Fast Food - Risk Factor For Alzheimer's

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Mice that were fed a diet rich in fat, sugar and cholesterol for nine months developed a preliminary stage of the morbid irregularities that form in the brains of Alzheimer's patients. The study results, published in a doctoral thesis from the Swedish medical university Karolinska Institutet (KI), give some indications of how this difficult to treat disease might one day be preventable.

Alzheimer's is the most common form of dementia, there being roughly 90,000 patients with the disease in Sweden today. The underlying causes of Alzheimer's disease are still something of a mystery, but there are a number of known risk factors. The most common is a variant of a certain gene that governs the production of apolipoprotein E, one of the functions of which is to transport cholesterol. The gene variant is called apoE4 and is found in 15-20 per cent of the population.

For her doctoral thesis, Susanne Akterin studied mice that had been genetically modified to mimic the effects of apoE4 in humans. The mice were then fed for nine months on a diet rich in fat, sugar and cholesterol, representing the nutritional content of most fast food.

"On examining the brains of these mice, we found a chemical change not unlike that found in the Alzheimer brain," says Ms Akterin, postgraduate at KI Alzheimer's Disease Research Center.

The change in question was an increase in phosphate groups attached to tau, a substance that forms the neurofibrillary tangles observed in Alzheimer's patients. These tangles prevent the cells from functioning normally, which eventually leads to their death. Ms Akterin and her team also noted indications that cholesterol in food reduced levels of another brain substance, Arc, a protein involved in memory storage.

"We now suspect that a high intake of fat and cholesterol in combination with genetic factors, such as apoE4, can adversely affect several brain substances, which can be a contributory factor in the development of Alzheimer's," says Susanne Akterin.

Previous research has shown that a phenomenon known as oxidative stress in the brain and a relatively low intake of dietary antioxidants can also increase the risk of Alzheimer's. Ms Akterin has now demonstrated in her thesis that two antioxidants are dysfunctional in the brains of Alzheimer patients, which can lead to nerve cell death.

"All in all, the results give some indication of how Alzheimer's can be prevented, but more research in this field needs to be done before proper advice can be passed on to the general public," she says. http://www.medicalnewstoday.com

Prebiotic-fortified fruit juice passes formulation test

Fructooligosaccharides (FOS) can be used to partially replace sucrose in fruit juices without detrimentally affecting physical characteristics of the juice, says new research from India. ...http://www.nutraingredients.com

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Alzheimer Society's Online Registry And Free Training Courses

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When someone with Alzheimer's disease becomes lost, finding them quickly is key to preventing a tragedy. In fact, research has shown that if the person is not found within 12 hours of last being seen, there is a 50 per cent chance that they will be found injured or dead from dehydration, drowning or hypothermia.

To help speed up search and rescue efforts, the Alzheimer Society, in partnership with the RCMP, developed a nationwide wandering registry. To date, 30,000 Canadians have registered. Now, people with Alzheimer's disease and their caregivers have the option of enrolling in the Safely Home program online, and managing their record through a new and improved website at http://www.safelyhome.ca.

Also, to ensure everyone is best prepared, the Alzheimer Society has also introducing two online courses to serve as a centralized resource for training people nationwide.

The first course, "Plan to be Prepared! Bringing people with Alzheimer's and related diseases Safely Home" is meant for care facilities' staff to help them better understand the characteristics of Alzheimer's disease, concepts of emergency preparedness and how to plan for and carry out search emergency procedures. The second course, "Search is an Emergency: Bringing people with Alzheimer's and related diseases Safely Home" was created for police and emergency services.

"Preventing people with Alzheimer's disease from becoming lost is our primary goal," says Mary Schulz, Education Director at the Alzheimer Society of Canada. "However, if they do, we want to ensure that everyone who supports people living with the disease, from family to health care workers to police officers, have the training and resources to find them as quickly as possible."

In March 2007, with the support of the RCMP, the Alzheimer Society of Canada received funding from the Search and Rescue Secretariat to implement a two year project known as the Safely Home Community Action Plan to increase public awareness and enhance the ability of the Safely Home program nationally. http://www.medicalnewstoday.com

A higher bar for infant nutrition

The infant nutrition market has shifted one notch upwards, adjusting to safety concerns and stricter requirements. Shane Starling speaks to DSM’s Fabiana Assis on how the firm has raised the bar in response. ...http://www.nutraingredients.com

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Drugs For Neurodegenerative Disease

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The Alzheimer's Drug Discovery Foundation (ADDF) announced today that it provided a grant of $185,000 to Varinel, Inc., an emerging pharmaceutical company dedicated to developing drugs that can prevent neuronal degeneration and improve brain function. The grant will assist Varinel in advancing the preclinical development of its multifunctional lead compounds, VAR10300 (also known as M30).

VAR10300 was tested successfully in cellular and animal models of Alzheimer's Disease (AD) reducing oxidative damage to mouse brain cells caused by iron-catalyzed free radical reactions and providing novel neuroprotective activity. The compound also improves levels of neurotransmitters, supports the growth of new neurons, and prevents cell death in preclinical models.

The lead compound, M30, was developed by Moussa B.H. Youdim, PhD, and his colleagues at the Technion Israel Institute of Technology, in collaboration with the Weizmann Institute of Science.

"We funded Professor Youdim's academic research on M30 and its derivatives for several years. We are now pleased to be able to further advance this M30-based drug development research being conducted by Varinel," said Howard Fillit, MD, ADDF's Executive Director. "The multifunctional approach shows great promise and, if successful, may yield an entirely new class of drugs for treatment of AD and other neurodegenerative diseases such as Parkinson's disease, Huntington's disease and ALS."

Varinel is one of the first biotechnology companies to receive funding through Novel Approaches to Drug Discovery for Alzheimer's Disease, a grant award program made possible by Elan. The purpose of the program is to catalyze and accelerate the discovery and development of innovative treatments for AD. Following extensive scientific review and due diligence, Varinel was selected as one of the top proposals for funding through this collaboration program. Novel Approaches has provided a total of $1,630,000 in research grants for AD research in the past three years.

