Tendulkar dedicates his 44th ODI century to Dungarpur

Mumbai, Sep. 16 (ANI): Condoling the death of former BCCI chairmen Raj Singh Dungarpur, master blaster Sachin Tendulkar dedicated his 44th ODI century to the man who selected him for international cricket in 1989.

“Wherever Rajbhai is he was definitely watching us yesterday and feeling happy for Indian team for having won yesterday. I’d like to take this opportunity to say that yesterday’s 100 was for Raj Bhai. We miss you Rajbhai,” Tendulkar said.

Dungarpur, 73, was suffering from Alzheimer’s and had died on Saturday.

Dugarpur belonged to the Dungarpur royal family and also played first class cricket for Rajasthan.

Tendulkar urged officials of Cricket Club of India, where Dungarpur played and also presided as president for almost a decade and a half, to name one of its gate after him.

“I know that here, CCI have named rooms after the ex-cricketers, the library is also named after a cricketer. Just like Prof. Shetty, I would like to request the management of CCI, I think the appropriate thing to do would be to name the main gate after Rajbhai because that is where I think is the right place for Rajbhai and I would strongly urge that,” said Tendulkar.

Veteran cricketers, Bapu Nadkarni, Dilip Vengsarkar, Sandeep Patil, Karsan Ghavri, Balwinder Singh Sandhu, Milind Rege and Ajit Agarkar were also present at the condolence meeting. (ANI)

Here’s what ups amyloid beta production in Alzheimer’s patients’ brains

Washington, September 4 (ANI): A new class of medicines to effectively treat Alzheimer’s disease may soon be available, for an international research group has shed light on how a fragment of a protein increases the production of the amyloid beta protein in the brain.

The researchers say that knowing that the N60 fragment of the RanBP9 protein increases the production of the amyloid beta protein, which is present in excessive amounts in the brains of people with Alzheimer’s disease, gives scientists a more specific focus for developing new drugs.

Most experts believe that if the creation of amyloid beta protein can be halted or slowed, the devastating effects of Alzheimer’s disease may also be stopped or slowed too, according to background information in a research article published in the FASEB Journal.

David Kang, assistant professor of neurosciences at the University of California, San Diego, and one of the researchers involved in the work, said: “Our study suggests that targeting RanBP9 expression and/or N60 fragment generation may lead to novel strategies to combat this devastating disease.”

During the study, Kang and his colleagues examined extracts from brains with Alzheimer’s disease and age-matched healthy controls.

The researchers found that the N60 section of RanBP9 was increased in Alzheimer’s brain.

“Alzheimer’s might seem hopeless to some, but this research shows that we’re closer than ever to unraveling both the protein tangles and mysteries surrounding this devastating disease,” said Dr. Gerald Weissmann, the Editor-in-Chief of The FASEB Journal. (ANI)

Macca says The Beatles became victims of success

Washington, Sep 2 (ANI): Brit singer Sir Paul McCartney has in an exclusive interview spoken out about the final days of ‘The Beatles’, and insisted that the group became victims of their own success when businessman Allen Klein took over their financial affairs.

According to music magazine Mojo, McCartney said that he and his bandmates struggled to come to terms with all the business decisions they were suddenly forced to make as they were recording their final album ‘Abbey Road’.

The fight between them over cash and contracts really became a huge burden.

“We were musicians, we were kids from Liverpool, we’d gone to grammar schools, we’d done Hamburg – we kind of knew all that,” Contactmusic quoted him as saying.

“But the idea that you were going to get this money and someone was going to take it off you…

“I think we all just thought, ‘You get the money, you put it in a bank, and it gradually gets bigger,’ and you say, ‘Thank you very much, and you live happily ever after.’ Then you suddenly get with accountants and they say, ‘No, you can’t just sit there’.

“Then there’s tax, and some business person is on a raid – it was a huge upheaval,” he said.

McCartney also admitted that the group’s business woes were poured into their new songs.

“George (Harrison) would write Piggies, and I knew exactly what he was talking about, and he wrote Taxman when we first found out about the tax system,” he said.

The rift between the group eventually led to a court battle before the band broke up, with many fans blaming Klein for contributing to the group’s split.

McCartney refused to be drawn into talking about Klein, but hinted that he still had not forgiven the businessman for things that would remain unspoken.

