The Seed Extract of Cassia obtusifolia Offers Neuroprotection

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Alzheimer’s disease (AD) is the most common age-related neurodegenerative disorder and its pathological hallmarks include β-amyloid (Aβ) plaques, dystrophic neurites associated with plaques, and neurofibrillary tangles composed of hyperphosphorylated tau protein. The gradual degeneration of nerve cells and the resultant loss of specific synaptic connections in the brain is the key pathological change associated with the emergence and progression of AD, with the amygdala, hippocampus, parahippocampal, and other adjacent cortical regions being particularly susceptible to such degeneration.

The precise causative factors in neurodegenerative diseases such as Alzheimer’s (AD) and Parkinson’s disease remain elusive, but mechanisms implicated comprise excitotoxicity, mitochondrial dysfunction, and in the case of AD, the amyloid beta peptide (Aβ). Current therapeutic strategies for such disorders are very limited; thus, traditional herbal medicines currently receive increased attention. The seeds of Cassia obtisufolia have long been used in traditional eastern medicine and more recently the ethanolic fraction of the seeds (COE) has been shown to attenuate memory impairments in mice. In this study, we set out to determine the effect of COE (range: 0.1 – 10 μg/ml) on calcium dysregulation and cell death models in mouse primary hippocampal cultures implicated in general neurodegenerative processes and in the pathogenesis of AD: excitotoxicity, mitochondrial dysfunction, and Aβ toxicity. It was found that treatment with COE attenuated secondary Ca2+ dysregulation induced by NMDA (700 μM), while a pre-application of COE also reduced NMDA-induced cell death. Furthermore, COE was neuroprotective against the mitochondrial toxin 3-NP (1 mM), while having no significant effect on cell death induced by incubation with naturally-secreted oligomers of Aβ (8.2 pg/ml). Collectively, these results are important for the therapeutic use of COE in the treatment of neurodegenerative disorders. http://www.jstage.jst.go.jp/article/jphs/107/4/380/_pdf

Science builds for L-carnitine and muscle ageing

Supplementation with L-carnitine may restore natural losses of the nutrient that occur naturally with age, according to a new study with rats. ...http://www.nutraingredients.com

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Zinc and copper ions induce the aggregation of Αβ peptides

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Alzheimer's disease (AD) is a neurodegenerative disease characterized by deposits of extracellular amyloid plaques and intracellular neurofibrillary tangles in the brain. The principal components of the plaques are fibrils formed of 40–42 residues long amyloid β-peptides (Αβ) derived from cleavage of amyloid precursor protein (APP) by β- and γ-secretases. Αβ aggregation is an established pathogenic mechanism of AD and therefore factors influencing the Αβ aggregation are of high interest. Aggregation of Αβ peptides is primarily affected by a variety of genetic and dietary factors leading to increased concentrations of Αβ peptides or to the excessive formation of Αβ peptides with increased tendency for aggregation i and copper ions may induce the aggregation of Αβ peptides and these ligands may act as seeding factors in the formation of amyloid plaques. Cu2+ and Zn2+ form complexes with Abeta peptides in vitro; however, the published metal-binding affinities of Abeta vary in an enormously large range. Authors studied the interactions of Cu2+ and Zn2+ with monomeric Abeta(40) under different conditions using intrinsic Abeta fluorescence and metal-selective fluorescent dyes. We showed that Cu(2+) forms a stable and soluble 1 : 1 complex with Abeta(40), however, buffer compounds act as competitive copper-binding ligands and affect the apparent K(D). Buffer-independent conditional K(D) for Cu(II)-Abeta(40) complex at pH 7.4 is equal to 0.035 micromol/L. Interaction of Abeta(40) with Zn2+ is more complicated as partial aggregation of the peptide occurs during zinc titration experiment and in the same time period (within 30 min) the initial Zn-Abeta(40) complex (K(D) = 60 micromol/L) undergoes a transition to a more tight complex with K(D) approximately 2 micromol/L. Competition of Abeta(40) with ion-selective fluorescent dyes Phen Green and Zincon showed that the K(D) values determined from intrinsic fluorescence of Abeta correspond to the binding of the first Cu2+ and Zn2+ ions to the peptide with the highest affinity. Interaction of both Zn2+ and Cu2+ ions with Abeta peptides may occur in brain areas affected by Alzheimer's disease and Zn2+-induced transition in the peptide structure might contribute to amyloid plaque formation. http://www3.interscience.wiley.com/cgi-bin

