates outside nerve cells, the study found. These mice also experienced a slower build-up of another protein in the brain, hyperphosphorylated-tau, that can lead to the formation of neurofibrillary tangles - twisted fibres in brain cells.

The Anti-Alzheimer's Diet

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New research suggests that oxidative stress which results from an accumulation of free radicals is involved in the neurodegeneration observed in dementias such as Alzheimer's and Parkinson's diseases, whilst the administration of anti-oxidants has the opposite effect and so might help in the control of these types of diseases. The research done by Doras Dias-Santagata, a Portuguese scientist, and colleagues, just published in the "Journal of Clinical Investigation" is exciting news for neurodegenerative patients all over the world.

Fruit becomes brown and butter becomes rancid - these are some of the everyday effects of oxidative stress. Free radicals are highly reactive molecules that result from the body energy producing mechanisms, and which are capable of oxidising and damaging DNA, proteins and cells in general. Oxidative stress (OS) by free radicals is fast becoming "the"[the] medical buzzword, with a growing number of diseases, from cancer to cataracts or just ageing, associated with it. Under normal circumstances the body is capable of neutralising free radicals by producing anti-oxidants but in modern societies things are not that balanced anymore. In fact, environmental factors and changes in our lifestyles, which have lead to exposure to higher levels of pollution and poor quality diets, mean that we are exposed to free radicals more than ever before. Brain cells are known to be specially sensitive to degeneration by these molecules and, worryingly, signs of OS have already been found in the brains of patients with several neurodegenerative dementias such as Parkinson's, Alzheimer' and Huntington's disease. However, whether OS is a cause or a result of disease is not clear.

To answer this question Dora Dias-Santagata, Mel B. Feany and colleagues at Brigham and Women's Hospital and Harvard Medical School in Boston and Howard University in Washington decided to analyse the effect of different levels of oxidative stress in an Alzheimer's model of fruit flies. In fact, most neurodegenerative dementias are characterised by having around the destroyed brain areas abnormal deposits of proteins which are believed to participate in the neurodegeneration. Dias-Santagata's flies have been mutated to have aberrant deposits of one such protein, tau (found in Alzheimer's brains) and show large destructed areas in their nervous system.

The team of researchers used two different approaches while testing OS effects in the fruit flies: on one hand they manipulated genes responsible for the production of anti-oxidant proteins and on the other hand administered vitamin E, a powerful anti-oxidant, to the mutant flies.

Dias-Santagata and colleagues found that reduction in the activity of two anti-oxidant proteins - SOD and Trxr by genetic manipulation led to increasing neurodegeneration in the brain of the mutant flies, while administration of vitamin E had the opposite effect. Control flies without tau, and consequently no signs of neurodegeneration, were not affected by either the genetic or the pharmacological manipulation. Both results strongly suggest that oxidative stress plays an important role in neurodegenerative dementias, at least in those where tau is involved, and if controlled can help controlling the disease. But they also indicate that, at least in this model, OS is not a primary cause for the illness.

Another interesting result of the study was to find that brain destruction in the mutated fruit flies was associated with activation of a stress-induced group of proteins called JNK. This needs to be further investigated but it might help to understand how and why neural cells die in these diseases.

In a world where more than 24 million people suffer from neurodegenerative dementias and where Alzheimer's disease, which for now is incurable, affects more than 5% of men and women above 60 years old Dias-Santagata and colleagues' results are very exciting. As lead author Dora Dias-Santagata says `This is exciting because antioxidants may prove to be a good therapeutic approach to treat Alzheimer's disease and ameliorate human neurodegeneration.´

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How brain protein becomes toxic in Alzheimer's

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The link between Alzheimer's disease and abnormalities in the way amyloid protein is processed in the brain has been confirmed at last. Usually harmless, the amyloid protein triggers neurological damage when it is broken down and transformed into toxic fragments of beta-amyloid. Previous studies have shown that people with Alzheimer's have reduced levels of several proteins involved in processing amyloid.

To find out whether low levels of any of these proteins could cause the production of toxic beta-amyloid, Peter St George-Hyslop at the University of Toronto in Canada and colleagues studied the DNA of 6861 people, 46 per cent of whom had Alzheimer's. Those with the disease proved significantly more likely to have variants of the gene SORL1, which usually produces a protein that binds amyloid and transports it to an area of the cell where it can be harmlessly recycled.

To demonstrate that mutations in SORL1 could trigger the disease, the researchers treated cells in the lab to deactivate the gene. This led to a substantial increase in the production of toxic beta-amyloid. "Where SORL1 is absent or defective, it allows the amyloid to float off into other areas where it is degraded," says St George-Hyslop. The team have identified two regions of SORL1 they believe harbour the disease-causing mutations, but have not yet found the mutations themselves.

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Nutrition to halt Alzheimer's

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Currently, about 12 million people in the US plus the EU suffer from Alzheimer's, with some estimates predicting this figure will have tripled by 2050. The direct and indirect cost of Alzheimer care is over $100 bn (€ 81 bn) in the US alone. The direct cost of Alzheimer care in the UK was estimated at £15 bn (€ 22 bn).

