Cytokines may be a marker of risk of Alzheimer's

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People whose blood shows signs of inflammation are more likely to later develop Alzheimer's disease than people with no signs of inflammation, according to a study published in the May 29, 2007, issue of Neurology®, the scientific journal of the American Academy of Neurology.

The study, which is part of the larger Framingham Heart Study, involved 691 healthy people with an average age of 79. Blood tests determined whether the participants had signs of inflammation. Then the participants were followed for an average of seven years. During that time, 44 of the participants developed Alzheimer's disease.

The participants' blood was tested for levels of cytokines, which are protein messengers that trigger inflammation. Those with the highest amount of cytokines in their blood were more than twice as likely to develop Alzheimer's disease as those with the lowest amount of cytokines. A total of 28 percent of the women and 30 percent of the men had high levels of cytokines, yet they made up 42 percent of the cases of Alzheimer's disease.

Harvard Medical School in Boston: "These results provide further evidence that inflammation plays a role in the development of Alzheimer's disease. The production of these cytokines may be a marker of future risk of Alzheimer's disease."

Calcium, vit D may cut breast cancer risk
Premenopausal women who consume higher amounts of calcium and vitamin D may lower their risk of developing breast cancer by almost 40 per cent, new research suggests.

The predictors of amyloid plaques in the brains

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A new study published in January's edition of Nature Biotechnology from researchers at the Institute for Systems Biology, USA; the University of California, USA; and Cellzome, Germany, highlights the benefits of a new computational technique to predict which peptide fragments should be observed for a given protein during LC/MS/MS.

Proteomics has been part of a radical transformation of biological and medical research, by studying which proteins are present in cells, how they interact and what they do. The differences in the abundance of different proteins in distinct samples has led to the identification of cellular functions and pathways affected by disease as well as enabling the detection of disease biomarkers.

Mass spectrometric (MS) peptide sequencing has become a key step in nearly all proteomic experiments but the results are often biased towards repeatedly detecting the protein fragment with the most intense MS signal, thus limiting the efficiency and depth of the analysis.

In fact, many peptides are never detected, either because they stick to the liquid chromatography (LC) column or they are too large or too small to be detected by the mass spectrometer. Typically, those fragments or peptide chains that are between seven and 30 amino acids long fall in the range detected by standard mass spectrometers.

The study found that, on average, the identification of only three distinct peptides is needed to identify the majority (95 per cent) of proteins, and for over 25 per cent of proteins only one peptide is needed for identification. These identifying protein fragments have been dubbed proteotypic peptides.

By defining approximately 500 physical and chemical properties of various peptides including charge, hydrophobicity and secondary structure, the researchers were able to find which properties best distinguished the proteotypic peptides from those peptides that are unobserved. Interestingly, the number of proteotypic peptides observed for a protein was not merely a function of the protein length, but factors such as amino acid composition and transmembrane domains also had a significant influence.

The predictors showed good agreement between observed and predicted peptides, even for human gamma-secretase, a protein associated with the development of amyloid plaques in the brains of Alzheimer's patients that is notoriously difficult to analyse.

According to one of the authors, Dr Bernhard Kuster, Cellzome's vice president of analytical sciences and informatics, "one of the motivations behind this research is that proteomics can be a bit hit and miss, we need to measure the proteins in a more quantitative way."

"We have found a number of proteins that we don't predict proteotypic peptides for, highlighting a blind spot of current LC/MS/MS techniques, some proteins have no peptides suitable for detection."

Even with the current state of the art methods of protein identification, some parts of the proteome are not detected. The use of these predictors could allow the development of new experimental methodologies that ensure that important proteins are not missed.

Kuster believes that the current techniques are "a good compromise between seeing everything and seeing enough," especially when it comes to high throughput screening, where speed is of the essence.

By using these new techniques in conjunction with its Kinobead technology, Cellzome can study the interaction of small molecules with over 200 kinase targets in a high throughput parallel assay. The active molecules, whether they are hits, leads, development candidates or marketed drugs, are tethered to a solid support and facilitate the isolation of those proteins that bind to the candidate.

The isolated proteins can then be identified by LC/MS/MS. According to Kuster: "the technique is much faster than in-vitro kinase assays and you can see many more kinases that you can't buy an assay for."

The new methodology will find application as a workflow improvement tool and will allow screening methods to be much faster by using an MS technique called multiple reaction monitoring (MRM). MRM allows the mass spectrometer to be focused on the detection of the specific signals from proteotypic peptides one after the other, rather than scanning the entire mass range.

The combination of using the predictors with LC/MS/MS/MRM will also help in the identification of serum biomarkers and monitoring how they change during pathological conditions. According to Kuster, these changes are often incredibly hard to detect, as the proteomic data is so noisy.

Cows can make skimmed milk, say scientists
Cows could be bred to produce only skimmed milk within the next five years, researchers have said, offering a new way of meeting consumer demand for lower fat dairy.

Pomegranate juice could halve proteins linked to Alzheimer's

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"This study is the first to show beneficial effects (both behavioral and neuropathological) of pomegranate juice in an animal model of AD," wrote lead researcher Richard Hartman from Loma Linda University in California.

Although the mechanism of Alzheimers is not clear, more support is gathering for the build-up of plaque from beta-amyloid deposits. The deposits are associated with an increase in brain cell damage and death from oxidative stress. It is against the oxidative stress that the polyphenols appear to offer protection.

Hartman and his co-workers supplemented the diets of transgenic mice (APPsw/Tg2576) with pomegranate juice. This strain of mice are engineered to express an amyloid precursor protein (APP) that leads to an early onset of neurological degeneration and subsequently Alzheimer's disease.

Between the ages of six and 12.5 months, the mice were divided into two groups and received either plain water or a pomegranate juice (PJ) made from concentrate (PomWonderful) diluted 1:160 or 1:80. "Since the PJ concentrate is four times more concentrated than regular strength PJ sold commercially, the dilutions of concentrate are approximately equivalent to dilutions of 1:40 or 1:20 of non-concentrated PJ," explained Hartman.