“I don’t want to speak ill of the dead,” he added.

Klein passed away in New York earlier this summer, after a long battle with Alzheimer’s disease. (ANI)

Heavy drinking ‘cuts dementia risk’

Washington, Aug 27 (ANI): People who drink up to 28 drinks a week in later life are less likely to develop dementia than people who abstain from alcohol consumption, according to a new study.

Professor Kaarin Anstey, from Canberra’s Australian National University, and colleagues compiled data from 15 international studies, including responses from more than 10,000 people.

They found that drinkers are better off when it comes to developing diseases affecting cognitive function, reports the Daily Telegraph.

The researchers found that those aged 60 and older who consumed between one and 28 alcoholic drinks each week, were almost 30 per cent less likely to have Alzheimer’s later on in life.

Light and moderate drinkers were also 25 per cent less likely to contract vascular dementia, and 26 per cent less likely to suffer from any form of dementia, the authors found.

The odds improved even more when comparing just drinkers with non-drinkers and ignoring exactly how much people consumed.

However, Anstey warned that this was not encouragement for people to start swilling 28 glasses of alcohol a week.

Even though, the study found imbibers, in general, had a 47 per cent reduced risk of contracting dementia compared with teetotalers, down to 44 per cent for Alzheimer’s.

Anstey said that there was a clear link between drinking and a reduced risk of dementia.

The researchers also found that the relationship between drinking and dementia was the same for men and women.

Although it was unclear exactly why light drinking provoked such a benefit, Anstey suggested that it might have something to do with alcohol’s ‘protective effect’ on reducing inflammation and heart disease.

The report was published in the July edition of the American Journal of Geriatric Psychiatry. (ANI)

Bird flu virus strain leaves survivors at increased Parkinson’s disease risk

Washington, August 20 (ANI): An animal study conducted by experts at St. Jude Children’s Research Hospital has suggested that at least one strain of the H5N1 avian influenza virus leaves survivors at significantly increased risk for Parkinson’s disease, and possibly other neurological problems later in life.

In their study report, the researchers write that mice that survived infection with an H5N1 flu strain were found to be more likely than uninfected mice to develop brain changes associated with neurological disorders like Parkinson’s and Alzheimer’s diseases.

Parkinson’s and Alzheimer’s involve loss of brain cells crucial to a variety of tasks, including movement, memory and intellectual functioning.

The researchers say that their study has shown that the H5N1 flu strain causes a 17 percent loss of the same neurons lost in Parkinson’s as well as accumulation in certain brain cells of a protein implicated in both diseases.

“This avian flu strain does not directly cause Parkinson’s disease, but it does make you more susceptible,” said Dr. Richard Smeyne, associate member in St. Jude Developmental Neurobiology.

“Around age 40, people start to get a decline in brain cells. Most people die before they lose enough neurons to get Parkinson’s. But we believe this H5N1 infection changes the curve. It makes the brain more sensitive to another hit, possibly involving other environmental toxins,” Smeyne added.

Smeyne revealed that the study focused on a single strain of the H5N1 flu virus, the A/Vietnam/1203/04 strain, and that the threat posed by other viruses, including the current H1N1 pandemic flu virus, was still being studied.

During the study, the researchers infected some mice with an H5N1 flu strain isolated in 2004 from a patient in Vietnam, which is still considered to be the most virulent of the avian flu viruses.

About two-thirds of the mice developed flu symptoms, primarily weight loss. After three weeks, there was no evidence of H5N1 in the nervous systems of the mice that survived.

However, the inflammation triggered by the infection within the brain continued for months, and it was found to be quite similar to inflammation associated with inherited forms of Parkinson’s.

Although the tremor and movement problems disappeared as flu symptoms eased, the researchers reported that 60 days later, mice had lost roughly 17 percent of dopamine-producing cells in SNpc, a structure found in the midbrain.

They also found evidence that the avian flu infection led to over-production of a protein found in the brain cells of individuals with both Alzheimer’s and Parkinson’s diseases.

“The virus activates this protein,” Smeyne said.

The study has been reported in the online early edition of the Proceedings of the National Academy of Sciences. (ANI)

MRI methods can show bone marrow stem cells’ viability as brain-repairing therapy

Washington, August 20 (ANI): Researchers at Tel Aviv University have offered new hope for people with incurable neurodegenerative diseases like Huntington’s, Alzheimer’s, and Parkinson’s by showing that the viability of stem cells created from a patient’s own bone marrow can be determined using MRI tracking methods.