Such is the interest in dietary approaches to improve brain health the world's largest food company, Nestlé, recently signaled its intention to get a head start on the competition with the signing of an agreement in November 2006 with the Swiss Federal Institute of Technology (EPFL) to investigate the role of nutrition in cognitive function.

The agreement with the EPFL, Nestlé's largest collaboration with a university of research institute, will see the company contributing up to CHF 5 million (€ 3.1 million) every year for five years, with a review after four years to potentially extend the project further.

The fundamental research, by scientists from Brigham and Women's Hospital and Harvard Medical School in Boston and Howard University in Washington, used genetic and pharmacological approaches to change the genetic expression of transgenic fruit flies so that they would express a disease-related mutant form of human tau protein.

Two different approaches was used by the researchers - on one hand they manipulated genes responsible for the production of anti-oxidant proteins and on the other hand administered the potent anti-oxidant vitamin E to the mutant flies.

The US-based researchers report that reduction in the activity of two anti-oxidant proteins - superoxide dismutase (SOD) and thioredoxin reductases (Trxr) – as a result of their genetic manipulation led to increasing neurodegeneration in the brain of the mutant flies, while administration of vitamin E reversed the effect.

Control flies that did not express the human tau protein did not show any signs of neurodegeneration, they said.

Both results are said to indicate that oxidative stress plays an important role in neurodegenerative dementias, at least in those where the tau protein is involved, and could therefore offer a nutritional/ dietary approach to improving brain health.

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Folic Acid Increases Mental Agility

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The scientists found that the group who took the folic acid improved on all aspects of cognitive functioning compared to the group that took the placebo.

Folic acid is a water soluble B vitamin and is found in yeast extract, green leafy vegetables, for example spinach, in dried beans and peas, some organ meats such as liver, fortified cereals, certain fruit and vegetables, and certain seeds, for example sunflower seeds. It plays an important role in the production of new cells, especially in the spinal cord an embryo, which is why it is important that pregnant women have their reference daily intake (RDI).

Adults and children need folic acid to generate red blood cells and DNA, and insufficient daily intake can result in anemia. The vitamin also helps to digest protein and make effective use of the resulting amino acids, and also to produce proteins that the body may be lacking. It also plays a role in regulating appetite.

Because of the discovery of the link between neural tube defects (NTD, such as that occurring in infants born with spina bifida), and insufficient folic acid governments have gradually introduced regulations that require certain foods to be fortified with folic acid, such as cereals, and in some countries bread and flour also.

Different countries recommend different RDI amounts, ranging from 400 micrograms a day in the US to 200 in Japan.

Some research studies have linked folic acid supplement taking with reductions in various age-related impairments such as hearing loss and Alzheimer's. Others are not so clear, but there seems to be consensus that it helps improve cognitive function in elderly people with high concentrations of the amino acid homocysteine in their blood, which could indicate increased riks of stroke, heart disease and Alzheimer's.

Concerns have been raised that folic acid interacts with Vitamin B12 and taking too much of it can cause problems, such as masking a deficiency in B12. This is particularly relevant to older people (over 50), who should ask their doctor to check their vitamin B12 levels if they considering taking folic acid supplements.

Eat five servings of fresh fruits and vegetables a day, and augment your diet with a high-quality supplement like TriVita’s Sublingual B-12, B-6 & Folic Acid. Providing over 100% of the recommended daily intake for B-12, B-6 and folic acid—and delivering these nutrients directly into your bloodstream—TriVita’s Sublingual B-12, B-6 & Folic Acid can help protect you and your loved ones from Alzheimer’s disease and vascular dementia.

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Good health - good brain function

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What causes the brain to degenerate as we age? Scientists cite three primary factors: genetic inheritance; nutrition; environmental toxins such as aluminum, lead, and pesticides that target the nervous system. These factors manifest themselves in the digestive system as well as the brain. Increased susceptibility to genetic factors and decreased ability to properly absorb nutrients tend to be part of the aging process. If a person shows early signs of Alzheimer's at a relatively young age, it would be a good idea to do a hair analysis to see if there are high levels of toxins in the body tissues.

Diet and Nutrition
There are nutritional elements and foods that are vital to good health, and foods that should be avoided. It seems unfair, but the older we get the more we have to watch what we eat because of insulin resistance, increased sensitivities to certain foods, and the diminished ability of the intestinal lining to absorb nutrients and process food through the alimentary canal.
More and more, nutritionists are sounding the alarm about the changes in the average American diet over the last 50 or 60 years, and the effect this has had on national disease statistics. The modern diet of highly processed and refined foods is low in fiber, and high in calories, carbohydrates, and fat. It is called "junk" food because it fills you up, but doesn't nourish you. Many of the dietary essentials that help control mental degeneration are lost in food processing, and many potentially harmful substances like pesticides, antibiotics, and hormones are added to food. Again, it seems unfair, but we have to make special efforts to find healthful, nutritious foods, insist on organically-grown foods, etc.

The foods that should be avoided. These include refined sugar, dairy products, wheat, deep fried, and high fat foods. Refined sugar (candy, cookies, desserts) are hardest for many people to give up because of the "sweet tooth" that is little short of an addiction. Many people notice that when they eat sweets, their mental processes start to seem a bit fuzzy or cloudy. Sugar can turn off your brain power.