"ADDF's generosity and its deep understanding of the treatment challenges associated with an Alzheimer's diagnosis has provided Varinel with both the financial and intellectual resources needed to meet our objective of bringing a unique multifunctional neuroprotective and neurorestorative anti-Alzheimer's drug into the clinic," said Dr. Vincent R. Zurawski, Jr., Varinel's President and CEO.http://www.medicalnewstoday.com

Calcium L-threonate safe for use in supplements, says EFSA

The European Food Safety Authority (EFSA) has backed the use of calcium L-threonate as a source of calcium in dietary supplements. ...http://www.nutraingredients.com

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Considerations And Innovative Alternatives

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World renowned dementia care expert David Sheard is hosting a one day event on Dementia Care Innovation at Richmond Villages Northampton on Thursday 4th December. The meeting will cover best practice based on person-centred care, introduce a new alternative in dementia care and establish a focus group to develop ideas to meet future challenges.

David Sheard, director of Dementia Care Matters, is a training consultant with the Alzheimer's Society and will present throughout the event. Richmond Villages will be launching a free training and support initiative for carers in the community. This initiative, called 'Yesterday, Today and Tomorrow', is for anyone who is a volunteer carer who would appreciate a greater insight and understanding of dementia. In addition, it is hoped that a support group will be set up to combat the feeling of isolation that many carers feel due to the lack of socialisation that their role can bring. http://www.medicalnewstoday.com

New Hansen probiotic cultures target low-fat dairy

Chr Hansen has launched two new probiotic cultures which it says allow manufacturers of low-fat yoghurt to add the healthy bacteria to their products while also maintaining a thick, creamy texture. ...http://www.nutraingredients.com

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Alzheimer's: polyphenols carried a one-two punch

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Scientists call it the "French paradox" - a society that, despite consuming food high in cholesterol and saturated fats, has long had low death rates from heart disease. Research has suggested it is the red wine consumed with all that fatty food that may be beneficial - and not only for cardiovascular health but in warding off certain tumors and even Alzheimer's disease.

Now, Alzheimer's researchers at UCLA, in collaboration with Mt. Sinai School of Medicine in New York, have discovered how red wine may reduce the incidence of the disease. They show how naturally occurring compounds in red wine called polyphenols block the formation of proteins that build the toxic plaques thought to destroy brain cells, and further, how they reduce the toxicity of existing plaques, thus reducing cognitive deterioration.

Polyphenols comprise a chemical class with more than 8,000 members, many of which are found in high concentrations in wine, tea, nuts, berries, cocoa and various plants. Past research has suggested that such polyphenols may inhibit or prevent the buildup of toxic fibers composed primarily of two proteins - Aß40 and Aß42 - that deposit in the brain and form the plaques which have long been associated with Alzheimer's. Until now, however, no one understood the mechanics of how polyphenols worked.

Teplow's lab has been studying how amyloid beta (Aß) is involved in causing Alzheimer's. In this work, researchers monitored how Aß40 and Aß42 proteins folded up and stuck to each other to produce aggregates that killed nerve cells in mice. They then treated the proteins with a polyphenol compound extracted from grape seeds. They discovered that polyphenols carried a one-two punch: They blocked the formation of the toxic aggregates of Aß and also decreased toxicity when they were combined with Aß before it was added to brain cells.

"What we found is pretty straightforward," Teplow, a UCLA professor of neurology:"If the Aß proteins can't assemble, toxic aggregates can't form, and thus there is no toxicity. Our work in the laboratory, and Mt. Sinai's Dr. Giulio Pasinetti's work in mice, suggest that administration of the compound to Alzheimer's patients might block the development of these toxic aggregates, prevent disease development and also ameliorate existing disease." http://www.medicalnewstoday.com

Early promise for almond’s prebiotic potential

Preliminary reports of a prebiotic potential of almonds are promising and intriguing, and impending human trials may reveal if the benefits can be translated from the lab to the layperson. ...http://www.nutraingredients.com

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A beverage-based prevention for Alzheimer's

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A combination of omega-3 fatty acids with the uridine and choline improved memory and learning in gerbils, and may have benefits for Alzheimer patients, suggests new research.

Animals fed the nutrient mix performed better in maze tests than animals not fed the combination, a result attributed to improved cognitive function, according to results published in the Federation of American Societies of Experimental Biology (FASEB) journal. Researchers from MIT are now taking the research a step further and have are exploring the potential of a beverage-based prevention for Alzheimer's and other brain diseases."It may be possible to use this [combination] to partially restore brain function in people with diseases that decrease the number of brain neurons, including, for example, Alzheimer's disease, Parkinson's, strokes and brain injuries. Of course, such speculations have to be tested in double-blind, placebo-controlled clinical trials," said senior author Richard Wurtman.

Trials are reportedly underway in Europe, and preliminary results have been submitted to the Alzheimer's Association International Conference on Alzheimer's Disease, to be held in Chicago at the end of this month.

Don't forget the gerbils

Wurtman and co-workers supplemented the diets of gerbils with uridine (in its monophosphate form, 0.5 per cent) and choline (0.1 per cent), and docosahexaenoic acid (DHA, 300 mg/kg/day) for four weeks. DHA is an omega-3 fatty acids obtained predominantly from marine sources. Choline is found in meats, nuts and eggs, and can also be made by the body. Uridine, on the other hand, is contained in breast milk and synthesized by the body - it cannot be obtained from food sources, however. At the end of the study, significant increases in phospholipid levels in the brain were observed when the compounds were given together, while administration of only DHA or UMP or UMP plus choline produced smaller increases.

When the animals were subjected to different maze tests, the combination of supplements produced the best results, indicating enhanced cognitive function.

Sparking the connections

The MIT researchers report that the benefits of the combination are due to the restoration of synapses, where information is passed between neurons. These play a critical role in learning and memory. All three dietary supplements used in the study are precursors to the fatty molecules that make up cell membranes, including the membranes of brain cells, which form synapses.

The researchers report that gerbils that received all three supplements had as much as 70 per cent more phospholipids in the cell membranes than control animals, suggesting the formation of new synapses. "The improvements in cognition observed in normal gerbils in this study and in rats with impaired cognition, in a previous study, correlate perfectly with the evidence of increased brain synapses, as shown biochemically and anatomically," said Wurtman. "This suggests that treating the animals with the experimental mixture affects behavior by increasing the number of synapses in important brain regions."