Cognitive function was evaluated by subjecting the mice to a water maze task, which requires the animal to swim and find a submerged platform in a pool of water. As performance improves, the time decreases for the mouse to escape the maze and the distance swum.

The mice given the pomegranate juice drink were found to negotiate the maze significantly quicker (about 35 per cent) and swam a more direct path (on average 3750 cm less) than the non-supplemented group, reported the authors in the Elsevier journal Neurobiology of Disease (doi: 10.1016/j.nbd.2006.08.006).

When the researchers examined the quantity of beta-amyloid deposits in the brain cortex of the mice, it was found that the pomegranate juice-supplemented groups had 50 per cent less of the protein than the non-supplemented group.

Being the first study into the potential protective role of pomegranate concentrate and the antioxidant polyphenols contained within, significantly more study is needed.

The data is based on pomegranate concentrate and no attempt was made by the authors to discriminate the potentially 'active' biochemicals in the fruit that may offer protection independently or synergistically, although they said the evidence suggests a complimentary effect of the polyphenols.

"The vast number of compounds in PJ, along with the evidence that these compounds may act together in a synergistic fashion, suggests that isolated components of pomegranate may not be as effective as dietary supplementation with either the whole fruit or its juice. These results suggest that further studies to validate and determine the mechanism of these effects, as well as whether substances in PJ may be useful in Alzheimer's Disease, should be considered," they concluded.

The work follows a recent epidemiological study into the possible role of fruit and vegetable juices reducing the risk of Alzheimer's (The American Journal of Medicine, Vol. 119, pp. 751-759), a result that was also linked to the polyphenol, rather than the vitamin content of the fruit and vegetables. The researchers from the Vanderbilt University Medical Center found that people drinking juices three or more times per week were 76 per cent less likely to develop signs of Alzheimer's disease than those who drank less than one serving per week. This was after taking into account dietary intake of vitamins E, C and beta-carotene.

A memory is not a static snapshot

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Scientists know little about how the brain assigns cells to participate in encoding and storing memories. Now a UCLA/University of Toronto team has discovered that a protein called CREB controls the odds of a neuron playing a role in memory formation. The findings, which are reported in Science, suggest a new approach for preserving memory in people suffering from Alzheimer's or other brain injury.

"Making a memory is not a conscious act," explained Alcino Silva, principal investigator and a professor of neurobiology and psychiatry at the David Geffen School of Medicine at UCLA. "Learning triggers a cascade of chemicals in the brain that influence which memories are kept and which are lost. "Earlier studies have linked the CREB protein to keeping memories stable," added Silva, a member of the UCLA Brain Research Institute. "We suspected it also played a key role in channeling memories to brain cells that are ready to store them."

Silva and his colleagues used a mouse model to evaluate their hypothesis. They implanted CREB into a virus, which they introduced into some of the cells in the animal's amygdala, a brain region critical to emotional memory. Next they tested the mouse's ability to recall a specific cage it had visited before. The cage was outfitted with patterned walls and a unique smell.

To visualize which brain cells stored the mouse's memories about the cage, the scientists tracked a genetic marker that reveals recent neuron activity. When the team examined the animals' amygdalas after the experiment, they found substantial amounts of CREB and the marker in neurons. "We discovered that the amount of CREB influences whether or not the brain stores a memory," said Silva. "If a cell is low in CREB, it is less likely to keep a memory. If the cell is high in CREB, it is more likely to store the memory."

Human implications of the new research could prove profound. "By artificially manipulating CREB levels among groups of cells, we can determine where the brain stores its memories," he explained. "This approach could potentially be used to preserve memory in people suffering from Alzheimer's or other brain injury. We may be able to guide memories into healthy cells and away from sick cells in dying regions of the brain." Our memories define who we are, so learning how the brain stores memory is fundamental to understanding what it is to be human, Silva observed.

"A memory is not a static snapshot," he said. "Memories serve a purpose. They are about acquiring information that helps us deal with similar situations in the future. What we recall helps us learn from our past experiences and better shape our lives."

How antibodies go inside brain cells

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Researchers at Weill Cornell Medical College have gotten much closer to understanding how immune-based therapies can treat Alzheimer's disease. There are currently no effective treatments to fight Alzheimer's disease, which now affects over 5 million Americans, according to the Alzheimer's Association. Scientists now project that unless new ways are found to prevent or treat the disease, the total could climb to 16 million by 2050.

"... internalization and activity of the antibody within the cell was a big surprise and something we really haven't appreciated in neurological medicine. It gives us new hope for the use of immunotherapy against Alzheimer's, while casting intriguing new light on other disease processes," says senior author Dr. Gunnar Gouras, associate professor of neurology and neuroscience at Weill Cornell Medical College and associate attending neurologist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center.

For years, the idea of an immune-based vaccine therapy against Alzheimer's has been a Holy Grail of research. In fact, in the past, researchers did have some clinical success with an antibody-directed immune therapy. "Still, the dream has remained very much alive -- especially since we know that antibodies to the beta-amyloid plaques associated with Alzheimer's can cross the blood-brain barrier, gaining access to the brain," Dr. Gouras explains.

"One of the things those earlier immunotherapy studies taught us was that antibodies can reduce amyloid plaques, which are a hallmark of the disease," he said. "The next logical question was -- how does it do that?" In their latest study, the researchers exposed amyloid-filled neurons from these mice to immune antibodies similar to those used in clinical trials. They then examined changes in these cells in the lab, using microscopy, immunofluorescence and other high-tech methods.

"What we found astounded us," Dr. Gouras says. "Instead of working outside the cell, we discovered that these antibodies to beta amyloid bind with a specific part of amyloid precursor protein (APP) -- a precursor molecule to beta amyloid -- as it lies on the outside of the affected cell. This complex then gets internalized within the cell, where it works to decrease levels of amyloid peptides, the building block of plaques that are found outside and between cells."