What foods should we eat? A lot of foods are great for our memories and reduce the risk of Alzheimer's, such as whole grains, soy products, legumes, fish, brewer's yeast, millet, rice, wheat germ, nuts (especially walnuts), black sesame seeds, pumpkin seeds, and sprouts. These foods are rich in vitamin B, beneficial proteins and many other nutrients. Also, make sure that you eat fruits and lightly-cooked vegetables every day.
Two nutritional building blocks that are key to optimum brain function are amino acids and the B-complex of vitamins, such as choline and B6. Amino acids are essential for building protein. Certain of the B vitamins can increase blood circulation in the brain, improve memory, and lower cholesterol, thus reducing the risk of hardening of the arteries and strokes.
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Maintaining brain cells and synapses in good condition is critical

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Maintaining brain cells and synapses in good condition is critical, since mental performance is totally reliant on the health of the brain's complex network of trillions of synapses. Deterioration or loss of synapses can result in changes in mood and cognition, and in alterations of brain functioning such as those associated with neurological disorders or aging.

Stress is a major cause of synapse dysfunction. Research shows that prolonged exposure to stress can interfere with the function of neurotransmitters. Excessive amounts of the excitatory neurotransmitter glutamate may accumulate in the synapse. In high concentrations, glutamate becomes a toxin that can interfere with learning and cause cell damage in the brain's memory regions. Research presented at the 2006 American Psychological Association convention suggests that repeated stress remodels the brain and causes neurons in the hippocampus and prefrontal cortex to shrink. Stress can also lead to depression, which is associated with memory difficulties.

A number of studies suggest that lack of stimulation is associated with a reduced number of synaptic connections in the brain, a factor that may increase vulnerability to Alzheimer's disease (AD). For example, scientists who used an electron microscope to compare post-mortem brain tissue from the prefrontal cortex of 16 subjects found that those whose professions required greater amounts of skill or education had 17 percent more synapses for each neuron than those with less education. Another study suggests that seniors who enjoy a variety of intellectually challenging activities (such as playing a musical instrument, solving puzzles or reading) have a lower risk of developing dementia. It is thought that the larger number of neuronal interconnections associated with regular intellectual activity may provide extra insurance against cognitive decline.

The synapses are vulnerable to neurotoxins, as well. Excessive alcohol consumption, exposure to certain pesticides and heavy metals, and to drugs such as phencyclidine (PCP) and ketamine can cause memory problems and synaptic loss. The toxin from the bacteria that causes poisonous botulism acts directly on the synapses by blocking transmission of neurotransmitters, as does the deadly toxin curare.

Following these tips may help you keep your mind active and alert by protecting and strengthening your synapses:

1. Reduce stress: Make time for leisure activities. Learn relaxation techniques such as meditation. Cut down on unnecessary responsibilities and avoid over-scheduling.

2. Stimulate your brain: Avoid routine. Enjoy new sensory experiences. Challenge your mind and body with new situations.

3. Exercise: A brisk walk or other cardiovascular workout oxygenates the brain and promotes brain growth factors.

4. Challenge your mind: Tackle puzzles, games and demanding intellectual tasks. Make an effort to learn new information through classes or reading

5. Stay healthy: Eat a nutritious diet, get adequate sleep, avoid smoking, and if you use alcohol, drink in moderation.

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CBF dysregulation associated with Alzheimer's

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Cerebral angiopathy contributes to cognitive decline and dementia in Alzheimer's disease (AD) through cerebral blood flow (CBF) reductions and dysregulation. We report vascular smooth muscle cells (VSMC) in small pial and intracerebral arteries, which are critical for CBF regulation, express in AD high levels of serum response factor (SRF) and myocardin (MYOCD), two interacting transcription factors that orchestrate a VSMC-differentiated phenotype. Consistent with this finding, AD VSMC overexpressed several SRF-MYOCD-regulated contractile proteins and exhibited a hypercontractile phenotype. MYOCD overexpression in control human cerebral VSMC induced an AD-like hypercontractile phenotype and diminished both endothelial-dependent and -independent relaxation in the mouse aorta ex vivo. In contrast, silencing SRF normalized contractile protein content and reversed a hypercontractile phenotype in AD VSMC. MYOCD in vivo gene transfer to mouse pial arteries increased contractile protein content and diminished CBF responses produced by brain activation in wild-type mice and in two AD models, the Dutch/Iowa/Swedish triple mutant human amyloid -peptide (A)-precursor protein (APP)- expressing mice and APPsw+/– mice. Silencing Srf had the opposite effect. Expression of SRF did not change in VSMC subjected to Alzheimer's neurotoxin, A. Thus, SRF-MYOCD overexpression in small cerebral arteries appears to initiate independently of A a pathogenic pathway mediating arterial hypercontractility and CBF dysregulation, which are associated with Alzheimer's dementia.

Isoflurane can lead to the death of brain cells

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The commonly used anesthetic isoflurane can lead to the death of brain cells and the production of amyloid-beta plaque, a hallmark of Alzheimer's disease, Harvard researchers report. Their study appears in the January issue of the Journal of Gerontology, which is devoted to the problems of dementia and delirium.