For the preliminary results of the clinical trial, we must await the end of the month to discover if similar benefits can be repeated in humans. http://www.nutraingredients.com/Research

Study backs dairy recommendations for weight loss

Cutting out dairy products during a weight loss programme may be misconceived, according to a new study from the US. ...http://www.nutraingredients.com

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n–3 Fatty acids and health:
DELAYED PASSING OF THE FRAIL?

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Two are prospective cohort studies based on n–3 FA biomarkers (as opposed to dietary intake estimates), and the third is a randomized controlled, dose-response study. Attesting to the pleiotrophic effects of the n–3 FAs, the endpoints in these studies ran the gamut from all-cause mortality and cognitive decline in the former 2 studies to mood and mental health in the latter study. In short, the story they tell is this: low in vivo concentrations of EPA (eicosapentaenoic acid) or DHA (docosahexaenoic acid) predict an increased risk of death in frail, hospitalized octogenarians from Norway and an accelerated cognitive decline in free-living septuagenarians from France. Hence, the ability of markers of n–3 FA biostatus continue to provide potentially relevant prognostic information for clinically important endpoints. On the other hand, intervention with EPA+DHA in the healthy elderly had no effect on mental well-being. Together, these findings suggest that dietary habits that include higher versus lower intakes of long-chain n–3 FAs may bring certain health benefits that short-term supplementation cannot provide. Supplementation can, of course, affect other factors (eg, serum triglyceride concentrations, susceptibility to arrhythmic events, and platelet aggregation, all with potential clinical relevance. American Journal of Clinical Nutrition, Vol. 88, No. 3, 595-596, September 2008

Oily fish may boost prostate cancer survival rate

An increased intake of fish and omega-3-rich seafood may improve prostate cancer survival by 38 per cent, according to a new study. ...http://www.nutraingredients.com

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APP processing and Abeta formation is important to the Alzheimer's

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Alzheimer's disease (AD) is a common neurodegenerative disease that affects cognitive function in the elderly. Large extracellular beta-amyloid (Abeta) plaques and tau-containing intraneuronal neurofibrillary tangles characterize AD from a histopathologic perspective. However, the severity of dementia in AD is more closely related to the degree of the associated neuronal and synaptic loss. It is not known how neurons die and synapses are lost in AD; the current review summarizes what is known about this issue. Most evidence indicates that amyloid precursor protein (APP) processing is central to the AD process. The Abeta in plaques is a metabolite of the APP that forms when an alternative (beta-secretase and then gamma-secretase) enzymatic pathway is utilized for processing. Mutations of the APP gene lead to AD by influencing APP metabolism. One leading theory is that the Abeta in plaques leads to AD because Abeta is directly toxic to the adjacent neurons. Other theories advance the notion that neuronal death is triggered by intracellular events that occur during APP processing or by extraneuronal preplaque Abeta oligomers. Some investigators speculate that in many cases there is a more general disorder of protein processing in neurons that leads to cell death. In the later models, Abeta plaques are a byproduct of the disease process, rather than the direct cause of neuronal death. A direct correlation between Abeta plaque burden and neuronal (or synaptic) loss should occur in AD if Abeta plaques cause AD through a direct toxic effect. However, histopathologic studies indicate that the correlation between Abeta plaque burden and neuronal (or synaptic) loss is poor. We conclude that APP processing and Abeta formation is important to the AD process, but that neuronal alterations that underlie symptoms of AD are not due exclusively to a direct toxic effect of the Abeta deposits that occur in plaques. A more general problem with protein processing, damage due to the neuron from accumulation of intraneuronal Abeta or extracellular, preplaque Abeta may also be important as underlying factors in the dementia of AD. Curr Mol Med. 2001 Dec;1(6):733-7

Seaweed gel may help reduce energy intake

Consuming a strongly gelled alginate drink may reduce daily energy intakes by about seven per cent and play a role in weight management, says a net study. ...http://www.nutraingredients.com

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The role of pharmacists in caring for individuals with Alzheimer's

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Alzheimer's disease is a progressive and fatal brain disease affecting as many as 5 million Americans and is the sixth-leading cause of death in the United States. Alzheimer's destroys brain cells, causing problems with memory, thinking and behavior severe enough to affect work, lifelong hobbies or social life. The number of people with this disease could increase to as many as 16 million people by 2050. Alzheimer's disease is the most common form of dementia, a general term for the loss of memory and other intellectual abilities serious enough to interfere with daily life. Vascular dementia, another common type of dementia, is caused by reduced blood flow to parts of the brain. In mixed dementia, Alzheimer's and vascular dementia occur together. Alzheimer's disease has no current cure but treatments for symptoms, combined with the right services and support, can make life better for the millions of Americans living with Alzheimer's.

The November/December issue of the Journal of the American Pharmacists Association (JAPhA) features an article titled: White paper on expanding the role of pharmacists in caring for individuals with Alzheimer's disease. The white paper presents a summary discussion from a meeting held on March 5-6, 2008 convened by the American Pharmacists Association (APhA) Foundation.

Leading national experts including representatives from the American Association of Retired Persons (AARP), the National Alzheimer's Association, the National Family Caregivers Association (NFCA) and the Partnership to Fight Chronic Disease (PFCD) met as a coordinating council to discuss the current levels of care and services provided by pharmacists to patients with Alzheimer's Disease. The White paper was developed to serve as a "blueprint document" to stimulate both discussion and action on how to help patients and family caregivers manage the burden of this devastating disease. Support for the coordinating council was provided by a grant from Forest Laboratories, Inc.

The coordinating council outlines several items that could involve pharmacists in improving care for patients with Alzheimer's disease. Those items include:

- Indentifying and publicizing best practices in collaborative care models
- Increasing continuing education programs provide not only clinical insights but information on caregiver issues
- Evaluating residencies, fellowships and other certification processes that enhance pharmacist skills
- Providing overall medication management for patients
- Provision of medication packaging options that promote patient independence and ease of use for caregivers

Another important issue discussed by the coordinating counsel was the need to develop and distribute a list of community referral sources, including healthcare professionals with specialized knowledge, individual and caregiver support groups, respite services and adult day care facilities.