Dr. Yoram Cohen, of TAU’s School of Chemistry, claims that he has been able to track the progress of the innovative cells called mesenchymal stem cells within the brain.

He says that initial studies indicate that it is possible to identify unhealthy or damaged tissues, migrate to them, and potentially repair or halt cell degeneration.

“By monitoring the motion of these cells, you get information about how viable they are, and how they can benefit the tissue. We have been able to prove that these stem cells travel within the brain, and only travel where they are needed. They read the chemical signalling of the tissue, which indicate areas of stress. And then they go and try to repair the situation,” he says.

During the study, Dr. Cohen and his colleagues tracked the activity of the live cells within the brain using the in-vivo MRI at the Strauss Centre for Computational Neuro-Imaging, with a view to establishing their viability as a therapy for neurodegenerative disease.

The researchers used magnetic iron oxide nanoparticles to label the stem cells, so that they could be identified as clear black dots on an MRI picture after being injected into the brain.

The stem cells were then injected into the brain of an animal that had an experimental model of Huntington’s disease, which suffered from a similar neuropathology as the one seen in human patients.

On MRI, it was possible to watch the stem cells migrating towards the diseased area of the brain.

“Cells that go toward a certain position that needs to be rescued are the best indirect proof that they are live and viable. If they can migrate towards the target, they are alive and can read chemical signalling,” says Dr. Cohen.

He believes that the benefits of using differentiated mesenchymal cells (MSC) may be numerous.

“Bone marrow-derived MSCs bypass ethical and production complications, and in the long run, the cells are less likely to be rejected because they come from the patients themselves. This means you don’t need immunosuppressant therapy,” he says.

Dr. Cohen has revealed that the next step in his research will be to develop a real-life therapy for those suffering from neurodegenerative diseases.

A researcher article on his study has been published in the journal Stem Cells. (ANI)

How to boost Alzheimer’s-fighting compounds’ value

Washington, August 18 (ANI): A team of researchers from Purdue University and Mount Sinai School of Medicine have shown that some of the polyphenols found in red wine, thought to help prevent Alzheimer’s disease, in fact reach the brain.

The researchers have found that the amount of polyphenols from grapeseed extract that can reach a rat’s brain is as much as 200 percent higher on the 10th consecutive day of feeding as compared to the first.

They point out that many past studies, in which absorption was measured after single or sporadic doses, often found very little of the bioactive polyphenols reaching brain tissues.

However, they add, more chronic exposure appears to improve absorption.

“This shows that reasonable and chronic consumption of these products may be the way to go, rather than single, high doses, similar to drugs. It’s like eating an apple a day, not a case of apples over two days every month,” said Mario Ferruzzi, a Purdue associate professor of food science, who collaborated on the research with Mount Sinai’s Dr. Giulio Pasinetti.

Pasinetti says that discovering how polyphenols are absorbed and distributed to the brain can impact the scientific understanding of the amount of grape products or red wine a person would need to consume to most effectively combat Alzheimer’s disease.

“The most important thing is that when we follow the repetitive administration of this compound, we were able to observe the transfer of the compound to the brain. This may help us figure out the proper concentration necessary to get these chemicals to the brain,” Pasinetti said.

Though the study dealt with polyphenols, Ferruzzi said that it could also be significant for determining proper doses of other compounds or drugs for patients.

“It could become important in terms of side effects. You could be overdosing because the body is adapting and absorbing or metabolising these compounds differently over time,” Ferruzzi said.

Ferruzzi said that further studies would focus on the mechanisms that control absorption of compounds during chronic consumption.

A paper detailing the findings has been published in the early online version of the Journal of Alzheimer’s Disease. (ANI)

How toxic various sizes of Alzheimer’s clusters can be to brain’s nerve cells

Washington, August 12 (ANI): In a breakthrough that may pave the way for an effective treatment for Alzheimer’s disease, scientists at the University of California-Los Angeles (UCLA) have created various sizes of clusters in their lab, which exactly match the clusters of the amyloid ß-protein (Aß) protein that form in the brains of those affected with the disease.

The researchers say that their work has shown that the ability of these grape-like clusters to kill nerve cells in the brain, scientifically known as toxicity, increases dramatically as they increase in size.