The Harvard study raises questions about the safety of isoflurane, which has been used for years for all ages of patients. "Many people, especially the elderly, who have anesthesia suffer from postoperative cognitive dysfunction, scrambling and delirium that can last six hours or two weeks or months," said lead researcher Rudolph Tanzi, a professor of neurology at the Genetics and Aging Research Unit of the Massachusetts General Institute for Neurodegenerative Disease. "To me, a big dose of isoflurane mimics a stroke or a bang to the head, and you don't want that as a risk factor for Alzheimer's disease at any age," Tanzi said.

In experiments with cells that had an amyloid-beta protein, Tanzi's team exposed them to isoflurane for six hours. The researchers found that isoflurane caused these cells to die. "It also caused the cell to overproduce the toxic molecule responsible for the pathology of Alzheimer's disease, particularly amyloid-beta," Tanzi said.

This is a warning, Tanzi said. "Isoflurane may be one reason why the elderly are more prone to cognitive dysfunction following anesthesia," he said. "Any trauma to the brain induces cell death. Isoflurane now joins that list of insults to the brain that can cause cell death and excessive production of this key molecule in Alzheimer's pathology," Tanzi. "This does increase the risk for Alzheimer's disease."

Alzheimer's drug rivastigmine

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Although only one type of medication is now available for use as an Alzheimer's disease therapeutic in Japan, a number of others are now in clinical trials, promising doctors a choice of treatments for symptoms.

Eli Lilly Japan KK and Wyeth KK, both arms of U.S. pharmaceutical firms, are each conducting phase I clinical trials on antibody drugs against beta-amyloid, the protein in the plaques associated Alzheimer's disease. Their efforts are the first Japanese trials of beta-amyloid antagonists.

GlaxoSmithKline KK, an arm of the U.K.'s GlaxoSmithKline Plc, has begun phase II trials on the use of Avandia -- a diabetes drug whose generic name is rosiglitazone maleate -- to treat patients with a certain Alzheimer's-related mutation. The rosiglitazone helps improve glucose metabolism in the brain and prevent inflammation of brain tissue.

Ono Pharmaceutical Co. (TSE:4528) and Novartis Pharma KK, an arm of Swiss giant Novartis AG, will soon enter into phase III trials on use of the Alzheimer's drug rivastigmine in the form of a transdermal patch. Rivastigmine is already available in more than 70 countries, but not in Japan and only in capsule and liquid forms.

SORL1 in Alzheimer's

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A huge international study has identified a gene that apparently can raise the risk of developing the most common form of Alzheimer's disease, a discovery that may help scientists develop new treatments.
Scientists analyzed DNA from more than 6,000 people from a variety of ethnic groups and found evidence implicating certain versions of the gene, called SORL1.
It's too soon to tell how much those gene versions raise the risk of getting Alzheimer's, or what percentage of cases they account for, the researchers said. They said the effect on risk appears to be modest.
The study, released Sunday on the Web site of the journal Nature Genetics, focused on Alzheimer's that appears after age 65, the most common type.
Only one gene, called APOE, has been firmly linked to raising susceptibility to the common form. A Harvard-based group lists about 20 other genes it considers promising candidates, based on research. Some authors of the new paper said they believe the evidence for SORL1 is unusually strong.
Experts familiar with the new work said SORL1 probably is involved in Alzheimer's, but cautioned that it will be important for other scientists to confirm that. "People will jump on it pretty fast," said Rudy Tanzi of Harvard Medical School.
Gerard Schellenberg of the University of Washington said the paper's evidence is "pretty solid, so I'm optimistic that it will be replicated."
Dr. Sam Gandy, a researcher who chairs the medical and scientific advisory council of the Alzheimer's Association, which helped finance the new study, said that he doubted SORL1 or any other gene plays as big a role in causing the disease as APOE does.
The new work was reported by Dr. Peter St. George-Hyslop of the University of Toronto, Lindsay Farrer of Boston University, Dr. Richard Mayeux of the Columbia University in New York, and others in the U.S., Germany, Israel and Japan.
The new paper implicates SORL1 in Alzheimer's in two ways. First, it shows that inheriting certain variants was associated with developing the disease in seven out of nine samples of people examined. The association appeared in African-American, Caribbean Hispanic, northern European and Israeli Arab groups.
In laboratory studies, researchers also found that when they suppressed the activity of SORL1, cells made greater amounts of amyloid beta, a substance thought to play a key role in causing Alzheimer's. Researchers believe the disease-promoting variants of SORL1 act by suppressing the gene's activity.

Bilingualism Has Protective Effect In Delaying Onset Of Dementia

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Canadian scientists have found astonishing evidence that the lifelong use of two languages can help delay the onset of dementia symptoms by four years compared to people who are monolingual. Now scientists with the Rotman Research Institute at the Baycrest Research Centre for Aging and the Brain have found the first evidence that another lifestyle factor, bilingualism, may help delay dementia symptoms. The study is published in the February 2007 issue of Neuropsychologia (Vol.45, No.2).

In this present study, researchers set out to answer that question by examining the diagnostic records of 184 patients who came to Baycrest's Sam and Ida Ross Memory Clinic between 2002 and 2005 with cognitive complaints. Of that group, 91 were monolingual and 93 were bilingual. The bilinguals included speakers of 25 different languages, the most prevalent being Polish, Yiddish, German, Romanian and Hungarian.