According to William Ellis, executive director of the APhA Foundation, "The coordinating council meeting and subsequent white paper highlighted the tremendous need and numerous opportunities for pharmacist involvement in helping patients and families deal with Alzheimer's disease." Ellis went on to state, "It is also important to recognize that many patients with Alzheimer's disease also suffer from other chronic conditions where a pharmacist's expertise and skills in medication therapy management can be valuable." http://www.medicalnewstoday.com

Lutein safe but won’t help infant eye function

The European Food Safety Authority (EFSA) has deemed lutein safe for use in infant formula in doses up to 250-300mg/l and 500mg/l in follow-on formula. ...http://www.nutraingredients.com

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Could people smoke marijuana to prevent Alzheimer's?

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Alzheimer's disease is the leading cause of dementia among the elderly, and with the ever-increasing size of this population, cases of Alzheimer's disease are expected to triple over the next 50 years. Consequently, the development of treatments that slow or halt the disease progression have become imperative to both improve the quality of life for patients and reduce the health care costs attributable to Alzheimer's disease. The research suggests that the development of a legal drug that contains certain properties similar to those in marijuana might help prevent or delay the onset of Alzheimer's disease. Though the exact cause of Alzheimer's remains unknown, chronic inflammation in the brain is believed to contribute to memory impairment.

Scientists demonstrate that the active component of marijuana, Delta9-tetrahydrocannabinol (THC), competitively inhibits the enzyme acetylcholinesterase (AChE) as well as prevents AChE-induced amyloid beta-peptide (Abeta) aggregation, the key pathological marker of Alzheimer's disease. Computational modeling of the THC-AChE interaction revealed that THC binds in the peripheral anionic site of AChE, the critical region involved in amyloidgenesis. Compared to currently approved drugs prescribed for the treatment of Alzheimer's disease, THC is a considerably superior inhibitor of Abeta aggregation, and this study provides a previously unrecognized molecular mechanism through which cannabinoid molecules may directly impact the progression of this debilitating disease.

The more research they do, the more evidence Ohio State University scientists find that specific elements of marijuana can be good for the aging brain by reducing inflammation there and possibly even stimulating the formation of new brain cells. Any new drug's properties would resemble those of tetrahydrocannabinol, or THC, the main psychoactive substance in the cannabis plant, but would not share its high-producing effects. THC joins nicotine, alcohol and caffeine as agents that, in moderation, have shown some protection against inflammation in the brain that might translate to better memory late in life. The most recent research on rats indicates that at least three receptors in the brain are activated by the synthetic drug, which is similar to marijuana. These receptors are proteins within the brain's endocannabinoid system, which is involved in memory as well as physiological processes associated with appetite, mood and pain response. This research is also showing that receptors in this system can influence brain inflammation and the production of new neurons, or brain cells. http://www.medicalnewstoday.com

Selenium may ease onset of metabolic syndrome: Study

An increased intake of selenium may decrease risk factors for metabolic syndrome and inflammation, suggests a new study from Spain. ...http://www.nutraingredients.com

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Ginkgo biloba extract does not prevent dementia

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The research was the work of the Ginkgo Evaluation of Memory (GEM) Study Investigators who are based at centers throughout the US, including the University of Pittsburgh, Pennsylvania, was working at the time of the investigation. Ginkgo biloba is taken by many people because of claims that it benefits memory and cognition and in some parts of the world it is prescribed for such. But there have been no substantial clinical trials to evaluate the effectiveness of the supplement in the primary prevention of dementia, wrote the authors.

The randomized, placebo-controlled clinical trial included 3,069 community-dwelling volunteers aged 75 and over and took place at five US medical research centers between 2000 and 2008. About half the volunteers were given a twice daily dose of 120mg extract of Ginkgo biloba and the other half took a placebo. None of the participants showed signs more advanced than mild cognitive impairment at the start (2,587 had normal cognition while 482 had mild cognitive impairment). They were followed for a median period of 6.1 years during which time they underwent 6-monthly assessments for dementia.

The results showed that:
During the period of the study, 523 participants were diagnosed with dementia: 16.1 per cent (246) in the placebo group and 17.9 per cent (277) in the Ginkgo biloba group.

92 per cent of all the dementia cases were classed as possible or probable Alzheimer's Disease (AD), or AD with evidence of the tell-tale signs of AD in the brain (vascular disease that shows as changes in the blood vessels).

The overall prevalence rate of dementia did not differ significantly between the two groups: 3.3 dementia cases per 100 persons per year of exposure for the Gingko biloba group and 2.9 per 100 for the placebo group.

There was a similar lack of significance for Alzheimer's prevalence: 3.0 persons per 100 per year of exposure in the Gingko biloba group and 2.6 per 100 in the placebo group.

Ginkgo biloba appeared to have no impact on the rate of progression to dementia in the participants who had mild cognitive impairment.

There were no significant differences between the groups in the rate of side effects.

The authors concluded that: Based on the results of this trial, Ginkgo biloba cannot be recommended for the purpose of preventing dementia. http://www.medicalnewstoday.com

Gum arabic shows prebiotic potential in humans: Study

Ten grams of gum arabic may produce a prebiotic effect in humans by boosting gut populations of specific bacteria, says a new study from Kerry. ...http://www.nutraingredients.com

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The treatment of Alzheimer's: Growth Hormone Drug or Resveratrol Like Compound?

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It is estimated that every 70 seconds, someone in the United States develops Alzheimer's disease. Medicines targeting amyloid beta that make up the clumps in the hallmark plaques are now in many phases of experimental testing. The hope is that clearing out amyloid beta before it accumulates could stave off the disease and reduce symptoms.

A new study shows that a drug that increases the release of growth hormone failed to slow the rate of progression of Alzheimer's disease in humans. Growth hormone is naturally produced in the body and stimulates the release of another hormone called insulin-like growth factor-1 (IGF-1). Studies on mice have suggested that IGF-1 helps reduce beta-amyloid, which is a form of plaque, from the brain. In the study, scientists used the investigational compound MK-677 to boost the blood levels of the hormone. The study found that MK-677 did not slow the symptoms of Alzheimer's disease even though MK-677 was effective in increasing levels of IGF-1. "This work suggests that targeting this hormone system may not be an effective approach to slowing the rate of Alzheimer's disease progression," says study author J.J. Sevigny, MD, of Merck Research Laboratories in North Wales, PA.