They say that though the larger clusters are more toxic than smaller ones, the larger formations are relatively rare.

Given that smaller versions are numerous, the researchers say, they are an inviting target for the development of new therapeutic drugs.

“We now have the best understanding yet of what types of toxic A-beta structures we should target with new classes of therapeutic drugs,” said senior author David Teplow, a professor of Neurology at UCLA.

The researchers have found that the larger the cluster, the greater the toxicity, but they also found that the increase in toxicity with these clusters is not linear.

“Clusters that contain two Aß molecules are more toxic than a single Aß molecule, and those with three molecules are more toxic that those with two,” said Teplow.

He pointed out that clusters composed of two Aß molecules are three-fold more toxic than the simple monomer compound, but those made of three molecules and four four molecules are more than 10-fold more toxic than are monomers.

This suggests that the larger, more toxic clusters should be the target for scientists trying to stop Alzheimer’s.

But Teplow notes that the relative amounts of the smaller clusters are far greater than that of the bigger clusters, and are, in total, more toxic.

So in an Alzheimer’s brain, the larger clusters are relatively rare, he said.

“Think of the molecules being wrapped in very weak Velcro. So a number of molecules can bind together to form large clusters, but they break apart very easily,” he said.

Having developed a process in the lab to be able to make pure forms of these Aß clusters of specific size will enable detailed study of their structures to show where every atom is.

“This will make development of drugs much easier and likely more successful,” he said. (ANI)

‘Heart healthy’ diet, exercise ‘protects against cognitive decline’

Washington, July 15 (ANI): A ‘heart healthy’ diet and taking moderate exercise can protect against cognitive decline, according to two new studies.

Researchers at Utah State University in the US found that over-65s on a diet full of green leafy vegetables, oily fish and the odd glass of red wine scored higher in mental tests.

A separate study at the University of California found that moderately physically active older adults might experience slower rates of mental decline.

In the first study, Heidi Wengreen, an assistant professor of nutrition at Utah State University, asked 3,831 adults, aged 65 and older, to complete a food survey. They then tested their cognitive skills over an 11-year period, beginning in 1995.

The researchers looked to see how well the participants followed the DASH diet, an eating regimen that protects against hypertension and heart trouble.

Those who followed the DASH diet more closely had higher scores on the cognitive tests at the start of the study and over time, Wengreen found.

In the second study, Deborah E. Barnes, of the University of California, San Francisco, followed more than 3,000 adults aged 70 to 79.

Those who were sedentary had the lowest level of cognitive function at the start and higher rates of decline over the course of the seven-year study.

The two studies were reported at the Alzheimer’s Association 2009 International Conference on Alzheimer’s Disease in Vienna. (ANI)

Study finds link between pesticide levels in blood and Parkinson’s disease

Washington, July 14 (ANI): In a new study, researchers at UT Southwestern Medical Center have found that people with Parkinson’s disease have significantly higher blood levels of a particular pesticide than healthy people or those with Alzheimer’s disease.

The researchers found the pesticide beta-HCH (hexachlorocyclohexane) in 76 percent of people with Parkinson’s, compared with 40 percent of healthy controls and 30 percent of those with Alzheimer’s.

According to researchers, the finding may provide the basis for a beta-HCH blood test to identify individuals at risk for developing Parkinson’s disease.

The results also point the way to more research on environmental causes of Parkinson’s.There’s been a link between pesticide use and Parkinson’s disease for a long time, but never a specific pesticide. This is particularly important because the disease is not diagnosed until after significant nerve damage has occurred. A test for this risk factor might allow for early detection and protective treatment,” said Dr. Dwight German, professor of psychiatry at UT Southwestern and a senior author of the paper.

The study involved 113 participants, ages 50 to 89. Fifty had Parkinson’s, 43 were healthy and 20 had Alzheimer’s. The researchers tested the subjects’ blood for 15 pesticides known as organochlorines.

These pesticides, which include the well-known DDT, were widely used in the U.S. from the 1950s to the 1970s but are more tightly regulated now. They persist in the environment for years without breaking down.

In the body, they dissolve in fats and are known to attack the type of brain nerves that die in Parkinson’s disease, the researchers said.