Researchers found that 132 patients met criteria for probable Alzheimer's; the remaining 52 were diagnosed with other dementias. Patient data included Mini-Mental State Examination (MMSE) scores (a measure of general cognitive functioning), years of education and occupation. The MMSE scores were equivalent for the monolingual and bilingual groups at their initial visit to the clinic, indicating comparable levels of impairment. The age of onset of cognitive impairment was determined by the interviewing neurologist at the first clinic visit who asked patients and their families or caregivers when symptoms were first noticed.

The researchers determined that the mean age of onset of dementia symptoms in the monolingual group was 71.4 years, while the bilingual group was 75.5 years. This difference remained even after considering the possible effect of cultural differences, immigration, formal education, employment and even gender as influencers in the results. "There are no pharmacological interventions that are this dramatic," says Dr. Freedman, who is Head of the Division of Neurology, and Director of the Memory Clinic at Baycrest, referring to the four-year delay in onset of symptoms for bilingual patients. "The data show a huge protective effect," adds co-investigator Dr. Craik, who cautioned that this is still a preliminary finding but nonetheless in line with a number of other recent findings about lifestyle effects on dementia.

The team is working on a follow-up study that will further examine bilingualism and dementia onset. They plan to conduct interviews and cognitive assessments on bilingual and monolingual patients in Baycrest's Memory Clinic and follow them for a few years.

Immunotherapy for Alzheimer's disease

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Alzheimer's disease, the most common form of dementia, is characterized by progressive loss of memory and cognition, ultimately leading to complete debilitation and death. A hallmark feature of Alzheimer's pathology is the presence of insoluble protein deposits known as beta-amyloid on the surface of nerve cells, which results from the accumulation of soluble beta-amyloid in the brain. The effects of the disease are devastating to the patients as well as the caregivers, with significant associated health care costs. It is estimated that there are over 12 million people suffering from Alzheimer's disease in the major markets worldwide with the number increasing as the global population ages. Currently marketed drugs transiently affect some of the symptoms of the disease, but there are no drugs on the market today that slow or arrest the progression of the disease. These symptomatic drugs are projected to generate approximately $4 billion in sales by 2008, indicating both the size of the market and the demand for effective treatment beyond symptomatic improvements.

Immunotherapy for Alzheimer's disease involves making an antibody molecule available to bind to the endogenous beta-amyloid toxin, thus promoting its clearance away from the brain. This therapeutic outcome can be achieved either by provoking the patient's immune system to generate such an antibody ("active immunization") or by administering an externally generated antibody ("passive immunization"). Both approaches have the potential to slow or arrest disease progression provided that key safety issues are addressed. Intellect has incorporated proprietary safety features into its technology platforms for both active and passive immunization, which provides the Company with a strong competitive advantage in this field.

Beta amyloid could attack red blood cell

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Work in the late 1990s showed fragments of beta amyloid could actually attack red blood cell membranes and cause them to destruct, says Dr. Hill, neuroscientist at the Medical College of Georgia and Veterans Affairs Medical Center in Augusta. "And, there is some evidence that red blood cells of Alzheimer's patients have been damaged so we think red blood cells are more fragile in some Alzheimer's patients allowing them to be more likely to break open.

Although the XmnI polymorphism's (which can significantly increase fetal hemoglobin expression in adults) protection mechanism is not clear, the researchers found in certain circumstances, adult hemoglobin bound better to beta amyloid, so if there are higher levels of fetal hemoglobin, there may not be as much interaction and subsequent injury, Dr. Hill says.

To determine the impact of the genetic mutation on Alzheimer's risk, studies need to be done on more Alzheimer's patients and their families, including taking blood levels of fetal hemoglobin, says Dr. Rodney T. Perry, UAB molecular geneticist and a study corresponding author. "More studies are needed to confirm the physiologic basis of the interaction," says Dr. Perry who already is working with Dr. Hill to submit a grant to pursue more answers. If they document higher fetal hemoglobin levels in healthy family members with the XmnI polymorphism, the hypothesis that it is providing some sort of protective measure is more likely, says Dr. Perry. Also the amount of disease protection has yet to be determined, he notes. "It may be a small protection."

Either way, the role needs pursuing, Dr. Perry says. "It helps in trying to fill in the pieces of the puzzle of what is going on in the pathogenesis and different etiologies of the disease, how it may come about." If they are right, the findings could open the doors to treatment approaches that increase fetal hemoglobin levels, Dr. Hill says. One such drug, hydroxyurea, already is used to treat sickle cells patients because fetal hemoglobin will not sickle.

The link between Alzheimer's and folic acid

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This connection led to the 1998 introduction of public health measures in the US and Canada, where all grain products are fortified with folic acid – the synthetic, bioavailable form of folate.

After an average of 6.1 years of follow-up, 192 cases of Alzheimer's disease had been diagnosed. After adjusting for potential confounding factors, like age, sex, ethnicity, cardiovascular history and B6 and B12 intake, Luchsinger and co-workers report that increasing folate intake, from both dietary and supplemental sources, was associated with a significantly reduced risk of Alzheimer's disease (50 per cent risk reduction).

Interestingly, neither dietary folate nor supplements alone were significantly linked to Alzheimer's disease risk; only the two in combination appeared to produce an effect. Vitamin B12 and B6 levels were not associated with Alzheimer's disease risk, said the researchers.