In fact, the antibodies cut down on intracellular amyloid accumulation by about one-third, the researchers found. How might antibodies working inside neurons decrease exterior plaque levels? The researchers still aren't sure, but they have already ruled out some of the most obvious answers. "We found no evidence that the antibody somehow inhibits the activity of either of the two cellular enzymes -- secretases -- that we know help produce beta amyloid," notes the study's lead author Dr. Davide Tampellini, a researcher in the Weill Cornell Laboratory of Alzheimer's Disease Neurobiology. "In fact, if anything the presence of the antibody appears to boost secretase activity," Dr. Tampellini says.

According to the researchers, it's possible that the antibody is affecting key trafficking mechanisms within the cell, thereby increasing the degradation of existing beta amyloid before it makes its way to the surface. "Most of the data we have supports this degradation model rather than an inhibition of beta-amyloid production," Dr. Gouras says. "More research is needed to clear up that mystery, however."

What is clear from the study is that immune-based therapy does work to rid brain cells of amyloid -- giving new impetus to the search for a safe, effective Alzheimer's vaccine. "A cure isn't likely as close as we are hoping for" Dr. Gouras cautions, "and new roadblocks to a successful vaccine might arise. But as we better understand how immunotherapy is working, we can better meet those roadblocks head-on." And the discovery that antibodies work their magic both inside and outside the cell could have profound implications for the investigation of other disease conditions, especially autoimmune disorders where the immune system mistakenly attacks it own tissues.

A wide range of health benefits

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An ever-growing body of science linking consumption to a wide range of health benefits, including lower risk of certain cancers, weight loss, heart health, and protection against Alzheimer's.

Salah-uddin Ahmed, from the University of Michigan Health System, told attendees at Experimental Biology 2007 in Washington, D.C. yesterday that the tea extract may also suppress the inflammatory products in the connective tissue of people with rheumatoid arthritis.

"Our research is a very promising step in the search for therapies for the joint destruction experienced by people who have rheumatoid arthritis," said Ahmed. Green tea contains between 30 and 40 per cent of water-extractable polyphenols, while black tea (green tea that has been oxidized by fermentation) contains between 3 and 10 per cent.

The four primary polyphenols found in fresh tealeaves are epigallocatechin gallate (EGCG), epigallocatechin, epicatechin gallate, and epicatechin. The research, which has not been seen in its entirety by NutraIngredients.com, focused on synovial fibroblasts - cells that form a lining of the tissue surrounding the capsule of the joints - from patients with rheumatoid arthritis. These fibroblasts were subsequently cultured in a growth medium and incubated with EGCG.

The pro-inflammatory cytokine interleukin-1 beta (IL-1beta) was then added to the culture medium. IL-1beta is an immune system protein reported to play an important role in causing joint destruction in people with rheumatoid arthritis. Ahmed told attendees that when untreated cells were stimulated with IL-1beta, a cascade of events occurred that resulted in production of the bone-destructive molecules interleukin-6 (IL-6) and cyclooxygenase-2 (COX-2). However, when the cells were incubated with EGCG the production of IL-6 and COX-2 was not observed.

The scientists revealed that work is ongoing with lab tests focusing on the inhibitory role of EGCG in gene expression. Animal studies will be used to test if EGCG can provide similar therapeutic or preventive effects against rheumatoid arthritis. Positive results could form a strong foundation for future testing of the green tea extract in humans with rheumatoid arthritis, said Ahmed.

One drink of alcohol a day may slow dementia

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In people with mild cognitive impairment, up to one drink of alcohol a day may slow their progression to dementia, according to a study published in the May, issue of Neurology. Mild cognitive impairment is a transitional stage between normal aging and dementia that is used to classify people with mild memory or cognitive problems and no significant disability.

Researchers evaluated alcohol consumption and the incidence of mild cognitive impairment in 1,445 people. They then followed 121 people with mild cognitive impairment and their progression to dementia. The participants, age 65 to 84, were part of the Italian Longitudinal Study on Aging and were followed for three-and-a-half years.

The study found people with mild cognitive impairment who had up to one drink of alcohol a day, mostly wine, developed dementia at an 85 percent slower rate than people with mild cognitive impairment who never drank alcohol. "While many studies have assessed alcohol consumption and cognitive function in the elderly, this is the first study to look at how alcohol consumption affects the rate of progression of mild cognitive impairment to dementia," said study authors Vincenzo Solfrizzi, MD, PhD, and Francesco Panza, MD, PhD, with the Department of Geriatrics at the University of Bari, in Bari, Italy. "The mechanism responsible for why low alcohol consumption appears to protect against the progression to dementia isn't known. However, it is possible that the arrangement of blood vessels in the brain may play a role in why alcohol consumption appears to protect against dementia. This would support other observations that drinking moderate amounts of alcohol may protect the brain from stroke and vascular dementia."

The study did not find any association between higher levels of drinking, more than one drink per day, and the rate of progression to dementia in people with mild cognitive impairment compared to non-drinkers. The study was supported by the Italian Longitudinal Study on Aging and by AFORIGE, an Italian association for aging research.

Immune Antibodies Penetrate Neurons To Clear Alzheimer's-Linked Amyloid
Researchers at Weill Cornell Medical College have gotten much closer to understanding how immune-based therapies can treat Alzheimer's disease — by studying how antibodies go inside brain cells to red...

Green tea-based products against Alzheimers

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In a bid to tap growing consumer demand for healthier products, India-based Tata Tea has entered a joint venture with a Chinese company to produce value-added beverages.

Tata this week announced that it would be working with Zhejiang Tea to develop polyphenol-rich drinks, like those using green tea extracts. The two companies also plan to develop a line of instant teas.

