We can reduce our chances of developing dementia

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A 60-year-old who is overweight/obese has more than twice the chance of developing dementia by the time he/she is 75 compared to a 60-year-old of normal weight. As rates of obesity in the United Kingdom rise alarmingly, it is possible the country may have 2.5 million people suffering from dementia by the middle of the century. Currently, about 700,000 people suffer from dementia/Alzheimer's disease in the UK.

According to the Alzheimer's Society (UK), there is a lot we can do to reduce our chances of developing dementia later in life. If dementia were delayed by five years, the total number of death from dementia would halve, says the Society.

According to Neil Hunt, chief executive of the Alzheimer's Society, "Over 100 000 people in the UK develop dementia each year. Evidence has shown that a healthy lifestyle can reduce your risk…we are encouraging people to Be Headstrong and challenge their risk of dementia. We must start to tackle dementia head on, even delaying dementia by five years will halve the number of deaths in the UK."

Professor Clive Ballard, director of research at Alzheimer's Society, said "We are only beginning to see how much a healthy lifestyle can reduce your risk of dementia. Some studies show that obesity can double your risk while a Mediterranean diet can lower your risk by as much as 40 per cent. It's time to act now to slow the rising tide of dementia."


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Low intake of vitamin B6 may increase a man's risk of colorectal cancer by 31 per cent, suggests a study from Japan.

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The many positive impacts of omega-3 fatty acids

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Omega-3 fatty acids were again proven to help serious symptoms coinciding with the memory decline characteristic for Alzheimer's disease, according to a recent study conducted by Yvonne Freund-Levi, M.D. from Sweden's Karolinska Institute. EPAX AS, a world-leading supplier of highly concentrated omega-3 EPA/DHA fatty acids, confirmed its EPAX 1050 TG oil was used in the study. Recently published in the International Journal of Geriatric Psychiatry, Freund-Levi's study was a randomised, double-blind, placebo-controlled clinical trial. It showed that carriers of a specific gene common to those with Alzheimer's disease who received the omega-3 supplements responded positively to the omega-3s in regards to agitation symptoms. Those without the gene showed an improvement in symptoms of depression.

"These findings are surely encouraging to the millions of people affected by Alzheimer's disease. This study helps demonstrate the many positive impacts of omega-3 fatty acids, whether one has specific health concerns or is simply looking to stay healthy. We are pleased that EPAX could play a role in this impressive clinical trial," said Bjorn Refsum, CEO of EPAX AS. A previous study, published in the Oct. 2006 issues of Archives of Neurology, conducted by Freund-Levi found that patients with early-stage Alzheimer's disease given EPAX 1050 TG omega-3 fatty acids showed significant improvement in memory decline compared to the control group.

EPAX 1050 TG is specially formulated for cognitive health. All of EPAX's oils are indication-specific and in addition to cognitive health, oils are available to address cardiovascular health, mood and mind health, joint health, pre-and post-natal health and weight management.

Probiotics may cut diarrhoea amongst the elderly
Probiotic-containing drinks may help reduce diarrhoea among older people receiving antibiotics, reports new research that could offer savings to public health services.

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Accera is developing the AD drug

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Accera, Inc. announced today that recent data from its Phase IIb study in Alzheimer's disease (AD) support findings showing that AD may effectively be thought of and treated as diabetes of the brain.

AD is widely believed to be caused by the accumulation of amyloid beta plaques in the brain, yet recent research from Brown University has shown that inducing insulin resistance in the brains of mice gives rise to some of the behavioral and pathological symptoms of AD. AD may therefore be thought of as brain-specific "type 3 diabetes," an idea that is further supported by brain images of AD patients showing decreased glucose metabolism.

All cells in the body require glucose, which is controlled with the aid of the hormone insulin. In type 2 diabetes, which accounts for 90% of the 180 million diabetes cases worldwide according to the World Health Organization, certain cells become resistant to insulin and therefore cannot take in enough glucose. When brain cells become insulin-resistant, as happens in AD, inadequate glucose leads to damage that results in impaired memory and cognition and brain shrinkage.

Because these metabolic defects in the brain often appear 10 to 20 years earlier than other AD symptoms, targeting them may allow for earlier treatment of the disease. Based on this hypothesis, Accera is developing the AD drug, Ketasyn(TM) (AC-1202), which provides glucose-deprived brain cells with an alternative energy source. Ketasyn is converted by the liver into ketone bodies, which brain cells can use for energy even when their ability to metabolize glucose is impaired.

