Glucose metabolism and progressive Alzheimer's

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Region specific declines in the cerebral glucose metabolism are an early and progressive feature of Alzheimer's disease (AD). Such declines occur pre-symptomatically and offer a potential point of intervention in developing AD therapeutics. Medium chain triglycerides (MCTs), which are rapidly converted to ketone bodies, were tested for their ability to provide an alternate energy source to neurons suffering from compromised glucose metabolism. The present study determined the short-term effects of ketosis in aged dogs, a natural model of amyloidosis. The animals were administered a 2 g/kg/day dose of MCTs for 2 months. Mitochondrial function and oxidative damage assays were then conducted on the frontal and parietal lobes. Amyloid-beta (Abeta), amyloid precursor protein (APP) processing and beta-site APP cleaving enzyme (BACE1) assays were conducted on the frontal, parietal and occipital lobes. Aged dogs receiving MCTs, as compared to age-matched controls, showed dramatically improved mitochondrial function, as evidenced by increased active respiration rates. This effect was most prominent in the parietal lobe. The improved mitochondrial function may have been due to a decrease in oxidative damage, which was limited to the mitochondrial fraction. Steady-state APP levels were also decreased in the parietal lobe after short-term MCT administration. Finally, there was a trend towards a decrease in total Abeta levels in the parietal lobe. BACE1 levels remained unchanged. Combined, these findings suggest that short-term MCT administration improves energy metabolism and decreases APP levels in the aged dog brain. ...http://www.ncbi.nlm.nih.gov

Blending cardiology with cooking

If heart healthy jambalaya sounds too good to be true, think again. Careful selection of ingredients can make any food heart healthy, without affecting the flavor, says Dr Richard Collins, MD, the Cooking Cardiologist. ...http://www.nutraingredients.com

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Alzheimers's disease: memory deficits - loss of dendritic spines?

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Using new scientific techniques, scientists have unlocked the cascade of molecular events that lead to Alzheimer's disease. The scientific findings published in the latest edition of Nature Medicine suggest a potential new target for the development of drug therapies to fight the irreversible and degenerative disease which affects some 29.8 million people worldwide. The total worldwide societal cost of dementia was estimated at somewhere in the region of US$315.4 billion in 2005.

Alzheimer's disease is marked by the build-up of plaques consisting of beta-amyloid protein fragments, as well as abnormal tangles of tau protein found inside brain cells. Early in the disease, Alzheimer's pathology is first observed in the hippocampus, the part of the brain important to memory, and gradually spreads to the cerebral cortex, the outer layer of the brain.

The team of Irish and international researchers have identified that the accumulation of a particular protein (called amyloid ß-protein - Aß) in the brain initiates Alzheimer's disease and that it directly alters the structure and function of brain cells. The findings place a significant emphasis on the development of new therapeutic strategies targeted at the reduction of the formation of Aß as opposed to the reduction of the plaque burden associated with the disease.

"Alzheimer's disease is a major personal and societal tragedy," says Professor Ciaran Regan from the UCD School of Biomolecular and Biomedical Science, University College Dublin, one of the co-authors of the report. "The disease progression is torturously long and debilitating, extorting a huge emotional and economic cost. The onset of the disease is insidious with the earliest symptoms often manifested as subtle and intermittent deficits of episodic memory," explains Professor Dominic Walsh, associate Professor of Pharmacology at the UCD Conway Institute, University College Dublin, another co-author of the report. "Our findings support the growing theory that Alzheimers's disease memory deficits may result from loss of dendritic spines and that this process is mediated by amyloid ß protein (Aß) oligomers, not monomer or plaque Aß as previously considered." ...http://www.medicalnewstoday.com

Zeaxanthin science fails safe supplements use

The use of rising eye health phytonutrient, zeaxanthin, in food supplements in doses of up to 20mg has been rejected by the European Food Safety Authority (EFSA). ...http://www.nutraingredients.com

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Intracellular calcium signaling may play a role in AD

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A new study uncovers a mechanism that directly links mutations that cause early onset Alzheimer's disease (AD) with aberrant calcium signaling.

AD is a devastating neurodegenerative disease that affects early 18 million people in the world. Most cases of AD occur spontaneously after the age of 60 but about 10% of cases are inherited and can develop decades earlier. Early onset familial AD (FAD) is caused by mutated amyloid precursor protein, which can lead to aggregation of sticky clumps of amyloid beta protein in the brain, and mutated presenilins (PS), enzymes which have been implicated in amyloid processing.

Recent research has also linked mutant PS expression with exaggerated intracellular calcium release in several model systems, including cells from FAD patients. The research, published by Cell Press in the June 26th issue of the journal Neuron, provides exciting molecular insights into the pathology of AD and may lead to new treatment strategies. "Accumulating evidence suggests that sustained disruption of intracellular calcium signaling may play an early role in AD pathogenesis," says study author Dr. J. Kevin Foskett from the University of Pennsylvania. Calcium plays a central role in many aspects of brain physiology including growth, plasticity and learning and memory as well as cell death and degeneration.

Dr. Foskett and colleagues found that biochemical interactions of FAD mutant PS with an intracellular calcium release channel, called inositol trisphosphate receptor (InsP3R), profoundly increased channel activity in a manner that could account for exaggerated calcium responses in cells exposed to normal stimulation and caused low level calcium signaling in unstimulated cells. The researchers went on to show that this enhancement of channel activity was directly involved in mutant PS-mediated amyloid beta generation, a hallmark of AD.