Green tea extract may lower blood pressure: study

Daily supplements of extracts from green tea (Camellia sinensis) may reduce blood pressure, cholesterol and markers of oxidative stress, and all within three weeks, says a new study. ...http://www.nutraingredients.com

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NP12 improves cognitive performance and reduces amyloid deposits

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Around 26 million people are affected by Alzheimer's disease worldwide, of which more than the half is entitled to seven major pharmaceutical markets (USA, Japan, Germany, UK, France, Italy and Spain). It is calculated that the number of AD sufferers worldwide will triple by the year 2050. The increase of the prevalence is a result of the progressive rise in life expectancy, the improvement in health care and diagnosis techniques.

Noscira, a company of Zeltia group devoted to the research and development of innovative drugs for the treatment of diseases of the nervous system, has received the approval of the Austrian health authorities and the Ethics Committee for the initiation of the first Phase II study with NP-12 for the treatment of Alzheimer's disease. NP-12, the first compound of Noscira's product pipeline, is an innovative drug of a new family of compounds. NP12 acts on the two main cellular processes that cause Alzheimer's disease, tau hyperphosphorylation and β-amyloid aggregation. Both in Alzheimer's disease and other neurodegenerative diseases, NP-12 may have a modifier and clinically relevant effect.

In Phase II clinical trials, NP12 will be administered to patients with Alzheimer's disease. Noscira is the only company in the world to have reached the clinical development stage with a compound for Alzheimer's disease, designed to inhibit the GSK3 enzyme. "This milestone reached by Noscira shows our progress in the search for new treatments, not only against cancer, through PharmaMar research activities, but also against other socially relevant diseases such as Alzheimer's disease" said Jose Maria Fernandez Sousa-Faro, President of Zeltia Group.

In words of Teodoro del Ser, Director of Clinical Development at Noscira, "We are pleased with the outcome of our work and with the efforts made at Noscira and we are confident that Phase II clinical trials results of NP12 will support our clinical expectations"

In animal models of Alzheimer's disease, it was demonstrated that NP12 improves cognitive performance and reduces amyloid deposits, hyperphosphorylation and tau aggregation, neuroinflammation and, most importantly, neuron loss, the ultimate cause of the clinical profile of progressive and widespread deterioration. Consistency of these findings supports the expectation that the compound may have a modifying effect of Alzheimer's disease when administered to patients. http://www.medicalnewstoday.com

Suck it and see: has the probiotic straw arrived?

The probiotic straw is a concept that has been a long time coming but one which may be about to move from its current niche status into the mainstream, according to Swedish probiotics supplier, BioGaia. ...http://www.nutraingredients.com

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2008

Amyloid beta clearance, transport and degradation

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Currently, the 'amyloid hypothesis' is the most widely accepted explanation for the pathogenesis of Alzheimer's disease (AD). According to this hypothesis, altered metabolism of the amyloid-beta (Abeta) peptide is central to the pathological cascade involved in the pathogenesis of AD. Although Abeta is produced by almost every cell in the body, a physiological function for the peptide has not been determined, and the pathways by which Abeta leads to cognitive dysfunction and cell death are unclear. Numerous therapeutic approaches that target the production, toxicity and removal of Abeta are being developed worldwide. Although therapeutic treatment for AD may be imminent, the value and effectiveness of such treatment are largely dependent on early diagnosis of the disease. This review summarizes current knowledge of Abeta clearance, transport and degradation, and evaluates the use of such information in the development of diagnostic tools. The conflicting results of plasma Abeta ELISAs are discussed, as are the more promising results of Abeta imaging by positron emission tomography. Current knowledge of Abeta-binding proteins and Abeta-degrading enzymes is analysed in the context of a potential therapy for AD. Transport across the blood-brain barrier by the receptor for advanced glycation end products and efflux via the multi-ligand lipoprotein receptor LRP-1 is also reviewed. Enhancing clearance and degradation of Abeta remains an attractive therapeutic strategy, and improved understanding of Abeta clearance may lead to advances in diagnostics and interventions designed to prevent or delay the onset of AD. Mol Psychiatry. 2008 Sep 16

Raw broccoli best for anti-cancer potential

Consuming cooked or processed broccoli may result in less of the potential anti-cancer compounds being available for absorption, suggests a new study from TNO Quality of Life. ...http://www.nutraingredients.com