With green tea-based products being linked by scientists to a lowered risk of certain cancers, improved heart health, weight loss, and protection against Alzheimers, the timing of the venture could be prudent.

Though the Chinese market for green tea remains consistently strong, global interest in the product is also on the rise as beverages touting health qualities grow in popularity. By combining its own facilities and marketing techniques with Zhejiang's, Tata expects the venture will be well positioned to meet the anticipated demand. Zhejiang Tea is estimated to account for about a 25 per cent of China's total export volume for tea, granting the joint-venture an immediate foothold within one of the leading markets for the production and consumption of the product.

Tata will hold a 70 per cent stake in the partnership, allowing it to boost its overall position within the dynamic market for teas. The global market for green tea is forecast to undergo volume growth of 3.9 per cent a year to 2010, faster than the expected average of 2.5 per cent for all teas, according to consumer analyst Euromonitor. At least one major manufacturer has felt the impact from the consumer shift toward healthier beverages, in particular green tea.

Coca-Cola last year blamed the move toward healthier beverages, citing green tea as an example, for the 10 per cent fall in sales of its carbonated beverages in South Korea. Meanwhile the company's green tea. Coca-Cola sales of carbonated beverages in the country fell by 10 per cent last year to about €40m. Meanwhile sales of the company's non-carbonated beverage ranges, like green tea, doubled over the same period to €36m.

Ethnic foods drive innovation from manufactures, flavour cos

Growth in the retail ethnic foods in Europe is outpacing growth in the overall foods and drink sector, according to Leatherhead, offering new opportunities to manufacturers and ingredient companies.

Fish oil plus exercise linked to...

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A combination of fish oil supplements and exercise led to reductions in fat mass by about 1.5 kg, as well as improving heart health markers and may cut the build-up of a certain protein linked to Alzheimer's.

The study adds to an ever-growing list of potential health benefits from the omega-3 polyunsaturated fatty acids, identified as one of the super-nutrients taking the food and supplements industry by storm.

Much of its healthy reputation that is seeping into consumer consciousness is based largely on evidence that it can aid cognitive function, may help protect the heart against cardiovascular disease, and could reduce the risk of certain cancers.

"Evidence is limited that fish oil supplementation can reduce body fat in overweight or obese subjects, and, in the studies that do provide evidence, little effort was made to control for the confounding influence of physical activity," wrote lead author Alison Hill in the American Journal of Clinical Nutrition.

"The present study is the first properly controlled trial to show an improvement in body composition in overweight or obese subjects after intervention with omega-3 fatty acids and regular aerobic exercise," she added.

The fish-oil supplements led to a decrease in blood triacylglycerols levels (14 per cent) and an increase plasma HDL cholesterol levels (10 per cent) relative to baseline amounts. The placebo sunflower oil decreased blood triacylglycerols levels and increase plasma HDL cholesterol levels by five and three per cent, respectively.

The combination of fish oil and exercise reduced fat mass by 1.6 kg, with no significant changes observed for fish oil alone, or placebo with or without exercise. No significant change in lean mass was observed for any of the groups.

"We have confirmed the independent benefits of supplementation with DHA-rich fish oil for triacylglycerols, [and] HDL cholesterol," said the researchers. "We also showed that both fish oil supplementation and regular moderate exercise reduced body fat in overweight or obese subjects who were at risk of CVD. Future research should evaluate the efficacy of this combined intervention over a longer duration and investigate the mechanism underlying the improvements in body composition," they concluded.

Genetic markers associated with late-onset Alzheimer’s

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Celera announced the publication of data from its research studies identifying several candidate genetic markers associated with late-onset Alzheimer’s disease. Two of these genes are PCK1, a gene that regulates blood glucose levels, and GALP, a gene that is modulated by insulin and regulates food intake, suggesting a link between Alzheimer’s disease and irregular glucose/insulin levels. This research paper has been accepted for publication in Human Molecular Genetics and is currently available on the publication’s website at http://hmg.oxfordjournals.org.

This is the first report of a genome-wide association study focused on testing genetic variants that are likely to change the function of a gene or protein. There were 19 single nucleotide polymorphisms (SNPs) that showed significant association with LOAD in an analysis of five independent case control sample sets, totaling 1,808 cases and 2,062 controls.

“This research study identifies genes that are likely risk factors for Alzheimer's disease, allowing us to narrow our biological focus as we strive toward an even better understanding of how these genes contribute to the development of this disease. Identifying susceptibility genes for Alzheimer's disease provides a knowledge base for the development of potential new diagnostic tests and novel therapies. These findings need to be looked at in other research samples to explore the consistency and the strength of these findings,” said Julie Williams, Ph.D., Professor of Neuropsychological Genetics at Cardiff University’s School of Medicine, and a lead author on the paper.

Celera intends to combine these markers with other previously identified markers into a Genetic Risk Score for late-onset Alzheimer’s disease that may identify individuals at elevated risk to develop the disease. Identification of individuals at elevated risk may also lead to more timely and cost-effective clinical drug trial designs. Other genetic variants that previously identified by Celera are in the death-associated protein kinase 1 (DAPK1) gene[1], in a homologue of the RPS3a gene[2], in members of the GAPD[3] (glyceraldehyde-3-phosphate dehydrogenase) gene family, and in the APPB2[4] (amyloid beta precursor protein binding family B member 2) gene. Patent applications for these Celera findings have been filed.

“This research holds promise for the development of diagnostic tests as well as new targets for drug discovery,” said Thomas White, Ph.D., Chief Scientific Officer at Celera. “As with our Genetic Risk Scores in other complex diseases such as risk of cirrhosis in hepatitis C virus infected individuals, and coronary heart disease and stroke that are currently in development, we now plan to combine these markers with others, and develop a predictive test that determines who might be at higher risk for Alzheimer’s disease.”

Australian funding aims for fitness in food formulation
Researchers at the University of Queensland today were awarded funding to devise healthier formulations for the food...