"We have discovered a mechanism that can account for altered calcium signaling in AD cells that involves a biochemical and functional interaction of FAD mutant PS with the InsP3R calcium release channel. These observations provide unique molecular insights into the calcium dysregulation hypothesis of AD pathogenesis and they suggest novel targets for therapeutic intervention," concludes Dr. Foskett.

In a related finding, published in the June 27th issue of the journal Cell, abnormal calcium signaling was also linked to the more common spontaneously occurring form of AD. In this study, Dr. Fabien Campagne from Weill Medical College, Dr. Philippe Marambaud from Albert Einstein College of Medicine and their colleagues discovered a mutation associated with late onset, sporadic AD that disrupted a previously uncharacterized brain calcium channel and led to subsequent accumulation of amyloid beta protein. Therefore, disregulation of intracellular calcium levels appears to play a role in both sporadic and hereditary AD. ...http://www.medicalnewstoday.com

Aloe vera thriving despite lack of science

The adage goes that if an ingredient is to gain favour with food and supplement makers as well as the public it should first get its scientific house in order. ...http://www.nutraingredients.com

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A more effective alternative to current Alzheimer's therapies

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Brain destruction in Alzheimer's disease is caused by the build-up of a protein called amyloid beta in the brain, which triggers damaging inflammation and the destruction of nerve cells. One in three people who live to be over 65 will end their lives with a form of dementia. 700,000 people in the UK have a form of dementia, more than half have Alzheimer's disease. In less than 20 years nearly a million people will be living with dementia. This will soar to 1.7 million people by 2051. 1 in 6 people over 80 have dementia.

Scientists had previously shown that preventing individual amyloid beta proteins from sticking to one another minimized brain lesions and protected nerve cells against damage.

The new study - a collaborative effort by researchers in Germany and the US - shows that an anti-inflammatory drug (called CNI-1493) may have the same effect. The drug - already tested in humans for the treatment of inflammatory diseases - protected nerve cells against amyloid beta-induced damage in culture. In mice prone to developing an Alzheimer's-like disease, the drug decreased brain inflammation and improved memory and cognitive function.

Other anti-inflammatory drugs, such as ibuprofen, have been shown to reduce Alzheimer's disease lesions in the brains of rodents, but CNI-1493 appears to be faster and more effective. If these results hold up in humans, CNI-1493 may provide a more effective alternative to current Alzheimer's therapies, which temporarily prolong the function of nerve cells but do not prevent their destruction. ...http://www.medicalnewstoday.com

Omega-3 ALA: Industry reacts to review

Following publication of a review that said the omega-3 from plant sources, alpha-linolenic acid (ALA), has been overlooked and misunderstood, industry sources have reacted.

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

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A more accurate diagnosis of Alzheimer's disease

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An automated system for measuring brain tissue with magnetic resonance imaging (MRI) can help physicians more accurately diagnose Alzheimer's disease at an earlier stage according to a new study published in the July issue of the journal Radiology.

In Alzheimer's disease, nerve cell death and tissue loss cause all areas of the brain, especially the hippocampus region, to shrink. MRI with high spatial resolution allows radiologists to visualize subtle anatomic changes in the brain that signal atrophy, or shrinkage. But the standard practice for measuring brain tissue volume with MRI, called segmentation, is a complicated, lengthy process. "Visually evaluating the atrophy of the hippocampus is not only difficult and prone to subjectivity, it is time-consuming," explained the study's lead author, Olivier Colliot, Ph.D, from the Cognitive Neuroscience and Brain Imaging Laboratory in Paris, France. "As a result, it hasn't become part of clinical routine."

In the study, the researchers used an automated segmentation process with computer software developed in their laboratory by Marie Chupin, Ph.D., to measure the volume of the hippocampus in 25 patients with Alzheimer's disease, 24 patients with mild cognitive impairment and 25 healthy older adults. The MRI volume measurements were then compared with those reported in studies of similar patient groups using the visual, or manual, segmentation method. The researchers found a significant reduction in hippocampal volume in both the Alzheimer's and cognitively impaired patients when compared to the healthy adults. Alzheimer's patients and those with mild cognitive impairment had an average volume loss in the hippocampus of 32 percent and 19 percent, respectively. Studies using manual segmentation methods have reported similar results. "The performance of automated segmentation is not only similar to that of the manual method, it is much faster," Dr. Colliot said. "It can be performed within a few minutes versus an hour."

According to the Alzheimer's Association, more than five million Americans currently have Alzheimer's disease. One of the goals of modern neuroimaging is to help in the early and accurate diagnosis of Alzheimer's disease, which can be challenging. When the disease is diagnosed early, drug treatment can help improve or stabilize patient symptoms. "Combined with other clinical and neurospychological evaluations, automated segmentation of the hippocampus on MR images can contribute to a more accurate diagnosis of Alzheimer's disease," Dr. Colliot said. ...http://www.medicalnewstoday.com

Solutions abound for polyphenol-fortified milk

Adding fruit flavours and cyclodextrin to milk may boost consumer acceptance of polyphenol-enriched dairy, without the need for added sugar, report New Zealand scientists.

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

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