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Aggregates of Amyloid beta induce neuronal cell cycle

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Neurons subject to degeneration in Alzheimer's disease (AD) exhibit evidence of re-entry into a mitotic cell cycle even before the development of substantial AD brain pathology. In efforts to identify the initiating factors underlying these cell cycle events , authors have characterized the appearance of the neuronal cell cycle events in the genomic-based transgenic mouse model of AD. Notably, the genomic-based transgenic mice exhibit neuronal cell cycle events in a reproducible temporal and spatial pattern that recapitulates the neuronal vulnerability seen in human AD. Neuronal cell cycle events first appear at 6 months in the frontal cortex layers II/III. This is 6-8 months before detectable amyloid beta (Abeta) deposition, suggesting that specific amyloid precursor protein (APP) processing products are responsible for the induction of neuronal cell cycle events. Furthermore, a reduction in the levels of Abeta dramatically delays the appearance of neuronal cell cycle events. More significantly, elimination of beta-secretase activity blocks the appearance of cell cycle events, providing direct genetic evidence that the amyloidogenic processing of APP is required for the induction of cell cycle events. Finally, in vitro preparations of oligomeric, but not monomeric, Abeta induce DNA synthesis in dissociated cortical neurons, and this response is blocked by antioligomer specific antibodies. Together, our data suggest that low molecular weight aggregates of Abeta induce neuronal cell cycle re-entry in mouse models of Alzheimer's disease. http://www.medicalnewstoday.com

Bilberry extract may ease the damages of stress: study

Extracts from bilberry may reduce stress-induced damage in the liver, according to a new study with mice. ...http://www.nutraingredients.com

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The development of AD therapeutics

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The past 25 years have seen an explosion of scientific investigations into the basic neurobiology of Alzheimer's disease (AD). At the same time, the gap between bench and bedside remains as vast as ever. Recent progress, however, has resulted in the development of novel, and in some cases, unconventional approaches for effective treatment. New therapies are currently undergoing preclinical investigation or are in clinical trial phase.

"The scientific community in general and the pharmaceutical industry in particular have invested heavily in just a few areas of AD therapeutics. The result is quite clear: symptomatic drugs are the best that can be offered to patients with this devastating disease," commented Dr. Chohan, Neuroimmunology Lab, Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities. "Despite the seemingly desperate state of affairs, we now see a steady influx of novel, unconventional therapeutic approaches."

Bringing together 14 contributions from worldwide experts, Dr. Chohan has assembled a two-part Special Issue. The first part concentrates mainly on preclinical studies and novel agents that are still in the experimental phase, while the second describes current clinical studies and some of the major issues involved.

The issue opens with a focus on immunotherapy. Einar Sigurdsson proposes active immunization against tau, while Michal Novak and his group elaborate on passive tau immunization. This is followed by an update on glycogen synthase kinase-3 (GSK-3) inhibitors by Daniel Perez and Anna Martinez, who lead a major AD clinical trial with a GSK-3 inhibitor. Although amyloid immunotherapy has been a particular focus of almost all large pharmaceutical efforts, there has been limited progress in that area. Beka Solomon proposes a completely novel approach based on phage-display technology which holds promise in amyloid-based vaccine development.

While there is growing literature on the involvement of oxidative stress in AD pathogenesis, clinical data have not shown substantial benefit from antioxidant agents. Two papers by Silvia Mandel and colleagues and Ashley Bush focus on a yet another novel approach: the role of metals and drugs based on the Metal Hypothesis. Kiminobu Sugaya and colleagues then discuss the promises and realities of cell replacement in the future of AD therapeutics. Finally, Antonio Cattaneo and colleagues discuss the potential of Nerve Growth Factor as a therapy for AD.

The development of AD therapeutics has been plagued with many failed and equivocal clinical trial outcomes. The second part of the special issue begins with a perspective from Saad Shafqat discussing the plight of dementia care in a developing country. This is followed by a series of stimulating analyses of current AD clinical trials both in the US and in Europe. First, Bruno Vellas and colleagues share their experience in the development of disease-modifying agents. Next, Robert Becker and colleagues and Cynthia Carlsson present an autopsy-style evaluation of failed AD clinical trials and make several important recommendations. Khalid Iqbal and colleagues wrap up the issue by discussing the multifactorial and heterogeneous nature of AD and the importance of patient stratification in the design of future clinical studies. http://www.medicalnewstoday.com (a special issue of the Journal of Alzheimer's Disease)