The study appears in the July issue of Archives of Neurology. (ANI)

Alzheimer’s disease drug may treat traumatic brain injury too

Washington, July 13 (ANI): A class of drugs used for the treatment of Alzheimer’s Disease (AD) has been found to be effective in treating traumatic brain injury as well, according to researchers from Georgetown University Medical Center (GUMC).

The scientists have found that the destructive cellular pathways activated in AD are also triggered after traumatic brain injury, indicating that a new therapy could successfully treat both conditions.

Now, the researchers are all set to show that deactivating these pathways in part by using a class of AD drug, called gamma secretase inhibitor, could reduce loss of neurons in animal models of traumatic brain injury.

The drug also protected the animals against motor and cognitive deficits.

“The goal for both diseases is to prevent neuronal cell death, and this study suggests that one therapy could possibly work for both,” said the study’s lead author, neuroscientist Dr. Mark Burns.

Both disorders are associated with build-up of beta amyloid, a toxic brain peptide.

Burns says that build-up of beta amyloid occurs in a second wave of damage that follows immediate “necrotic” death of nerve cells after traumatic brain injury.

This secondary injury can last months, if not years, resulting in large holes within brain tissue.

Amyloid peptides are produced when a long brain protein known as the amyloid precursor protein (APP) is cut in two by the enzyme beta secretase, and then cut once again by a second enzyme known as gamma secretase.

Agents that inhibit the activity of gamma secretase are now being studied as treatment for Alzheimer’s disease.

In the study, researchers used mice that were either treated with DAPT, an experimental gamma secretase inhibitor, or mice which were “BACE knock-outs” -genetically altered in such a way that they could not produce beta secretase.

It was found that DAPT and BACE knockout mice had brain lesions that were as much as 70 percent smaller than control animals and they experienced minimal impairment.

Burns said that the findings further cement the connection between Alzheimer’s disease and traumatic brain injury.

In addition, the study showed that “modulation of beta and gamma secretase may provide novel therapeutic targets for the treatment of traumatic brain injury.”

The findings of the study will be presented at the Alzheimer’s Association 2009 International Conference on Alzheimer’s Disease. (ANI)

New compound could be a promising treatment for Alzheimer’s disease

Washington, July 13 (ANI): A compound called NIC5-15 has been found to be a safe and effective treatment to stabilize cognitive performance in Alzheimer’s disease patients, according to a study.

The two researchers in the study, Dr. Giulio Maria Pasinetti, and Dr. Hillel Grossman, have presented the Phase IIA preliminary clinical findings, and have said that NIC5-15′s potential to preserve cognitive performance will be further evaluated in a Phase IIB clinical trial.

Early evidence has suggested that NIC5-15 is a safe and tolerable natural compound that may reduce the progression of Alzheimer’s disease-related dementia by preventing the formation of beta-amyloid plaque.

Beta-amyloid plaque is a waxy substance that accumulates between brain cells and impacts cognitive function.

“With Alzheimer’s disease affecting 5.2 million Americans, another 5 million with early-state disease, and nearly a half million new cases reported annually, treatments like NIC5-15 would make a significant difference in the lives of many Alzheimer’s patients. We are hopeful that the follow up clinical study will support this preliminary evidence,” said Pasinetti.

Grossman said: “There are no FDA-approved Alzheimer’s disease modifying drugs available today.”

He added: “Current drugs approved for use help maintain cognitive function, but only for a limited time. NIC5-15 is part of a new class of natural compound we found to have the potential of precluding the generation of _-amyloid and, eventually, attenuating cognitive deterioration in preclinical models of Alzheimer’s disease.”

The Phase IIA preliminary clinical findings of the study were presented at the Alzheimer’s Association 2009 International Conference on Alzheimer’s Disease (ICAD) in Vienna. (ANI)

Alzheimer’s patients may not benefit from eating ‘brain food’ fish

London, July 13 (ANI): People with Alzheimer’s disease may not benefit from eating fish, even though it is considered to be a “brain food”, say American researchers.

Two pieces of research have shown that the chances of getting the disease may be reduced, or its progression prevented, by consuming a fish-based diet, but further work is needed.

Two studies were carried out to determine the effects of DHA, an omega-3 fatty acid found in oily fish.

While studies conducted in the past have suggested that fish oil rich in omega-3 can protect the brain from age-related dementia, the new research has cast doubt on the claims.