Scientists at the Feinstein hope to develop this natural substance, called resveratrol, or synthetic versions, for the treatment of Alzheimer's. Scientists have discovered that a specific kinase - AMPK - controls Abeta levels. AMPK is an interesting protein because it is a metabolic sensor in the cells and throughout the body. It senses levels of ATP, the body's fuel source. When ATP levels drop, AMPK is activated to prepare the cells to adjust to the metabolic change in the body - when fuel is low. It's like a driver moving along at 50 and slowing down when it realizes that there is trouble ahead. Resveratrol activates AMPK and in turn this protein lowers Abeta levels. This is an important finding because the scientists identified a new potential molecular target - AMPK - to lower Abeta levels in Alzheimer's. It also opens the door to considering more potent analogs of resveratrol. Feinstein scientists are now screening libraries of substances to see whether there are any compounds that could mimic the effects found in this substance. As it is, the amounts found in grapes and wine are small and it would not be feasible to ingest enough to have a benefit. The Feinstein chemists have identified several compounds that are now in different stages of testing. http://www.medicalnewstoday.com

EFSA says no to Valio probiotic gut health claim

A health claim submission linking probiotic consumption and gastro-intestinal has not been supported after scientific assessment by the European Food Safety Authority (EFSA). ...http://www.nutraingredients.com

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A role of nutrition in the prevention of Alzheimer Disease

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Alzheimer Disease is the most prevalent form of dementia, i.e. diseases showing severe loss of cognitive ability, during aging. Alzheimer Disease is a heterogeneous neurodegenerative disorder, clinically characterized by progressive and irreversible cognitive deficits and behavioral alterations that affect memory and learning ability, activities of daily living and quality of life, already in an early stage of the disease. The prevalence of Alzheimer Disease is only 1% above the age of 60 but increases dramatically to 40% above the age of 85. In addition to the increased life expectancy, also the association between nutrition and life style disorders may add to the predicted global burden of Alzheimer Disease considerably as well.

There is a growing interest in the role of nutrition in aging diseases such as dementia, in particular sporadic or late-onset Alzheimer Disease. The evidence to date supports a contribution of food and food components particularly in the prevention of and risk on Alzheimer's Disease. Older people may already be at nutritional risk because of changes in taste and smell, impaired digestion, absorption or utilization of nutrients due to chronic diseases or drug-nutrient interactions. Although epidemiological studies sometimes report conflicting results, specific associations between nutritional components and the risk for Alzheimer Disease have been found, especially in frail elderly people at risk of deficiencies. These include the potential protective effects of, for instance, specific polyunsaturated fats, B-vitamins and antioxidants. These macro- and micronutrients are dietary components that can influence brain structure and function.

Nutritional intake may provide specific nutrients that can be used as building blocks for membrane and synapse formation and neurotransmitter production but can also directly influence the availability of nutrients, energy and oxygen to the brain. The neuronal loss, amyloid and Tau protein pathology in the Alzheimer brain, as well as possible dysfunction of the cerebrovascular system and energy metabolism may act together to accelerate the downhill cascade in cognitive and behavioral function. The potential of nutrition for neuronal maintenance rather than as an energy substrate is illustrated by the increasing evidence that nutrients not only stimulate neural plasticity but also ameliorate the ongoing neurodegenerative process and show the ability to reduce the pathological burden in the brain. With the limited therapeutic utility of current pharmacological treatments for Alzheimer Disease, the question arises what nutrition may contribute to our toolbox to address the specific needs of the Alzheimer patient. We advocate that a multi-nutrient composition specifically targeting membrane formation has the capacity to modulate all of these processes and may provide a useful way, in conjunction with the pharmaceutical route, to treat the Alzheimer patient effectively.

The contribution of both macro- and micronutrients in this respect is supported by epidemiological data that emphasize the relevance of diet context (i.e. a multi-nutrient approach) rather than single nutrients, and also by recent findings from our lab and others. In addition, recent mechanistic studies specifically support benefits of selective nutritional components in counteracting some of the neurodegenerative and pathological processes. The potential synergy between nutritional components to stimulate neuronal plasticity and function and reduce neuropathology provides a solid basis to investigate the potential benefits of such nutrient combinations in a clinical setting. The modulating capacity of such a specifically designed nutritional approach may show disease modifying capacity rather than symptomatic, especially during the prodromal and early stage of Alzheimer's Disease. European Journal of Pharmacology Volume 585, Issue 1, 6 May 2008, Pages 197-207

'Call to action' issued for raising vitamin D levels

Recommended daily intakes of vitamin D should be raised to 2,000 International Units, says a group of 18 scientists from the University of California. ...http://www.nutraingredients.com

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The newly identified compounds - promise in halting of Alzheimer's

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Researchers at Southern Methodist University (SMU) and The University of Texas at Dallas (UTD) have identified a group of chemical compounds that slow the degeneration of neurons, a condition behind old-age diseases like Alzheimer's, Parkinson's and amyotrophic lateral sclerosis (ALS).

Their findings are featured in the November 2008 edition of Experimental Biology and Medicine. SMU Chemistry Professor Edward R. Biehl and UTD Biology Professor Santosh D'Mello teamed to test 45 chemical compounds. Four were found to be the most potent protectors of neurons, the cells that are core components of the human brain, spinal cord and peripheral nerves.

The most common cause of neurodegenerative disease is aging. Current medications only alleviate the symptoms but do not affect the underlying cause - degeneration of neurons. The identification of compounds that inhibit neuronal death is of urgent and critical importance.

The synthesized chemicals identified by Biehl and D'Mello, called "3-substituted indolin-2-one compounds" are derivatives of another compound called GW5074 which was shown to prevent neurodegeneration in a past report published by the D'Mello lab. While effective at protecting neurons from decay or death, GW5074 is toxic to cells at slightly elevated doses, which makes it unsuitable for clinical testing in patients.

The newly identified, second generation compounds maintain the protective feature of GW5074 but are not toxic - even at very high doses - and hold promise in halting the steady march of neurodegenerative diseases like Alzheimer's and Parkinson's.