Lutein and zeaxanthin can benefit colon cancer, say researchers

Korean researchers have found alga-extracted carotenoids such as lutein and zeaxanthin can reduce colon cancer growths. ...http://www.nutraingredients.com

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Aβ Oligomers Induce Neuronal Cell Cycle Events in Alzheimer's

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Amyloid plaques are the defining characteristic of Alzheimer's disease (AD), but several studies suggest that soluble amyloid protein is more damaging to neurons. In fact, many signs of neurodegeneration occur before amyloid plaques appear. One such sign is neuronal re-entry into the cell cycle, which occurs in several neurodegenerative diseases. In humans with mild cognitive impairment, DNA replication and expression of cell cycle proteins (e.g., cyclins) appear in brain regions that undergo neurodegeneration in AD. Using transgenic mouse models of AD, Varvel et al. found that cyclins were expressed in frontal cortex many months before plaques appeared, and they were expressed even in mice that never develop plaques. Cyclin expression was prevented by blocking the abnormal processing of amyloid precursor protein that produces amyloid β. Furthermore, amyloid oligomers triggered DNA replication and cyclin expression in primary cortical neurons in vitro, indicating that this early characteristic of degeneration is triggered by soluble amyloid. http://www.medicalnewstoday.com

EFSA says yes to calcium

The latest batch of European Food Safety Authority (EFSA) opinions has surfaced with the assessor giving the thumbs up to three claims revolving around calcium, vitamin D and bone health. ...http://www.nutraingredients.com

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Statin therapy provides benefit in individuals with Alzheimer's

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Alzheimer's disease (AD) is the leading cause of dementia in the elderly, afflicting an estimated 4.5 million people in the U.S. Nymox Pharmaceutical Corporation holds U.S. and global patent rights for the use of statin drugs for the prevention and treatment of AD, including for patients at risk for AD because of vascular-related risk factors or disease. An important new study has found that ongoing statin drug use was associated with a 67% reduction in the risk of AD. The authors concluded that the "data suggest that statins produce a significant reduction in the risk of AD."

In the study, 2,233 people aged 70 years or older from six U.S. centers were followed for 4 years with annual assessments of cognitive changes. Subjects with suspected cognitive decline were referred for an in-depth evaluation for dementia and AD diagnosis. The study also tracked the use of statin and other cholesterol-lowering agents. Subjects who were taking statin drugs were found to have a statistically significant 67% reduction in the risk of AD.

The study authors also reviewed the other published studies assessing the effect of statin use on later risk of AD in the elderly and noted that 13 out of 15 of these studies had reported reduced risk for AD associated with cholesterol-lowering therapy. They concluded: "Overall, the evidence, with limited exceptions, suggests that statin therapy provides some level of benefit in treating individuals with AD, and prior statin use may reduce the risk of AD later in life."

Statins are widely used cholesterol-lowering drugs with a well-established track record of safety. They have an estimated global market over $25 billion and represent a potential new way of treating or preventing AD. Statin drug use has been shown to be associated with a lower risk of neuropathological changes in the brain of AD.

This press release contains certain "forward-looking statements" as defined in the United States Private Securities Litigation Reform Act of 1995 that involve a number of risks and uncertainties. There can be no assurance that such statements will prove to be accurate and the actual results and future events could differ materially from management's current expectations. The conduct of clinical trials and the development of drug products involve substantial risks and uncertainties and actual results may differ materially from expectations. Promising early results do not ensure that later stage or larger scale clinical trials will be successful or will proceed as expected. Such factors are detailed from time to time in Nymox's filings with the United States Securities and Exchange Commission and other regulatory authorities. http://www.medicalnewstoday.com

Tart cherries can reduce ‘belly fat’: rat study

Tart cherries, a relatively new entrant to the superfruit category, have been shown to benefit heart health as well as body weight, in a study on obese rats.

...http://www.nutraingredients.com

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Specific fatty acids may contribute to Alzheimer's

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US scientists working with laboratory mice have discovered that complete or partial removal of an enzyme that regulates fatty acid levels lessened the memory and learning deficits of Alzheimer's and could one day lead to a new treatment for the neurodegenerative disease in humans. The research was conducted by scientists at the Gladstone Institute of Neurological Disease (GIND) in San Francisco, California, the University of California San Francisco (UCSF), and other research centres in the US, and was published in the 19 October advanced online issue of Nature Neuroscience. The researchers said they found specific fatty acids that may contribute to Alzheimer's and this could open a door to a new kind of treatment.