Milk nutrients may prevent Alzheimer's

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According to a recent study published in the medical journal Neurology, elderly persons who consume low levels of vitamin B-12 and folate may have an increased risk of developing Alzheimer's disease (AD).

Milk is a good source of vitamin B-12. In fact, three cups of milk provide the entire amount of vitamin B-12 needed by most adults each day.

The study followed 370 people, ages 75 and older, for three years and found that the risk for developing AD doubled among participants who had low levels of vitamin B-12 in their blood when compared to those with normal levels.

"The human body does not produce vitamin B-12 naturally, so it is important to incorporate these nutrients into the diet throughout a person's lifetime," said Susan Adams, MS, RD, an extension agent at the Washington State University Cooperative Extension Family Nutrition Education Program.

"Older adults should keep in mind that they need about the same amount of vitamins and minerals everyday as when they were younger. Although caloric needs generally decrease as people age, older adults still need to find ways to incorporate adequate amounts of these important nutrients into their diets."

The Center for Disease Control recently reported that deaths from Alzheimer's disease in 1999 surpassed the totals for other major causes of death, including motor vehicle accidents and breast cancer. According to the Alzheimer's Association, between now and 2050, the number of people with Alzheimer's disease will increase from an estimated 4 million to 14 million.

"The Neurology study is another indication of the true value of Alzheimer's research," said Helen Payton, development director at the Alzheimer's Association, Western and Central Washington Chapter. "Each study may lead us closer to ultimately finding a means of prevention or a cure for the disease."

ALZHEIMER'S DISEASE AND DAIRY.
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Neurologists at the Boston University School of Medicine obtained blood
samples from 1092 elderly healthy subjects over an eight year period.
During the course of the study, 111 of those subjects developed dementia,
diagnosed as Alzheimer's Disease.

Those who developed Alzheimer's had enormous increases of homocysteine
in their blood when compared to those who did not develop dementia.
There are 28 amino acids in nature. Your body's liver manufactures 19 of them. The other 9 are
called "essential", which means that they must be obtained in the foods you eat. Methionine is one such "essential"
amino acid. I have previously written about homocysteine and methionine. After ingestion, methionine converts to
homocysteine.

Homocysteine has been linked to heart disease by William Castelli, senior investigator of the largest clinical heart
study in history, the Framingham Study. Dairy causes heart disease. Homocysteine has also been linked to osteoporosis.
Ingestion of sulfur-containing amino acids causes an acid condition in the bloodstream which the body neutralizes by
leeching calcium from bones. Animal proteins contain greater amounts of methionine than do plant proteins. Milk is
liquid meat, and dairy products contain high levels of methionine, which has sulfur as its center atom. The sulfur
converts to sulfates and causes an acid condition in the blood that results in cellular destruction.

Here are some values of methionine for 100 gram portions of various foods. You will find that a result of eating
meat or consuming dairy products is the creation of a methionine-rich, and subsequent homocysteine-rich environment
of Alzheimer-causing substances human blood serum.

Cow's milk = .083 grams of methionine
Soy milk = .040 grams
Mori-Nu silken soft tofu = .074 grams
Chicken (broiled breast meat, no skin) = .859 grams
Swiss cheese = .784 grams
Parmesan cheese = .958 grams

Cow's milk contains twice as much methionine as does soy milk. Chicken has nearly 12 times the amount of methionine
as does tofu, and Parmesan cheese has an unlucky 13 times more methionine than does tofu.

The neurologists who conducted this study did not consider how or why people have high levels of methionine. Pity.
They were close to determining the cause and cure of Alzheimer's.

These neurologists who published the study in the New England Journal of Medicine suggest that folic acid reduces
levels of homocysteine. Folic acid can be found in green leafy vegetables, grains, and fruits, particularly citrus.
However, the best cure may very well be to not eat what causes the problem.

Scientific research has provided the proof that Alzheimer's Disease can be controlled or prevented by eliminating the
standard American diet that includes milk and dairy products as its foundation.

Milk can reduce the risk of developing Alzheimer's

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Organic milk consumption, compared to non-organic milk, can reduce the risk of developing Alzheimer's. According to the researchers from Aberystwyth, Wales, organic milk contains 64% more Omega 3 fatty acids than non-organic milk. In some cases organic milk contains 240% more Omega 3 acids.

The researchers also say that behaviour problems often improve if you switch your child to organic milk. Giving children organic milk can help their concentration and behaviour.

When cows are fed clover, their organic milk is much richer, they say. The downside in all this is that organic milk is much more expensive than non-organic.

Asda reformulates to cut out artificial additives

UK supermarket Asda has said it is removing all artificial colours and flavours from all of its private label food and beverage products - the biggest indication to date of the shift towards natural ingredients.

Predicting Alzhemer's with Proteomics

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A new study published in January's edition of Nature Biotechnology from researchers at the Institute for Systems Biology, USA; the University of California, USA; and Cellzome, Germany, highlights the benefits of a new computational technique to predict which peptide fragments should be observed for a given protein during LC/MS/MS.

Proteomics has been part of a radical transformation of biological and medical research, by studying which proteins are present in cells, how they interact and what they do. The differences in the abundance of different proteins in distinct samples has led to the identification of cellular functions and pathways affected by disease as well as enabling the detection of disease biomarkers.

Mass spectrometric (MS) peptide sequencing has become a key step in nearly all proteomic experiments but the results are often biased towards repeatedly detecting the protein fragment with the most intense MS signal, thus limiting the efficiency and depth of the analysis. Many peptides are never detected, either because they stick to the liquid chromatography (LC) column or they are too large or too small to be detected by the mass spectrometer. Typically, those fragments or peptide chains that are between seven and 30 amino acids long fall in the range detected by standard mass spectrometers.

The study found that, on average, the identification of only three distinct peptides is needed to identify the majority (95 per cent) of proteins, and for over 25 per cent of proteins only one peptide is needed for identification. These identifying protein fragments have been dubbed proteotypic peptides.