Funded by the Alzheimer’s Disease Co-operative Study (ADCS), the first trial lasted 18 months, during which it compared the effects of DHA and a dummy placebo on 402 volunteers with an average age of 76 who had been diagnosed with mild to moderate Alzheimer’s.

The researchers associated with the trial say that, at the end of the study, there was nothing to conclusively show that omega-3 supplements improved participants’ memory and mental performance scores.

The second trial ran for six months, during which a DHA manufacturer tested one of its products on a group of 485 healthy people.

It did show some improvement in one test of memory and learning. However, those participating in the trial did not have Alzheimer’s disease or any other form of dementia.

The findings of both trials were presented at the International Conference on Alzheimer’s Disease (ICAD) in Vienna.

“These trial results do not support the routine use of DHA for patients with Alzheimer’s,” the Scotsman quoted Dr. Joseph Quinn, from Oregon Health and Sciences University, who led the ADCS study, as saying.

However, the researchers presenting the findings did say that there was some evidence that DHA might help people with a particular genetic make-up.

“These studies show that using omega-3 fatty acids as a treatment late on may not be effective against Alzheimer’s,” Dr Simon Ridley, research manager at the Alzheimer’s Research Trust, said.

“But with previous population studies suggesting that fish oils could reduce dementia risk, getting oily fish, such as mackerel, herring, salmon and sardines into our weekly menus could still be good advice.

“This shouldn’t spell the end of research into omega-3, however. It could be that omega-3 given very early in the disease process could make a difference, but for that to happen we must drive forward studies that improve our methods of diagnosing Alzheimer’s disease,” he added.

Dr William Thies, chief medical and scientific officer at the Alzheimer’s Association, said: “These two studies – and other recent Alzheimer’s therapy trials – raise the possibility that treatments for Alzheimer’s must be given very early in the disease for them to be truly effective. For that to happen, we need to get much better at early detection of Alzheimer’s.” (ANI)

Fish oil supplements can cut memory loss in the elderly

London, July 13 (ANI): A study carried out by American bioscience company Martek suggests that taking fish oil supplements can reduce memory loss in old age.

Dr Karin Yurko-Mauro, a researcher associated with the company, has revealed that taking a supplement of omega 3 for six months had a beneficial effect on people with age-related forgetfulness and loss of learning ability during the study.

The research team tested the affect of docosahexaenoic acid (DHA), the most commonly found in fish oil, on 485 healthy people with an average age of 70, and found that memory and general brain function increased significantly.

According to the study report, taking 900mg capsules every day was found to be the equivalent of turning back the clock three years.

The researchers hope that future studies will provide promising results suggesting that the fatty acid may help stave off Alzheimer’s disease, if new techniques can be found to diagnose it before it take holds.

Dr Yurko-Mauro said that the participants who took the supplements had “almost double the reduction in errors on a test that measures learning and memory performance.”

“The benefit is roughly equivalent to having the learning and memory skills of someone three years younger,” the Telegraph quoted him as saying.

Dr. William Thies, Chief Medical and Scientific Officer at the Alzheimer’s Association, feels that it is “too early” to make a recommendation about use of DHA supplements to prevent loss of mental function.

“In high doses, DHA does have side effects, so you would want to see a benefit to justify the risk you are taking. We need more work for that,” he said.

A presentation on the study was made at the international Alzheimer’s Association meeting in Vienna, Austria. (ANI)

Diets bad for the teeth may be bad for the body too

Washington, July 10 (ANI): Dental disease may be a warning that the high-glycemic diet that led to dental problems in the short term may, in the long term, cause harm to the body.

“The five-alarm fire bell of a tooth ache is difficult to ignore,” says Dr. Philippe P. Hujoel, professor of dental public health sciences at the University of Washington (UW) School of Dentistry in Seattle.

Hujoel weighed two contradictory viewpoints on the role of dietary carbohydrates in health and disease. The debate surrounds fermentable carbohydates: foods that turn into simple sugars in the mouth.

Fermentable carbohydrates are not just sweets like cookies, doughnuts, cake and candy. They also include bananas and several tropical fruits, sticky fruits like raisins and other dried fruits, and starchy foods like potatoes, refined wheat flour, yams, rice, pasta, pretzels, bread, and corn.