GIND director and senior author of the study, Dr Lennart Mucke said: "Several different proteins have been implicated in Alzheimer's disease, but we wanted to know more about the potential involvement of lipids and fatty acids." The brain takes up fatty acids and incorporates them into phospholipids, a type of fat that makes up the membrane that surrounds cells and protects them from the external environment. Using large scale profiling of fatty acids, an approach known as "lipidomics", Mucke and colleagues compared the fatty acids in the brains of normal mice with mice genetically bred to have a condition with physiological and memory symptoms similar to Alzheimer's in humans.

Lead author Dr Rene Sanchez-Mejia said: "The most striking change we discovered in the Alzheimer mice was an increase in arachidonic acid and related metabolites in the hippocampus, a memory center that is affected early and severely by Alzheimer's disease. Arachidonic acid likely wreaks havoc in the Alzheimer mice by causing too much excitation, which makes neurons sick. By lowering arachidonic acid levels, we are allowing neurons to function normally." Sanchez-Mejia said that a lot more work was needed before a treatment based on regulating fatty acid levels, for example by diet or drugs, could be proven in humans, and the study's main contribution was it showed that "inhibition of PLA2 activity might help prevent neurological impairments in Alzheimer's disease".

Scientists already knew that an enzyme called group IVA phospholipase A2 (or PLA2) released arachidonic acid from phospholipids in the brain, so Mucke and colleagues lowered the levels of PLA2 in the Alzheimer mice by genetic engineering to see what happened. They found that either removal or even partial reduction of PLA2 prevented memory and learning deficits and other behavioural abnormalities in the Alzheimer mice.

Rebecca Wood, Chief Executive of the Alzheimer's Research Trust in the UK, where there are 700,000 people living with Alzheimer's, said the study gave: "Cause for cautious optimism, as fatty acid levels can be controlled to some extent by diet and drugs. However, it is not yet clear if these findings are applicable to humans, and a lot more research is needed before any human trials can be conducted. The Alzheimer's Research Trust is funding several projects in this area," added Wood. http://www.medicalnewstoday.com

Yoghurt can benefit bladder cancer, say researchers

Two servings of yoghurt per day can reduce the risk of developing bladder cancer by up to 40 per cent, say Swedish scientists. ...http://www.nutraingredients.com

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Amyloid plaques are the direct cause of Alzheimer's

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Amyloid precursor protein (APP), whose cleavage product, amyloid-b (Ab), builds up into fibrous plaques in the brains of Alzheimer's disease patients, jumps from one specialized membrane microdomain to another to be cleaved, report Sakurai et al.

Although there is no definitive evidence that Ab plaques are the direct cause of Alzheimer's disease, there is much circumstantial evidence to support this. And working on this hypothesis, scientists are investigating just how the plaques form and what might be done to stop or reverse their formation. APP, a protein of unknown function, is membrane associated and concentrates at the neuronal synapse. Certain factors such as high cellular cholesterol and increased neuronal or synaptic activity are known to drive APP cleavage, and Sakurai and colleagues' paper pulls these two modes of Ab regulation together.

APP associates with membrane microdomains high in cholesterols (lipid rafts). These lipid rafts can also contain the enzyme necessary for APP cleavage, BACE. Synaptic activity is known to involve a very different type of membrane microdomain high in an excytosis-promoting factor called syntaxin. Sakurai et al. now show that although APP preferentially associates with syntaxin microdomains, upon neuronal stimulation APP instead associates with microdomains that contain BACE.

It's unclear why APP should be associated with syntaxin, though it might suggest a role for APP in vesicle trafficking and exocytosis. Also unclear is why neuronal activity should cause APP to jump from syntaxin domains to BACE domains. What is clear, however, is that the process is an active one, requiring a kinase called cdk5. Furthermore, treating neurons with a cdk5 inhibitor called roscovitine, which is currently in trials for cancer treatment, reduced APP's association with BACE microdomains and reduced APP cleavage. http://www.medicalnewstoday.com

Doctors advise more vitamin D for infants

The American Academy of Pediatrics has doubled its advice on... ...http://www.nutraingredients.com

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Arachidonic acid likely wreaks havoc in the Alzheimer

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Scientists at the Gladstone Institute of Neurological Disease (GIND) and the University of California have found that complete or partial removal of an enzyme that regulates fatty acid levels improves cognitive deficits in a mouse model of Alzheimer's disease (AD). Their findings, which will be published in today's issue of Nature Neuroscience, identified specific fatty acids that may contribute to the disease as well as a novel therapeutic strategy.