“We found that higher folate intake was independently related to lower AD risk in a predominantly Hispanic and African American cohort of elderly persons with a high prevalence of vascular risk factors,” wrote the researchers. Higher folate intake was modestly correlated with lower homocysteine levels, "indirectly suggesting that a lower homocysteine level is a potential mechanism for the association between higher folate intake and a lower Alzheimer's disease risk," said the authors.

The link between Alzheimer's and homocysteine involves the accumulation of amyloid proteins in the brains. In vitro studies have reported that folate deficiencies and high homocysteine levels may enhance the effects of amyloid-beta, which in turn would indicate an increase in Alzheimer risk factors.

The researchers stress that no definitive conclusion about the role of folate in the development of Alzheimer's disease can be made, since the findings are at odds with previously published studies.

"Thus, the decision to increase folate intake to prevent Alzheimer's disease should await clinical trials," they concluded. Clive Ballard, director of research for British charity the Alzheimer's Society agreed that a controlled trial is necessary to “determine the full value of this research.” "It is worth noting that follow-up studies within communities are notoriously difficult to interpret because there are other external factors that can influence the results,” siad Ballard in a statement. “These latest findings add weight to growing evidence about the important role that dietary factors can play in preventing Alzheimer's disease,” he said.

The B-Vitamin Treatment Trialists' Collaboration should soon be better able to address the link between B-vitamins, homocysteine levels, and cognitive function. The effects of three to seven years of treatment with B vitamins on cognitive function should eventually be available on about 20,000 of the 50,000 participants with previous cardiovascular or renal disease from 12 large homocysteine-lowering trials.

Poor Heart Health Linked To Mental Impairment

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Mental impairment and decline in cardiac health are two common complaints of advancing age. A new study, published in Journal of the American Geriatrics Society, suggests that there may be a link between the conditions; specifically, a decline in heart health may lead to cognitive impairment in elderly women.

According to study author Dae Hyun Kim, a healthy heart naturally varies its rate and rhythm throughout the day in response to physical and mental demands. "Advancing age and disease can lower the heart's ability to change its rate and rhythm, which can be associated with changes in mental function," says Kim. How this occurs is not clearly known.

Kim says that further research into the connection between cardiac and mental health is important. “Mental impairment in the elderly is a major public health issue, and has significant effects on caregivers, the healthcare system and society.” Identifying contributing risk factors, such as heart health, could help seniors to avoid this debilitating condition.

The primary goal of the Journal of the American Geriatrics Society is to publish articles that are relevant in the broadest terms to the clinical care of older persons. Such articles may span a variety of disciplines and fields and may be of immediate, intermediate, or long-term potential benefit to clinical practice. For more information, please visit blackwellpublishing.com/jgs.

Alzheimer's disease and herpes virus

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A gene known to be a major risk factor for Alzheimer's disease puts out the welcome mat for the virus that causes cold sores, allowing the virus to be more active in the brain compared to other forms of the gene. The new findings, published online in the journal Neurobiology of Aging, add some scientific heft to the idea, long suspected by some scientists, that herpes somehow plays a role in bringing about Alzheimer's disease.

The work links a form of the ApoE gene known as ApoE-4, which after advanced age is the leading known risk factor for getting Alzheimer's disease, with the form of herpes - herpes simplex 1 or HSV - that infects more than 80 percent of Americans and causes cold sores around the mouth. The findings from a group at the University of Rochester Medical Center show that the particular form of the gene that puts people at risk also creates a fertile environment for herpes in the brain, allowing the virus to be more active than other forms of the ApoE gene permit.

Scientists have known for more than 15 years that the ApoE-4 gene is a player in Alzheimer's disease, but the idea that it works in concert with the herpes virus is new.

The team is exploring different ways that herpes might affect the development of Alzheimer's disease. In one study the team looking at the role of Nectin-1, a cell adhesion molecule that herpes uses as one route to infect a cell. Nectin-1 plays a crucial role in forming synapses, the structures between brain cells that move information and signals from one cell to the next. The team is studying whether herpes somehow disturbs the receptor, possibly altering the structure and function of the synapse. Damage to synapses is one of the earliest signs of Alzheimer's disease.

Another possibility is that the body's immune response against herpes somehow damages the brain, and that such damage is worse in people with the ApoE-4 copy of the gene. Earlier this year Federoff's team published a study that showed inflammation is the earliest change that could be detected in a brain affected by Alzheimer's disease, before any of the hallmark plaques or tangles and certainly long before any behavioral changes are seen. Such inflammation often is a byproduct when the immune system fights an infection.

Non-Drug Treatments For Dementia
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Memory training and other non-drug treatments may one day help older adults ward off declines in mental function, according to researchers from Wake Forest University School of Medicine.

The authors say that matching cognitive training with an individual's risk factor profile is an intriguing possibility. For example, training that focuses on memory may be best for those at risk for Alzheimer's disease.