One viewpoint is that certain fermentable carbohydrates are beneficial to general health and that the harmful dental consequences of such a diet should be managed by the tools found in the oral hygiene section of drugstores.

A contrasting viewpoint suggests that fermentable carbohydrates are bad for both dental and general health, and that both dental and general health need to be maintained by restricting fermentable carbohydrates.

The close correlation between the biological mechanisms that cause dental decay and the factors responsible for high average levels of glucose in the blood is intriguing.

Hujoel explains that eating sugar or fermentable carbohydrates drops the acidity levels of dental plaque and is considered an initiating cause of dental decay.

“Eating these same foods, he says, is also associated with spikes in blood sugar levels. There is fascinating evidence that suggests that the higher the glycemic level of a food, the more it will drop the acidity of dental plaque, and the higher it will raise blood sugar. So, possibly, dental decay may really be a marker for the chronic high-glycemic diets that lead to both dental decay and chronic systemic diseases. This puts a whole new light on studies that have linked dental diseases to such diverse illnesses as Alzheimer’s disease and pancreatic cancer,” Hujoel said.

The report has been published in the Journal of Dental Research. (ANI)

Having chocolate, red wine regularly may help protect against Alzheimer’s

London, July 10 (ANI): Regular intake of chocolate, fruits, vegetables, red wine and tea could help protect against Alzheimer’s disease, according to an expert.

Dr Robert Williams, a biochemist at Kings College London, says that all contain chemicals called flavonoids that may also help existing dementia sufferers.

Flavonoids are naturally occurring antioxidants, which help beat cancer and the ageing process by protecting cells from damage. They also mop up potentially harmful oxygen molecules in the body.

New research is emerging that suggests flavonoids do not act only as antioxidants but exert their effects in other ways.

“There have been some intriguing epidemiological studies that show the consumption of flavonoid-rich vegetables, fruit juices and red wine delays the onset of the disease,” the Daily Express quoted Williams as saying.

Williams and his colleagues have focused their own cellular studies on a flavonoid called epicatechin, found in many foodstuffs, including cocoa.

“We have found that epicatechin protects brain cells from damage but through a mechanism unrelated to its antioxidant activity and have shown in laboratory tests that it can also reduce some aspects of Alzheimer’s disease pathology,” he said.

Central to the development of Alzheimer’s disease is beta-amyloid peptide, a substance normally produced in the brain but which in Alzheimer’s is deposited abnormally.

Williams has shown that flavonoids can protect brain cells against the toxic actions of beta-amyloid.

“The challenge now is to identify the single flavonoid or combination of flavonoids that exert the most positive effects,” he said.

Williams will present his findings at the British Pharmacological Society’s Summer Meeting in Edinburgh. (ANI)

Most cognitive tests fail to predict Alzheimer’s, vascular dementia

Washington, July 9 (ANI): Most of the cognitive tests fail to predict whether someone has Alzheimer’s disease or vascular dementia, say researchers.

Both Alzheimer’s disease and vascular dementia affect learning and memory, behaviour and day-to-day function.

The researchers suggest when older people are confused and forgetful, doctors should base their diagnoses on many different types of information, including medical history and brain imaging.

Dr Jane Mathias and Jennifer Burke, M.Psych.(Clinical), both from the University of Adelaide, analysed 81 previously published studies that compared the cognitive testing of people diagnosed with dementia of the Alzheimer’s and vascular type .

Of the 118 different tests that were used only two were able to adequately differentiate between Alzheimer’s and vascular dementia.

The Emotional Recognition Task (the ability to identify facial expressions in photographs and match emotional expressions to situations, at which people with Alzheimer’s were better) and Delayed Story Recall (at which people with vascular dementia were better), were the only tests that appeared to reliably tell the two groups apart.

Many commonly used tests-such as Digit Span (repeating a set of numbers forward, backward), verbal fluency (generating words by first letter or category, such as animals), drawing tasks and more – were unable to distinguish between dementia types. While these tests may assist in diagnosing dementia, they do not adequately discriminate between Alzheimer’s disease and vascular dementia,” wrote the authors.

They suggest that all cognitive tests should be used cautiously and only in conjunction with other information (imaging, medical history) when diagnosing patients.

The study appears in the journal Neuropsychology. (ANI)

Inflammation may lead to Alzheimer’s disease

Washington, July 9 (ANI): A new study has revealed that inflammation might lead to development of Alzheimer’s disease.