AD causes a progressive loss of cognitive functions and results in death. Over 5 million Americans are living with this condition. Although there are treatments to ease the symptoms, these treatments are not very effective and researchers have yet to discover a cure. "Several different proteins have been implicated in Alzheimer's disease," said Lennart Mucke, M.D., GIND director and senior author of the study, "but we wanted to know more about the potential involvement of lipids and fatty acids."

Fatty acids are rapidly taken up by the brain and incorporated into phospholipids, a class of fats that form the membrane or barrier that shields the content of cells from the external environment. The scientists used a large scale profiling approach ("lipidomics") to compare many different fatty acids in the brains of normal mice with those in a mouse model of Alzheimer's disease that develops memory deficits and many pathological alterations seen in the human condition. "The most striking change we discovered in the Alzheimer mice was an increase in arachidonic acid and related metabolites in the hippocampus, a memory center that is affected early and severely by Alzheimer's disease," said Rene Sanchez-Mejia, M.D., lead author of the study.

In the brain arachidonic acid is released from phospholipids by an enzyme called group IVA phospholipase A2 (or PLA2). The scientists lowered PLA2 levels in the Alzheimer mice by genetic engineering. Removal or even partial reduction of PLA2 prevented memory deficits and other behavioral abnormalities in the Alzheimer mice.

"Arachidonic acid likely wreaks havoc in the Alzheimer mice by causing too much excitation, which makes neurons sick. By lowering arachidonic acid levels, we are allowing neurons to function normally," said Dr. Sanchez-Mejia. Dr. Mucke added, "in general, fatty acid levels can be regulated by diet or drugs. Our results have important therapeutic implications because they suggest that inhibition of PLA2 activity might help prevent neurological impairments in Alzheimer's disease. But a lot more work needs to be done before this novel therapeutic strategy can be tested in humans." http://www.medicalnewstoday.com

Science: The wider impacts of gut health

In the final part of our gut health series, NutraIngredients.com reviews the science behind the ‘friendly bacteria’ and the prebiotics fibres that ‘fuel’ them. ...http://www.nutraingredients.com

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People with more education and mentally demanding have protection against Alzheimer's

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People with more education and more mentally demanding occupations may have protection against the memory loss that precedes Alzheimer's disease, according to a study published in the October 21, 2008, issue of Neurology®, the medical journal of the American Academy of Neurology. The study involved 242 people with Alzheimer's disease, 72 people with mild cognitive impairment, and 144 people with no memory problems. Mild cognitive impairment is a transition stage when some memory problems are occurring beyond what is normal for a person's age but not the serious problems of Alzheimer's disease.

Researchers tested the participants' memory and cognitive skills and used brain scans to measure the amount of brain glucose metabolism, which shows how much the brain has been affected by the plaques and tangles of Alzheimer's disease. The participants were followed for an average of 14 months. During that time, 21 of the people with mild cognitive impairment developed Alzheimer's disease.

The study found that in people with the same level of memory impairment, people with more education and more mentally demanding jobs had significantly more changes and damage in their brains from Alzheimer's disease than people with less education and less mentally demanding jobs. "The theory is that education and demanding jobs create a buffer against the effects of dementia on the brain, or a cognitive reserve," said study author Valentina Garibotto, MD, of the San Raffaele University and Scientific Institute and the National Institute of Neuroscience in Milan, Italy. "Their brains are able to compensate for the damage and allow them to maintain functioning in spite of damage. There are two possible explanations. The brain could be made stronger through education and occupational challenges. Or, genetic factors that enabled people to achieve higher education and occupational achievement might determine the amount of brain reserve. It isn't possible to determine which accounts for our findings."