"These studies illustrate the promise of non-drug treatments," said Shumaker. "The medications available today produce only low to moderate improvements in mental function. And they can have adverse side effects. Showing that cognitive training can protect mental function means that individuals who cannot tolerate existing drugs would have additional treatment options." "Once they are standardized and developed for mass markets, cognitive training programs might be available to seniors through churches, schools and senior centers," said Shumaker. "Importantly, cognitive training programs may give individuals a greater sense of control over the disturbing prospect of cognitive decline and have a beneficial effect on their quality of life," says the editorial.

Resolutions for a Brain-Healthy from Alzinfo.org

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New Year resolutions may be good for more than just your body. Recent studies continue to point to the benefits of an active, heart-healthy lifestyle to help keep the mind sharp and alert. While there are many factors that we can't control, such as the genes we inherit, a few simple steps may even help to prevent Alzheimer's disease years down the road.

1. Keep on exercising. Exercise is beneficial at any age, not just for the heart and muscles but for the brain as well. Doctors in Scotland who examined 460 men and women who had been participants in a long-running national survey found that, as a group, the more physically robust an individual was in old age, the more likely he or she was to have an intact memory.

2. Eat a heart-healthy diet. A Mediterranean-style diet may be good not just for the heart but for the brain as well. Doctors at Columbia University in New York found that seniors who ate plenty of fruits, vegetables, legumes, cereals, olive oil, and fish; moderate amounts of wine; and little red meat or high-fat dairy products had a lower risk of getting Alzheimer’s disease.

3. Eat your fish. Do what the Scandinavians do: Eat fish for the New Year. Recent findings from the large and ongoing Framingham Heart Study found that people with high levels of a fatty acid known as DHA, a “good” fat found in fish, may have a lower risk of developing Alzheimer's disease.

4. Drink juice. Older men and women who drank fruit and vegetable juices more than three times a week were 76 percent less likely to develop Alzheimer’s disease than those who drank juices less than once a week, a new study found. Researchers point to disease-fighting substances called polyphenols that are naturally found in fruits and vegetables as a possible source of protection.

5. Turn off the TV. Watching too much television not only keeps you on the couch; it may also dull the brain. A recent survey from Australia found that men and women who reported watching less than an hour a day of TV performed better in numerous memory tasks, including remembering items on a shopping list, recalling names and faces and people’s occupations, and long-term memory skills.

6. Try computer games. More and more senior centers are adding computer games and other mental challenges to the roster of daily activities. One recent study found that men and women with Alzheimer’s disease benefited from computer-based “games” designed to provide mental stimulation and enhance brain activity. The findings provide more evidence that mental challenges, such as doing crossword of Sodoku puzzles, solving brain teasers, or playing a musical instrument, can provide a mental boost, regardless of age or health.

7. Seek counseling. Spouses who cared for a loved one with Alzheimer’s disease were much less likely to place their partner in a nursing home if they received targeted counseling and support. These findings, from a long-running study led by Dr. Mary Mittelman and colleagues at the Silberstein Institute at the New York University School of Medicine, underline the importance of counseling and social support for any family touched by Alzheimer’s disease.

8. Finally, relax. Scientists at the University of California at Irvine found that mice injected with a drug that mimics stress in people had high levels of beta-amyloid, a toxic protein that builds up in the brains of those with Alzheimer’s disease. The findings suggest that managing stress may be important parts of an Alzheimer’s care plan. [see the alzinfo.org ]

Let’s Weigh-in On The Risks

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More than 280,000 Canadians aged 65 and over have AD. As populations around the world continue to age, AD will become even more prevalent. By 2031, more than 750,000 Canadians are expected to have AD and related dementias. "Almost 25 per cent of Canadians have someone with AD in their family. Research into the causes of, or solutions to AD is significant as research may hold the key to unlocking new means of preventing, treating and curing it," says Dr. Rémi Quirion, based in Montreal and Scientific Director of the CIHR Institute of Neurosciences, Mental Health and Addiction (CIHR-INMHA).

"Aside from its impacts on those who suffer from it, AD can be a significant burden for families and for the health care system," says Dr. Anne Martin-Matthews, based in Vancouver and Scientific Director of the CIHR Institute of Aging (CIHR-IA). "CIHR recently launched RAPID (Research to Action Program In Dementia), an initiative which seeks to accelerate the translation of research about AD and dementia by linking researchers with communities."

Recent studies have highlighted several life style risk factors for the development of AD. Does the long-term intake of caffeine reduce the risk of AD? Does physical activity have a role to play in staving off the risk of AD? What about the so-called Mediterranean diet which is high in olive oil and said to be protective against age-related memory problems? Some studies say eating fish just two to three times a week may also protect your brain as you age. And others have shown that fruits, vegetables and juices have a role to play in reducing risk.

The Canadian Institutes of Health Research (CIHR) is the Government of Canada's agency for health research. CIHR's mission is to create new scientific knowledge and to catalyze its translation into improved health, more effective health services and products, and a strengthened Canadian health care system. Composed of 13 Institutes, CIHR provides leadership and support to more than 10,000 health researchers and trainees across Canada. http://www.cihr-irsc.gc.ca.

Cardiac health and Mental impairment

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Mental impairment and decline in cardiac health are two common complaints of advancing age. A new study, published in Journal of the American Geriatrics Society, suggests that there may be a link between the conditions; specifically, a decline in heart health may lead to cognitive impairment in elderly women.