Two research studies published by William A. Banks has shown how inflammation triggers disease, and how can it be treated.

It is believed that the toxic levels of amyloid beta protein, the substance responsible for Alzheimer’s disease, accumulate in the brain because a pump that pushes it into the blood and past the blood-brain barrier malfunctions.

The blood-brain barrier is a system of cells that regulates the exchange of substances between the brain and the blood.

The blood-brain barrier transporter known as LRP is the pump that removes amyloid beta protein from the brain and into the bloodstream.”LRP malfunctions like a stop light stuck on red, and keeps amyloid beta protein trapped in the brain,” said Banks.

Inflammation, which is part of the body’s natural immune response, occurs when the body activates white blood cells, and produces chemicals to fight infection and invading foreign substances.

“We induced inflammation in mice and found that it turned off the LRP pump that lets amyloid beta protein exit the brain into the bloodstream,” Banks said.

“It also revved up an entrance pump that transports amyloid beta into the brain. Both of these actions would increase the amount of amyloid beta protein in the brain,” he added.

Banks said that treatment with drug indomethacin prevented inflammation from turning off the LRP (exit pump). (ANI)

New discovery can help thwart Parkinson’s disease

Washington, July 8 (ANI): Scientists from King’s College London say that blocking the release of chemical glutamate in the brain may help prevent Parkinson’s disease.

Dr. Susan Duty said that one of the contributing factors to nerve cell death is an excess of the chemical glutamate in the motor control pathways in the brain.

An excess of this chemical changes the way these pathways operate, and makes movement even less well controlled.

She said that stimulating ‘trigger points’ responsible for the release of a chemical that can kill brain cells can help thwart Alzheimer’s.

“The way we hope to achieve this is by stimulating protein targets on the nerve cell called metabotropic glutamate receptors. Certain types of these receptors, when stimulated, are known to prevent release of glutamate in other brain regions,” said Duty.

“We, and others, have now taken these ideas into regions relevant to Parkinson’s disease in the hope of reversing both the clinical signs and cell death associated with this condition.

“We, and others, have now taken these ideas into regions relevant to Parkinson’s disease in the hope of reversing both the clinical signs and cell death associated with this condition,” she added.

Duty said that current drugs could only treat the symptoms but not the underlying cause of the disease.

“They provide relief of symptoms by replacing the chemical, dopamine, which the dying cells would normally secrete in order to maintain proper control of movement,” she said.

“However, they do little to combat the ongoing progressive cell death meaning that symptoms get worse, higher doses of drug are needed to control the worsening symptoms, the result being appearance of disabling side-effects such as involuntary flailing limb movements and painful twisting of joints.

“Given the disease is progressive in nature, the continued death of cells in the substantia nigra leads to gradual worsening of symptoms and decline in patients’ quality of life over time.

“Finding drugs that can provide protection or repair to the dying cells – as well as relieve the clinical signs of Parkinson’s – is therefore a key area of interest in this field,” she added.

The study was presented at The British Pharmacological Society’s Summer Meeting in Edinburgh. (ANI)

Severe COPD linked to cognitive impairment

Washington, July 8 (ANI): A new study by researchers at Mount Sinai School of Medicine has shown that severe chronic obstructive pulmonary disease (COPD) is associated with lower cognitive function in older adults.

COPD is caused by noxious particles or gas, most commonly from smoking, which trigger an abnormal inflammatory response in the lung.

In the study, researchers compared cognitive performance in over 4,150 adults with and without COPD and found that individuals with severe COPD had significantly lower cognitive function than those without, even after controlling for confounding factors such as comorbidities.

“Our findings should raise awareness that adults with severe COPD are at greater risk for developing cognitive impairment, which may make managing their COPD more challenging, and will likely further worsen their general health and quality of life,” said lead author of the study, William W. Hung, M.D., M.P.H., assistant professor at Mount Sinai School of Medicine.

Patients with COPD may experience periods of hypoxia-low oxygen levels-that might lead to brain abnormalities that could reduce cognitive capacity.

Alternatively, hypoxia may cause or exacerbate diseases that are characterized by cognitive impairment, such as Alzheimer’s disease.

The results were published in the July 15 issue of the American Journal of Respiratory and Critical Care Medicine. (ANI)