By defining approximately 500 physical and chemical properties of various peptides including charge, hydrophobicity and secondary structure, the researchers were able to find which properties best distinguished the proteotypic peptides from those peptides that are unobserved. Interestingly, the number of proteotypic peptides observed for a protein was not merely a function of the protein length, but factors such as amino acid composition and transmembrane domains also had a significant influence.

The predictors showed good agreement between observed and predicted peptides, even for human gamma-secretase, a protein associated with the development of amyloid plaques in the brains of Alzheimer's patients that is notoriously difficult to analyse.

According to one of the authors, Dr Bernhard Kuster, Cellzome's vice president of analytical sciences and informatics, "one of the motivations behind this research is that proteomics can be a bit hit and miss, we need to measure the proteins in a more quantitative way. We have found a number of proteins that we don't predict proteotypic peptides for, highlighting a blind spot of current LC/MS/MS techniques, some proteins have no peptides suitable for detection."

Even with the current state of the art methods of protein identification, some parts of the proteome are not detected. The use of these predictors could allow the development of new experimental methodologies that ensure that important proteins are not missed. By using these new techniques in conjunction with its Kinobead technology, Cellzome can study the interaction of small molecules with over 200 kinase targets in a high throughput parallel assay. The active molecules, whether they are hits, leads, development candidates or marketed drugs, are tethered to a solid support and facilitate the isolation of those proteins that bind to the candidate.

The new methodology will find application as a workflow improvement tool and will allow screening methods to be much faster by using an MS technique called multiple reaction monitoring (MRM). MRM allows the mass spectrometer to be focused on the detection of the specific signals from proteotypic peptides one after the other, rather than scanning the entire mass range. The combination of using the predictors with LC/MS/MS/MRM will also help in the identification of serum biomarkers and monitoring how they change during pathological conditions such as Alzheimer.

The cholinesterase treatments had a 70 per cent reduction in Aβ

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The first study into the effects of cholinesterase inhibitors on the human brain provides important new evidence of how the progression of dementia is altered by the drugs. Key proteins linked to plaques in the brain associated with Alzheimer's disease and other dementias were 70 per cent less in people prescribed the only-available treatments for the condition compared to untreated patients.

Researchers led by Professor Clive Ballard, director of research at the Alzheimer's Society, measured the levels of β-amyloid (Aβ) and tau, in people with Lewy bodies dementia. The Aβ and tau proteins are both associated with the onset of Alzheimer's disease and other types of dementia and are key to plaques and tangles found in the brains of people with Alzheimer's disease. The cholinesterase drugs, donepezil, rivastagmine and galantamine work by protecting the communication process between brain cells. The study found people with dementia prescribed the cholinesterase treatments had a 70 per cent reduction in Aβ in the brain in comparison to people who had not received the drugs. The results are the first-ever evidence of how the anti-dementia drugs curb the physical progression of dementia and appear in the May 15, 2007, issue of Neurology®, the scientific journal of the American Academy of Neurology.

Professor Ballard: 'We knew there may be some reduction in the levels of Aβ among people prescribed cholinesterase drugs, but the sheer magnitude of the reduction was a real surprise. The study looked at dementia with Lewy bodies but Aβ is also a hallmark in Alzheimer's disease. The results suggest that if we want to slow down the progression of these diseases the earlier we start prescribing these treatments the better. Our study indicates cholinesterase inhibitors go beyond a symptomatic benefit for people with dementia and also modify the disease in the brain'.

The cholinesterase inhibitors used in the study are the only licensed treatments currently available to people with Alzheimer's disease and are prescribed to more than 58,000 people in England and Wales. In November last year the National Institute for Health and Clinical Excellence (NICE) recommended the drugs should be restricted to people in the moderate stages of Alzheimer's disease. The Alzheimer's Society will go to the High Court next month as part of a judicial review of NICE's recommendation on access to these treatments.

Neil Hunt, chief executive of the Alzheimer's Society: 'People with Alzheimer's disease and their carers have known about the life-changing benefits of these drugs for some time now and this study provides the first hard evidence of the physical benefits of the same treatments. It is completely unethical that this sole lifeline is being snatched away from people in the name of economic efficacy. NICE's process in this case was fatally flawed, and we look forward to challenging it in court.'

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Fruit juice consumption could help protect against Alzheimer's

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There is a high degree of consumer awareness of the term 'antioxidant' and its relation to health and well-being - even if many people do not understand the mechanism. The study, said to be the first of its kind in the UK, could encourage more people to include juices in their diet as a relatively minor change that could potentially have a role in avoiding chronic illness.

In particular lead researcher Professor Alan Crozier said his team's findings are relevant to consumers wishing to reduce their risk of age-related dementia, in the light of a study published last year that indicated long-term fruit juice consumption could help protect against Alzheimer's disease.

"Phenolic antioxidants are bioactive compounds in fruits, vegetables and beverages that play an active role in the human body. By quenching free radicals they help maintain oxidative balance and are thought to play a key role in maintaining and improving health," explained Prof Alan Crozier.

The new study draws particular attention to the juice of Concord grapes, which came out on top in terms of highest overall antioxidant capacity and the highest and broadest range of polyphenols.

Alan Crozier, Professor of Plant Biochemistry and Human Nutrition, who conducted the study, said: "Not all fruit juices are the same. The findings reveal that the variety of phenolic compounds and antioxidant capacity of the individual juices varied markedly."

Other top scorers were cloudy apple juice and cranberry juice.
Crozier and his team assessed the total phenolic content of 13 commercially available fruit juices and juice drinks deemed to be the most popular in the UK using the Folin-Ciocalteu assay.