"Sadly, neurodegenerative diseases are a challenge for our elderly population," D'Mello said. "People are living longer and are more impacted by diseases like Alzheimer's, Parkinson's and Amyotrophic Lateral Sclerosis (ALS) than ever before - which means we need to aggressively look for drugs that treat diseases. But most exciting now are our efforts to stop the effects of brain disease right in its tracks. Although the newly discovered compounds have only been tested in cultured neurons and mice, they do offer hope." http://www.medicalnewstoday.com

Naturex has grape expectations

French supplier Naturex is aiming the grape extract it acquired in January to the energy drinks market and shunning the traditional heart health marketing that accompanies antioxidants. ...http://www.nutraingredients.com

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Can Grapes Prevent Brain Aging?

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As healthcare costs continue to escalate, the concept of disease prevention is becoming more and more attractive. The use of vaccines is well accepted by all reasonable people and even mandated by law in some cases. In terms of drug therapy, the use of tamoxifen for the prevention of breast cancer, celebrex for the prevention of colon familial polyps, and aspirin for the prevention of cardiovascular disease or cancer is well established. It is likely that additional vaccines will be developed in due course, and it is likely that new drug therapies will be implemented as part of overall disease prevention strategies. In terms of disease prevention, a concept that must constantly be remembered is the creed of the physician: first, do no harm. This concept is distinctly related to the 5-A-Day for Better Health campaign.

Should the grape be included among the group of fruits and vegetables recommended for health maintenance or disease prevention? Based on existing data, the answer is yes. Grapes are a valuable source of numerous phytonutrients, including the intensively studied constituent, resveratrol. A question worth addressing is the potential of dietary grape consumption to positively modulate human health. Many studies have suggested cardiovascular benefits, and some work has indicated cancer chemopreventive activity. Data are particularly compelling in the area of skin cancer prevention. With financial support provided by the California Table Grape Commission, novel and exciting preliminary data are emerging from independent research suggesting beneficial activity against other less prevalent but devastating illnesses, such as Alzheimer's disease and urinary bladder dysfunction. It is further suggested that some of the copious amounts of data obtained with resveratrol may be relevant to grape consumption, especially responses that can be mediated by low concentrations of the substance. Whether future specific health claims will be sought from or allowed by regulatory authorities is not known, but based on existing data, it is clear that grapes should be considered an integral component of fruit and vegetable enriched diets that are recommended by health authorities and widely accepted as beneficial for human health and disease prevention. J Agric Food Chem. 2008 Aug 27

Blackcurrant compounds target Alzheimer’s progression

Armed with a ₤60 million war chest from the Scottish government, researchers in Aberdeen are aiming to slow the progress of Alzheimer’ with bioactive compounds from blackcurrants. ...http://www.nutraingredients.com

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A fragment of ribonucleic acid is regulating the development of Alzheimer's

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The most common form of dementia, Alzheimer's Disease is a fatal, age-related neurodegenerative disorder characterized clinically by the progressive erosion of cognition and memory, and neuropathologically by defective gene expression and increased inflammatory cell signaling. According to the Alzheimer's Foundation of America, it is estimated that Alzheimer's disease currently affects more than 5 million Americans and it is projected that the number could more than triple to 16 million by mid-century.

Researchers at the LSU Health Sciences Center New Orleans Neuroscience Center of Excellence has shown that this tiny piece of RNA, or microRNA, called miRNA-146a is found in increased amounts in stressed human brain cells and in Alzheimer's disease, and that it plays a crucial role in the regulation of inflammation and disease-related neuropathology thought to be integral to the Alzheimer's disease process. They demonstrated in human brain cells in primary culture that MiRNA-146a targets the messenger RNA of an important anti-inflammatory regulator called complement factor H (CFH). Testing both control cells and Alzheimer's disease-affected tissues, they found that miRNA-164a appears to reduce the amount and bioavailability of CFH, promoting the inflammation of brain cells and contributing to the development of Alzheimer's disease.

"The goal of these neuroscience research studies is to further our understanding of the molecular biology and genetic mechanisms associated with Alzheimer's Disease and to advance the design of therapeutic strategies to counteract this common and tragic neurological disorder," said Dr. Lukiw. http://www.medicalnewstoday.com

The pros and cons of antioxidant claims

Stephen Daniells canvases views on the use of the term 'antioxidant' and whether the industry is storing up future problems by over-egging their potential. ...http://www.nutraingredients.com

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A therapy that reverses symptoms of Alzheimers's

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"We found a unique approach for delivering drugs to the brain," says William A. Banks, M.D., professor of geriatrics and pharmacological and physiological science at Saint Louis University. "We're turning off the guardian that's keeping the drugs out of the brain."

The brain is protected by the blood-brain barrier (BBB), a gate-keeping system of cells that lets in nutrients and keeps out foreign substances. The blood-brain barrier passes no judgment on which foreign substances are trying to get into the brain to treat diseases and which are trying to do harm, so it blocks them without discrimination. "The problem in treating a lot of diseases of the central nervous system - such as Alzheimer's disease, HIV and stroke - is that we can't get drugs past the blood-brain barrier and into the brain. Our new research shows a way of getting a promising treatment for these types of devastating diseases to where they need to be to work," says Banks, who also is a staff physician at Veterans Affairs Medical Center in St. Louis.

The therapy - known as PACAP27 - is a hormone produced by the body that is a general neuro-protectant. PACAP stands for pituitary adenylate cyclase-activating polypeptide. "It is a general protector of the brain against many types of insult and injury," Banks says. He compares a specific guarding mechanism in the BBB - efflux pumps - to bouncers at exclusive nightclubs. While they welcome those on the approved guest list, they look for trouble-makers trying to crash the party, refuse to let them in and evict them if they do get in.

The scientists isolated the particular gatekeeper than evicts PACAP27. Then they designed an antisense, a specific molecule that turned off the impediment. They used mouse models of Alzheimer's disease and stroke to test what would happen if PACAP27 could get into the brain. "The mice that had a version of Alzheimer's disease became smarter and in the stroke model, we reduced the amount of damage caused by the blockage of blood to the brain and improved brain recovery. We went after the guard and essentially told him to go on break for a while so PACAP27 could get into the brain. We reversed the symptoms of the illnesses," Banks says.