According to study author Dae Hyun Kim, a healthy heart naturally varies its rate and rhythm throughout the day in response to physical and mental demands. "Advancing age and disease can lower the heart's ability to change its rate and rhythm, which can be associated with changes in mental function," says Kim. How this occurs is not clearly known.


Kim says that further research into the connection between cardiac and mental health is important. “Mental impairment in the elderly is a major public health issue, and has significant effects on caregivers, the healthcare system and society.” Identifying contributing risk factors, such as heart health, could help seniors to avoid this debilitating condition.

The primary goal of the Journal of the American Geriatrics Society is to publish articles that are relevant in the broadest terms to the clinical care of older persons. Such articles may span a variety of disciplines and fields and may be of immediate, intermediate, or long-term potential benefit to clinical practice. For more information, please visit blackwellpublishing.com/jgs.

Lithium & Alzheimer's disease

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New laboratory research suggests that lithium and other drugs that inhibit a particular enzyme, GSK-3 beta, should be used with caution in treating Alzheimer's disease because too high a dose can impair, rather than enhance, neuronal function.

Lithium is currently in clinical trials for treating Alzheimer's. Pharmaceutical companies are interested in producing other GSK-3 beta inhibitors for the disease because these drugs are relatively easy to make and lithium has been shown to be safe in low doses in treating people with manic-depressive illness, said Dr. William D. Snider, professor of neurology, cell and molecular physiology at the University of North Carolina at Chapel Hill's School of Medicine.

"People might think that if you make the inhibitor stronger and stronger, that would be better. Our in-vitro experiments show that you will have to be careful with how you use GSK-3 beta inhibitors, because if you use too much, it will interfere with and possibly kill neurons," said Snider, who also is director of UNC's Neuroscience Center

The results, published online in the journal Neuron, were surprising because GSK-3 beta inhibitors have been shown at some doses to improve neuronal function. "It's known that when GSK-3 beta is inactivated that tends to allow the processes inside the cell it regulates to function normally," Snider said. But when the researchers strongly inhibited GSK-3 beta in mouse neurons in cell culture, the growth of axons, which carry messages between nerve cells, was markedly reduced.

The researchers inhibited GSK-3 beta using RNA silencing. "RNA silencing allows you to specifically knock down the level of a particular protein inside the cell," Snider said. In a second set of experiments, the researchers treated mouse neurons with a low dose and a high dose of a GSK-3 beta inhibitor similar to lithium. The high dose impaired neuronal function, while the low dose improved it. Snider's group plans to further investigate the effect of inhibiting GSK-3 beta in a whole-mouse model. "We will take a conditional mutagenesis approach in mice to knock out the GSK-3 beta in the nervous system," Snider said. "We'll be able to find out if we get the same effect in the whole animal that we got using RNA silencing in the culture dish."

The researchers will also work to understand how GSK-3 operates in relation to a protein called Tau, which is implicated in Alzheimer's.

Mental training and physical activity

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Memory training and other non-drug treatments may one day help older adults ward off declines in mental function, according to researchers from Wake Forest University School of Medicine in an editorial in the current issue of the Journal of the American Medical Association.

"The latest research suggests that mental training and physical activity both have promise for preventing declines in cognition," said Sally A. Shumaker, Ph.D., lead author on the editorial. "It's possible to envision a future treatment approach that combines lifestyle and drug treatments to meet the specific needs of each individual."

Shumaker, a professor of public health sciences and associate dean for research at Wake Forest, said the findings suggest opportunities for studying other non-drug treatments, such as meditation, to prevent or slow declines in cognition, which includes concentration, language, memory and abstract reasoning. "Cognitive decline is a rapidly growing problem because of our aging population," said Shumaker. "It is probably one of the biggest fears that older adults have - the loss of your mind and your competency and independence. It seriously threatens the ability of the aging population to live independently."

In the editorial, Shumaker and co-authors Claudine Legault, Ph.D., and Laura H. Coker, Ph.D., also from Wake Forest, discuss the results of a recent multicenter study involving cognitive training, as well as other advances in the field. The Advanced Cognitive Training for Independent and Vital Elderly (ACTIVE) study involved almost 3,000 participants. Half received 10 sessions of cognitive training and half received no special training. Participants who had the training showed immediate improvements in memory, reasoning and speed of processing. When the participants were tested five years later, the improvements had been sustained.

Other recent research showing that sedentary older adults perform less well on measures of memory suggests that physical activity may also be able to improve memory, according to the editorial. "These studies illustrate the promise of non-drug treatments," said Shumaker. "The medications available today produce only low to moderate improvements in mental function. And they can have adverse side effects. Showing that cognitive training can protect mental function means that individuals who cannot tolerate existing drugs would have additional treatment options."

"The ACTIVE study is an important step toward demonstrating the feasibility of enrolling older adults in a long-term study of a cognitive training intervention," according to the editorial. The authors say that matching cognitive training with an individual's risk factor profile is an intriguing possibility. For example, training that focuses on memory may be best for those at risk for Alzheimer's disease. "Once they are standardized and developed for mass markets, cognitive training programs might be available to seniors through churches, schools and senior centers," said Shumaker. "Importantly, cognitive training programs may give individuals a greater sense of control over the disturbing prospect of cognitive decline and have a beneficial effect on their quality of life," says the editorial.