The products were: Spray Classic Cranberry; Welch's Purple Grape; Tesco Pure Pressed Red Grape; Pomegreat Pomegranate; Tesco Pure Apple (clear); Copella Apple (cloudy); Tesco Pure Grapefruit; Tesco Value Pure Orange (concentrate); Tropicana Pure Premium Smooth Orange (squeezed); Tropicana Pure Premium Tropical Fruit; Tesco Pure Pressed White Grape; Tesco Pure Pineapple; Del Monte Premium Tomato.

Individual phenolic compounds were identified and quantified, and catechin content and degree of polymerization of proanthocyanidins were analyzed. The main components in purple grape juice were flavan-3-ols, anthocyanins, and hydroxycinnamates, together accounting for 93 per cent of the total phenolic content. The results for the red grape juice were said to be equal to those for a Beaujolais red wine. Interestingly, white grape juice, mainly containing hydroxycinnamates, had the lowest total phenolic content.

The early diagnosis of Alzheimer's

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The new technique, soon to undergo clinical trials, could help with the early diagnosis of Alzheimers disease as well as tracking disease progression. Currently, there is no diagnostic test for Alzheimer's and clinical trials rely on cognitive end-point tests. The technique has been licensed by UCLA to Siemens, which plans to begin clinical trials under an investigational new drug (IND) application agreed by the Food and Drug Administration (FDA).

The test could also increase the speed of clinical trials of new drugs, increasing the efficiency of Alzheimer's drug development, speeding the current generation of Alzheimer's drugs along the pipeline.

Commenting on the new technique, Professor Clive Ballard, Alzheimer's Society director of research, said: "This new research could prove significant in the early diagnosis of Alzheimer's disease. The ability to diagnose at the earliest possible stage is of huge importance to people with Alzheimer's disease. This exciting study aims to track the progression of Alzheimer's disease by imaging amyloid using PET (positron emission tomography) scan. Amyloid is the protein at the core of plaques which are known to occur with the onset of Alzheimer's disease, and we look forward to further developments in this area of research."

The technique works by the intravenous injection of a Fluorine-18 labeled short-lived radio-tracer molecule FDDNP, that specifically binds to the amyloid protein. The radio-tracer molecule can then be located using positron-emission topography (PET). The study indicated that patients with Alzheimer's disease have a significantly higher retention of FDDNP biomarker in the brain than control subjects or dementia sufferers. The FDDNP-PET scan showed considerably better differentiation between sufferers and non-sufferers than magnetic resonance imaging and PET scans using other imaging agents.

Neuropathological studies have shown that beta-amyloid and another protein called tau, accumulate in abnormal patterns during ageing and particularly during the onset of Alzheimer's disease. The build-up of these lesions may even begin before the age of 30. A spokesperson for the Alzheimer's society told DrugResearcher.com that approximately 55 per cent of the 18000000 worldwide dementia sufferers have Alzheimer's disease and this number is predicted to grow to 34000000 by 2050.

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Omega-3 fatty acids and Alzheimer's disease

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Nutritionists have long endorsed fish as part of a heart-healthy diet, and now some studies suggest that omega-3 fatty acids found in the oil of certain fish may also benefit the brain by lowering the risk of Alzheimer's disease. In order to test whether an omega-3 fatty acid can impact the progression of Alzheimer's disease, researchers supported by the National Institute on Aging (NIA), part of the National Institutes of Health, will evaluate one in a clinical trial, the gold standard for medical research.

The study will be conducted nationwide by the Alzheimer's Disease Cooperative Study (ADCS), a consortium of leading researchers supported by NIA and coordinated by the University of California, San Diego. The trial will take place at 51 sites across the United States and seeks 400 participants age 50 and older who have mild to moderate Alzheimer's disease. Joseph Quinn, M.D., associate professor of neurology at Oregon Health and Science University, is directing the study.

Researchers will be evaluating primarily whether the omega-3 fatty acid DHA (docosahexaenoic acid), taken over many months, slows the progression of both cognitive and functional decline in people with mild to moderate Alzheimer's. During the 18-month clinical trial, investigators will measure the progress of the disease using standard tests for functional and cognitive change.

"The evidence to date in observational and animal studies on omega-3 fatty acids and Alzheimer's disease warrants further evaluation in a rigorous clinical trial," says NIA Director Richard J. Hodes, M.D. "This study is one of a number we are undertaking in the next few years through the ADCS to test compounds that might play a role in preventing or delaying the symptoms of this devastating disease."

"By participating in this study, volunteers will make an invaluable contribution to Alzheimer's disease research progress," says Quinn, the study's principal investigator. "We are indebted to those who graciously volunteer to participate in clinical studies."

The trial will use DHA donated by Martek Biosciences Corporation of Columbia, Md. Participants will receive either two grams of DHA per day or an inactive placebo pill. About 60 percent of participants will receive DHA, and 40 percent will get the placebo. Doctors and nurses at the 51 research clinic sites will monitor the participants in regular visits throughout the trial. To ensure unbiased results, neither the researchers conducting the trial nor the participants will know who is getting DHA and who is getting the placebo.

In addition to monitoring disease progression through cognitive tests, researchers will also evaluate whether taking DHA supplements has a positive effect on physical and biological markers of Alzheimer's, such as brain atrophy and proteins in blood and spinal fluid.

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Myelination of the brain and Alzheimer's

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Wisdom comes with age (doesn't it?), but not without a process that takes place in the brain called myelination. Myelin is the fatty sheath that coats the axons of the nerves, allowing for efficient conduction of nerve impulses. It is key to the fast processing speeds that underlie our higher cognitive functioning, including, yes, wisdom.

Myelination continues sheathing axons until we reach the age of about 50, but in these later stages, the myelin becomes more and more susceptible to damage. Now, in a report in the April issue of the journal Alzheimer's & Dementia, Dr. George Bartzokis, UCLA professor of neurology, suggests that it is the breakdown of this late-stage myelin that promotes the buildup of toxic amyloid-beta fibrils that eventually deposit in the brain and become the plaques which have long been associated with Alzheimer's disease.