Simply turning off the gatekeeper that kept PACAP27 out of the brain allowed enough of the hormone that already is in the body to get inside the brain, where it effectively treated strokes. However, the mice that had a version of Alzheimer's disease needed both an extra dose of PACAP27 and the antisense that turned off the gatekeeper to improve learning. "These findings are significant for three reasons. We have found a therapy that reverses symptoms of Alzheimers's disease and stroke in a mouse model. We have isolated the particular roadblock that keeps the treatment from getting into the brain. And we have found a way to finesse that obstacle so the medicine can get into the brain to do its work," Banks says. "This could have implications in treating many diseases of the central nervous system." http://www.medicalnewstoday.com

In search of probiotics' oral potential

UK-based Leatherhead Food International (LFI) is seeking commercial interest for a research project that will explore the potential of probiotics to deliver oral health benefits. ...http://www.nutraingredients.com

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Education interacts with Alzheimer burden

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Individuals with higher education levels appear to score higher on cognitive tests despite having evidence of brain plaques associated with Alzheimer's disease, according to a report in the November issue of Archives of Neurology.

The cognitive reserve hypothesis holds that individuals with greater cognitive (thinking, learning and memory) abilities are able to delay symptoms of Alzheimer's disease despite underlying changes in the brain, according to background information in the article. Education is commonly used as a substitute measure of cognitive reserve. "Adjusting for level of Alzheimer disease pathological burden determined at autopsy, greater education has been associated with better cognitive function during life," the authors write. "Education interacts with Alzheimer disease pathological burden such that a greater pathological burden is required to show an effect on cognition among persons with more education."

Catherine M. Roe, Ph.D., and colleagues at the Washington University School of Medicine, St. Louis, studied 37 individuals with dementia of the Alzheimer type and 161 individuals without dementia between 2003 and 2008. Participants reported their education history and took cognitive tests. They were injected with a marker known as carbon 11-labeled Pittsburgh Compound B ([11C]PiB) and then underwent a 60-minute positron emission tomography (PET) scan of the brain. Recent studies have shown that [11C]PiB adheres to beta-amyloid brain plaques associated with Alzheimer's disease, allowing researchers to identify these characteristics of the disease in living patients.

The level of [11C]PiB uptake interacted significantly with years of education in predicting cognitive test scores. Among individuals whose brains took up higher levels of [11C]PiB, indicating the presence of beta-amyloid plaques, performance on the test increased with increasing education levels. Education was not associated with cognitive scores among those with low [11C]PiB uptake, indicating no plaques.

"The results support the hypothesis that cognitive reserve influences the association between Alzheimer disease pathological burden and cognition," the authors write. "Based on autopsy data, there may be a ceiling effect when extensive beta-amyloid pathological burden is present as in late-stage dementia of the Alzheimer type. Presumably, as the Alzheimer disease pathological burden increases, a greater proportion of highly educated participants reaches the threshold for dementia and the initial advantage provided by cognitive reserve decreases. Longitudinal imaging of beta-amyloid pathology in vivo will soon allow us to determine whether these inferences from cross-sectional studies are accurate." http://www.medicalnewstoday.com

Hibiscus tea can lower blood pressure: researchers

Drinking hibiscus tea can lower blood pressure in pre-hypertensive and mildly hypertensive adults, according to new research presented to the American Heart Association (AHA). ...http://www.nutraingredients.com

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Neuromelanin in the substantial nigra and Alzheimer

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The neuromelanins recognized here are present throughout the human brain and accumulate over a lifetime. Reduced neuronal content of neuromelanin in substantia nigra has been reported in patients with Parkinson's disease, Alzheimer's disease, and Rett syndrome. Their production and accumulation in putamen, premotor cortex, cerebellum, and substantia nigra during aging appear to be an important physiological process that serves both to remove toxic quinones and to bind and immobilize toxic metals. Because they have no turnover, neuromelanins constitute an effective and stable system for immobilizing/detoxifying the reactive/toxic metals in human body over its life span. Because substantial amounts of neuromelanins are found in all major brain regions, their detoxifying role is relevant throughout the human brain, and because neuromelanin accumulation takes place over the entire life span, the neuromelanin pigments contains the story of one's life exposure to several endogenous and environmental metals. http://www.pnas.org/content/105/45

Brain link to mother’s high fat diet and offspring’s obesity

A high fat diet during pregnancy may bring about changes in the offsring’s brain that makes them more prone to over-eating and obesity throughout their lives, according to a new rat study that may help explain the rise in childhood obesity. ...http://www.nutraingredients.com

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Antioxidant use is beneficial for cognitive function

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Aging in most species studied to date is accompanied by the progressive accumulation of oxidative damage in many tissues . The brain, in particular, is highly vulnerable to oxidative damage as it is consumes approximately 20% of the body’s total oxygen, has a high content of polyunsaturated fatty acids, and lower levels of endogenous antioxidant activity relative to other tissue. Normal metabolic processes result in the release of reactive oxygen species (ROS), which in turn can lead to oxidative damage to proteins, lipids, DNA and RNA. ROS are produced primarily from mitochondria, intracellular organelles that are themselves vulnerable to oxidative damage . Oxidative damage in the brain may lead to cognitive impairments in aged humans. Further, in age-associated neurodegenerative disease, oxidative damage may be exacerbated and associated with additional neuropathology. Epidemiological studies in humans show both positive and negative effects of the use of antioxidant supplements on healthy cognitive aging and on the risk of developing Alzheimer disease (AD). This contrasts with consistent behavioral improvements in aged rodent models. In a higher mammalian model system that naturally accumulates human-type pathology and cognitive decline (aged dogs), an antioxidant enriched diet leads to rapid learning improvements, memory improvements after prolonged treatment and cognitive maintenance. Cognitive benefits can be further enhanced by the addition of behavioral enrichment. In the brains of aged treated dogs, oxidative damage is reduced and there is some evidence of reduced AD-like neuropathology. In combination, antioxidants may be beneficial for promoting healthy brain aging and reducing the risk of neurodegenerative disease. http://www.springerlink.com/content/y10838132m02x7n7/fulltext.html

Probiotics to enhance the body's resistance to seasonal infections

HOWARU™ Protect represents an efficient preventive solution to strengthen the body natural defenses, particularly during the cold & flu season. To view the HOWARU™ Protect webinar. ...http://www.nutraingredients.com

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Pharmacology of Alzheimer's disease