The results were found in both people with Alzheimer's and people with mild cognitive impairment who developed Alzheimer's during the study, suggesting that the cognitive reserve is already in effect during the mild cognitive impairment phase before Alzheimer's begins, Garibotto said. People with Alzheimer's disease and people with mild cognitive impairment who developed Alzheimer's during the study had metabolic dysfunction in the areas of the brain consistent with Alzheimer's disease, whereas the healthy people and those with mild cognitive impairment who did not develop Alzheimer's disease had no brain metabolism problems.
http://www.medicalnewstoday.com

Science: The wider impacts of gut health

In the final part of our gut health series, NutraIngredients.com reviews the science behind the ‘friendly bacteria’ and the prebiotics fibres that ‘fuel’ them. ...http://www.nutraingredients.com

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A reduction in high blood pressure because of cognitive decline

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A new study published in Bioscience Hypotheses, a recently launched Elsevier journal, proposes that some people suffering from Alzheimer's disease experience a reduction in their high blood pressure because of cognitive decline.

Publications relating to dementia and blood pressure have been reviewed by the paper's author Dr Sven Kurbel of the Osijek Medical Faculty in Croatia. The cognitive problems suffered by some Alzheimer's patients have previously been put down to low blood pressure (arterial hypotension). The hypothesis put forward by Dr Kurbel is that the opposite is true. He suggests that as the patient's memory fails, they forget the causes of anxiety and worry that was causing high blood pressure: failing memory causes hypotension, not vice versa.

Hypertension itself is a cause of disease, including strokes, so paradoxically, Dr. Kurbel's hypothesis suggests, treatments which alleviate memory loss could affect other causes of illness. If this hypothesis is correct it could have a significant effect on the treatment of conditions such as metabolic syndrome, which involves increased weight and high blood pressure. Dr. Kurbel concludes that "An important question is would reduction of stressful memories and of stress exposure in everyday life help diminish the risk of getting hypertension or metabolic syndrome in the years to come."

If confirmed by further studies, this will affect how doctors treat the elderly, helping to target drugs more effectively and reduce risks of stokes and heart attack It also suggests that heart disease could be substantially reduced in old people simply by making them happier about themselves and their lives.

Dr. William Bains, editor of Bioscience Hypotheses, said "This is a fascinating piece of lateral thinking, one with real health implications, and just the sort of stimulating, practical idea that we hoped Bioscience Hypotheses would be able to publish for other scientists to think about". http://www.medicalnewstoday.com

Science: The wider impacts of gut health

In the final part of our gut health series, NutraIngredients.com reviews the science behind the ‘friendly bacteria’ and the prebiotics fibres that ‘fuel’ them. ...http://www.nutraingredients.com

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Vitamin B: No Cognitive Decline In Alzheimer's

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A clinical trial led by Paul S. Aisen, M.D., professor of neurosciences at the University of California, San Diego School of Medicine, showed that high-dose vitamin B supplements did not slow the rate of cognitive decline in patients with mild to moderate Alzheimer disease. The study will be published in the October 15 issue of the Journal of the American Medical Association (JAMA).

Aisen is director of the Alzheimer's Disease Cooperative Study (ADCS), a multi-center network spanning the United States and Canada, which conducted the clinical trial to determine if reduction of an amino acid called homocysteine would reduce the risk of Alzheimer's disease or slow its progression. Homocysteine is known to be involved in neurological disease, including Alzheimer's, and its metabolism is affected by B vitamins. Therefore, it was thought that B vitamin supplements might offer a new therapeutic approach in treating Alzheimer' disease.

"Prior studies using B vitamin supplementation to reduce homocysteine levels in patients with Alzheimer's weren't large enough, or of long enough duration to effectively assess their impact on cognitive decline," said Aisen. "This study of several hundred individuals over the course of 18 months showed no impact on cognition, although it resulted in lower levels of homocysteine in these patients."

The study included supplementation with folic acid and vitamins B6 and B12 for 18 months in 409 individuals with mild to moderate Alzheimer's disease. Participants were randomly assigned to two groups of unequal size; to increase enrollment, 60 percent were treated with high-dose supplements and the remaining 40 percent treated with identical dosages of placebo. A total of 340 participants (202 in active treatment group and 138 in placebo group) completed the trial while taking study medication. Cognitive abilities were measured via testing with the Alzheimer Disease Assessment Scale (ADAS-cog).

The researchers found that the ADAS-cog score did not differ significantly between treatment groups, but that symptoms of depression were more common in the high-dose supplement group. "Our study does not support the treatment of individuals with mild to moderate Alzheimer's disease and normal vitamin levels with B vitamin supplements," the authors conclude. http://www.medicalnewstoday.com

Apples and onions may protect athletes from flu: Study

Quercetin, the compound most commonly associated with onions, may boost the immune system and protect against flu, according to results of a study with mice. ...http://www.nutraingredients.com

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Alzheimer

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