Long-term vision for vitamin C and diabetic eye health?
Long-term supplementation with vitamin C may one day help prevent...

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Accera is developing the AD drug

.
Alzheimer's Donation
Donate Online Now
.

Accera, Inc. announced today that recent data from its Phase IIb study in Alzheimer's disease (AD) support findings showing that AD may effectively be thought of and treated as diabetes of the brain.

AD is widely believed to be caused by the accumulation of amyloid beta plaques in the brain, yet recent research from Brown University has shown that inducing insulin resistance in the brains of mice gives rise to some of the behavioral and pathological symptoms of AD. AD may therefore be thought of as brain-specific "type 3 diabetes," an idea that is further supported by brain images of AD patients showing decreased glucose metabolism.

All cells in the body require glucose, which is controlled with the aid of the hormone insulin. In type 2 diabetes, which accounts for 90% of the 180 million diabetes cases worldwide according to the World Health Organization, certain cells become resistant to insulin and therefore cannot take in enough glucose. When brain cells become insulin-resistant, as happens in AD, inadequate glucose leads to damage that results in impaired memory and cognition and brain shrinkage.

Because these metabolic defects in the brain often appear 10 to 20 years earlier than other AD symptoms, targeting them may allow for earlier treatment of the disease. Based on this hypothesis, Accera is developing the AD drug, Ketasyn(TM) (AC-1202), which provides glucose-deprived brain cells with an alternative energy source. Ketasyn is converted by the liver into ketone bodies, which brain cells can use for energy even when their ability to metabolize glucose is impaired.

Long-term vision for vitamin C and diabetic eye health?
Long-term supplementation with vitamin C may one day help prevent...

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The first phase of human clinical trials for a beta-secretase inhibitor

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"Millions of people suffer from this devastating disease and treatment options are very limited," said Arun Ghosh, the Purdue professor who led the creation of the treatment molecule. "Current drugs manage the symptoms, but this could be the first disease-modifying therapy. It may be able to prevent and reverse the disease."

A drug based on the design of a Purdue University researcher to treat Alzheimer's disease began the first phase of human clinical trials this week. CoMentis Inc., a biopharmaceutical company based in San Francisco, is initiating the clinical trials of the experimental drug CTS-21166. Ghosh, who has dual appointments in the departments of chemistry and medicinal chemistry, is a scientific co-founder of the company with Jordan Tang, the J.G. Puterbaugh Chair in Medical Research at the Oklahoma Medical Research Foundation.

The collaborative work of Ghosh and Tang led to the development of a treatment that could intercept and disable the disease at an early stage. In 2000, Tang identified beta-secretase, a key enzyme in the progression of Alzheimer's that triggers the formation of amyloid plaques in the brain. Various stages in plaque formation produce toxic proteins that harm the brain, causing damage that eventually leads to dementia. Later that year, Ghosh built a molecule that binds to this key enzyme and inhibits its activity, a beta-secretase inhibitor.

"These molecules fit together like puzzle pieces," Ghosh said. "We created a molecule that fits with a key piece of the Alzheimer's disease puzzle. When the treatment molecule binds to the enzyme, it changes the shape of that puzzle piece so that it no longer fits in its original spot. This halts the chain reaction that leads to the devastating symptoms of Alzheimer's disease." Since 2000, Ghosh has been leading the structure-based design of beta-secreatase inhibitors for therapeutic intervention of Alzheimer's disease. His most recent work was published in the May 17 issue of the Journal of Medicinal Chemistry. Ghosh also helped direct CoMentis in the generation of beta-secretase inhibitor drugs. The treatment molecule, beta-secretase inhibitor CTS-21166, is the culmination of this work. "The molecule is both highly potent and highly selective, meaning it does not appear to affect other enzymes important to brain function or cause harmful side effects," Ghosh said. "It took years of work and evaluation of hundreds of molecules to achieve one with the strength and safety necessary for clinical potential."

The trial, comprised of 48 healthy volunteers, will measure safety, tolerability and pharmacokinetics of CTS-21166 at various doses. The company expects to begin generating human clinical data by the end of 2007 and to begin phase II studies in Alzheimer's patients in 2008. The drug could be administered at any stage of the disease, Ghosh said. These clinical trial phases are the first steps in a lengthy process necessary before the Food and Drug Administration approves a drug to be available on the market.

Blueberries may reduce Alzheimer risk
Eating a diet rich in blueberries may reduce the severity of neurodegenerative diseases such as Alzheimer's or cognitive disorders relating to ageing, if results from an animal study can be translated into humans.

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