These amyloid products in turn destroy more and more myelin, according to Bartzokis, disrupting brain signaling and leading to cell death and the classic clinical signs of Alzheimer's. If correct, the research suggests a broader approach to therapeutic interventions for the disease. And in a unique twist for modern-day science, Bartzokis tested his myelin model of Alzheimer's by comparing modern imaging results with maps of cortical myelination that were published in the medical journal The Lancet back in 1901.

"Myelination is the single most unique aspect in which the human brain differs from those of other species," said Bartzokis, who also directs the UCLA Memory Disorders and Alzheimer's Disease Clinic. Myelin is produced by oligodendrocytes, specialized glial cells that themselves become more vulnerable with age. "Myelination of the brain follows an inverted U-shaped trajectory, growing strongly until middle age. Then it begins to breakdown," Bartzokis said. "Before the advent of modern medicine, very few persons lived beyond age 50 and therefore, as a species, we evolved to continue myelinating over our entire natural life span."

As a result, the volume of myelinated white matter increases to a peak at about age 50, then slowly begins to reverse and decline in volume as we continue to age. The myelin that is deposited in adulthood ensheaths increasing numbers of axons with smaller axon diameters, and so spreads itself thinner and thinner, he said. As a result, it becomes more susceptible to the ravages of age in the form of environmental and genetic insults and slowly begins to break down.

"The myelin breakdown process mimics the developmental process of myelination, but this time in reverse," Bartzokis said. "That's what we think underlies the progressive spread of the neuritic plaques from the late-myelinating regions toward the earlier-myelinating regions."

Bartzokis noted that a similar progression has been described clinically of the cognitive, functional and neurologic declines that accompany Alzheimer's disease.

Oligodendrocytes and myelin have the highest levels of iron of any brain cells, Bartzokis said, and circumstantial evidence supports the possibility that brain iron levels might be a risk factor for age-related neurodegenerative diseases like Alzheimer's. In the study, he suggests that myelin breakdown in the late-myelinating regions releases iron, which promotes the development of the toxic amyloid oligomers and plaques, which in turn destroy more myelin.

Bartzokis tested his hypothesis by examining published images of amyloid deposition acquired in living individuals; the images were made using radiolabeled ligands, molecules that bind to amyloid plaques in the brains of Alzheimer's patients. Next, he compared the physical location of these plaques to much earlier work published in a 1901 edition of The Lancet that mapped the locations in the brain where late-stage myelination occurs. The two matched up perfectly.

"It was pretty striking," Bartzokis said. "And the results are easily testable using currently available imaging methods. What's important is that these results have implications for novel therapeutic interventions that could target oligodendrocytes, myelin and iron deposits in the brain."

Sony PS3 powers Alzheimer's research

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Sony announced that its PS3 console will be able to partake in Stanford University's Folding@home project. The distributed computing project has been running since 2000 and takes advantage of the unused power of subscriber's home PCs to conduct protein folding research. The results are then sent back to the US scientists to analyse.

"Millions of users have experienced the power of PS3 entertainment. Now they can utilise that exceptional computing power to help fight diseases," said Masayuki Chatani, chief technical officer at Sony Computer Entertainment. "In order to study protein folding, researchers need more than just one super computer, but the massive processing power of thousands of networked computers. Previously, PCs have been the only option for scientists, but now, they have a new, more powerful tool - PS3."

The structure of proteins is critical to their function and yet, the process of protein folding is, in many ways, still a mystery. Also, proteins folding incorrectly or not at all have been implicated in several diseases, including Alzheimer's, Mad Cow (BSE), Huntington's, Parkinson's and several cancers.

Unfortunately, there is a significant time barrier to further understanding this process through computational research - protein folding simulations can take up to 30 years for a single computer to complete. The first project run by Grid.org was in conjunction with scientists from Oxford University and searched for new anti-cancer drugs - screening billions of small molecules against numerous proteins associated with cancer. Grid.org are currently also running a project that tries to unravel the secrets of protein folding.

The 'Cell' processor at the heart of the PS3 is much faster than common, mainstream processors in PCs and could enable performance previously only possible with supercomputers, according to the scientists at Stanford. The advanced graphics capabilities of the console will allow users to display the actual folding process in real-time and also rotate and look at the protein from different angles in real-time.

PS3 owners can join in once the latest software update becomes available at the end of March. A Folding@home icon will be added to the network menu on the machine to allow users to join the project. But users need not worry about their games slowing down - the programme can be set to run automatically only when the console is idle.

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Brain scans of people with MCI show signs of early Alzheimer's

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Brain scans of people with mild cognitive impairment (MCI) show signs of early Alzheimer's disease.
According to a study published in the May 8, 2007, issue of Neurology®, PET scans were performed on the brains of 13 elderly men and women with mild cognitive impairment (MCI) and 14 elderly people without memory problems. The scans were used to measure uptake of PIB, which is an imaging agent that allows doctors to see and measure abnormal protein aggregation growth, otherwise known as amyloid plaque, in the brain. Abnormal protein aggregation growth is a signature of Alzheimer's disease. Until recently, Alzheimer's disease couldn't be officially diagnosed until after death with an autopsy.

The study found people with MCI had as much as 39 percent more PIB uptake in some parts of the brain than people without MCI. And about half of the MCI patients had PIB uptake in the Alzheimer's disease range.

"This pattern of increased PIB in patients with MCI resembles what's seen in Alzheimer's disease and is suggestive of an early Alzheimer's disease process," said study author Juha O. Rinne, MD, PhD, with the University of Turku in Turku, Finland, and Fellow of the American Academy of Neurology. "Our findings are similar to what's seen in post-mortem studies in which abnormal protein aggregation growth is found in people who had been diagnosed with probable Alzheimer's disease." Rinne says larger studies and extended follow-up is needed since identifying people with MCI who have abnormal protein aggregation growth will become increasingly important as treatments affecting such plaque amyloid accumulation become available.

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