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Alzheimer's disease is an ever-increasing health concern among the aging population, and as we research new and existing treatments for this disease we begin to uncover possibilities for its prevention. Observational studies and animal models have provided promising findings and generated excitement, but placebo-controlled clinical trials are required to demonstrate true efficacy for these treatments.In the past two decades, clinical trials have led to the approval of symptomatic treatments for Alzheimer's disease, including cholinesterase inhibitors and, more recently, an NMDA receptor antagonist. Clinical trials have also examined antioxidants, NSAIDs, hormone replacement, nutritional supplements and nonpharmacological interventions for the treatment and prevention of Alzheimer's disease. Ten years after the introduction of the first drug for the treatment of Alzheimer's disease, tacrine, it seems appropriate to reappraise the pharmacological processes of innovation in the field of research in dementia. The aim of this review is to pinpoint concrete improvements achieved in this field, in terms of experimental methods and clinical evaluation of the compounds, as well as the neurochemistry of the disease and cellular targets deserving of initial consideration. * The article first considers the use of animal models of Alzheimer's disease, which are classified according to two categories: animals with lesions of some neuronal pathways specifically implicated in clinical symptoms (i.e. lesions of the nucleus basalis of Meynert, the origin of cholinergic projections to the cortex underlying memory processes); and transgenic models, which are intended to reproduce some of the neuropathological hallmarks of Alzheimer's disease. Drugs can be tested in animals with such alterations for their effect on neuropathology, neurochemistry and behavioural disturbances. More recently, in silico models have been developed, which offer the possibility of simulating the pharmacodynamic effects of drugs in specific areas of the brain. These experiments are helpful in distinguishing purely symptomatic effects from disease-modifying effects, the latter being the ultimate goal of the modern pharmacology of dementia. * The second breakthrough considered in this article is the codification and standardisation of clinical methods for obtaining a more accurate and earlier diagnosis (the recent introduction of the concept of "Mild Cognitive Impairment", which includes patients who will later develop a true clinical dementia syndrome). In that respect, the determination of the biological markers of Alzheimer's disease (apolipoprotein E, amyloid substance, protein-tau, isoprostane) as well as progress in neuroimaging (functional positron emission tomography [fPET]-scan, single photon emission-computed tomography [SPECT], functional nuclear magnetic resonance [fNMR]) are discussed in terms of their potential as new tools in the early stages of drug development (surrogate markers). The methods used during the comparative clinical trials (phase III) have been elaborated and internationally standardised during the assessment of the different acetylcholinesterase inhibitors (AChE-I), with the knowledge that, since 1994, four of these have been officially approved: tacrine, donepezil, rivastigmine and galantamine; the same methods have been used for developing memantine, a recently-launched modulator of glutamatergic neurotransmission. The validated scales now take into consideration not only the cognitive dimensions of Alzheimer's disease but also the behavioural symptoms, with the introduction of the concept of BPSD (behavioural psychological symptoms of dementia). Some proposals to improve this clinical assessment of anti-dementia drugs are presented here. * The section of this article dealing with prospective issues considers the main pathways of interest in drug innovation and the elucidation of new targets for the future compounds. As well as their symptomatic effects on the different components of cognition, drugs should be neuroprotective and limit the lesions documented in Alzheimer's disease, with the aim of progressing far beyond the amyloid hypothesis (immunisation, beta-sheet breakers, secretase inhibitors). The field of excitotoxicity (which is mainly glutamate dependent) appears fruitful, because of the possibility of pharmacological intervention at the different steps in the excitotoxic process. All the new directions presented in this article support the concept of true disease-modifying agents. While the results of many of these trials have been disappointing, new mechanisms targeting the hallmark pathology of Alzheimer's disease are currently under investigation, including immunotherapy and secretase modulation, targeted at reducing the amyloid burden, for which we await the results. http://www.medicalnewstoday.com

Ocean Spray launches all-natural cranberry paste

Ocean Spray’s Ingredient Technology Group (ITG) has introduced an additive-free cranberry puree for use in both sweet and savoury applications, including fruit fillings and glazes for baked goods. ...http://www.nutraingredients.com

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PROTECTING YOUR BRAIN WITH SUPPLEMENTS

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The Protective Effects of Fish Oil

Eating fish regularly decreases your chances of developing Alzheimer’s, and research shows that it’s the DHA (docosahexaenoic acid) in fish that’s offering the protection. Older people with the highest blood levels of DHA were about half as apt to develop dementia and 39% as apt to develop Alzheimer's as those with lower blood levels of DHA over a nine-year period, according to Tufts University researchers. Those with the highest blood levels consumed about 180 mg of DHA a day—the amount found in three servings of fish a week. DHA decreases the formation of amyloid plaque, researchers say.

Vitamin D Boosts Mood and Memory

We now know that vitamin D affects virtually all body tissues, including the brain, and a new study suggests that getting enough D can improve some mood and memory problems. In a group of older people, those with low blood levels of vitamin D were more likely to have mild depressive symptoms such as lack of interest or indecisiveness than people with adequate blood levels. Deficiency was also linked to poor thinking skills like memory, judgment and problem-solving.

Folic Acid Adds Years to Your Brain

Dark leafy greens contain folic acid, which protects your brain two ways: it helps to reduce inflammation, by lowering neurotoxic homocysteine levels, and it seems to interfere with expression of the genes involved in dementia. Dutch researchers studied 818 subjects aged 50 to 70 with high homocysteine levels. They found that those who took 800 mcg of folic acid daily for three years had better memory and information-processing speed than those taking a placebo. The difference was dramatic. On memory tests, those taking 800 mcg of folic acid daily scored as well as people 5.5 years younger.

Don’t Forget B12

With so much new research on nutrition and the brain, it’s easy to forget about vitamin B12, a nutrient long known for its critical role in nerve and brain function. B12 is needed to keep nerves working properly throughout the body. Plus, it works with folic acid and vitamin B6 to neutralize neurotoxic homocysteine. New research from Tufts University shows just how important vitamin B12 really is to brain function. They looked at B12 and folic acid status in people age 60 or older. Not unexpectedly, they found that people’s thinking abilities were best when they had adequate blood levels of both vitamins. Surprisingly though, cognitive abilities were worst in seniors with low vitamin B12 and high serum folate levels. Anemia and impaired thinking were observed nearly five times as often for people with this combination than among people with normal B12 and folate levels. This finding led researchers to conclude that, although it’s important to get enough folic acid, in seniors, too much folic acid and too little B12 is just as bad. You need both. http://www.stopagingnow.com