Dual-tasking test could differentiate between Alzheimer's and depression

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London, Nov 9 (ANI): Scottish researchers have developed a novel diagnostic test that can help distinguish between symptoms of depression
and early Alzheimer's.


People developing Alzheimer's face mild levels of impaired reasoning and memory that are easily mistaken for signs of depression, which in turn can lead to many patients with dementia
being misdiagnosed and missing out on early treatment that could make a difference.

Now, researchers at the University of Edinburgh found that asking patients to perform two mental tasks at the same time can help tell the conditions apart.


Led by Professor Sergio Della Sala, the researchers compared the "dual-tasking" ability of 89 Alzheimer's patients, sufferers of chronic depression and healthy elderly individuals with no memory impairment.


The findings showed that people with Alzheimer's performed significantly worse than the other two groups.


This was true even when allowances were made for individual memory differences.


"This is the first piece of research to compare the performance of dual tasks in Alzheimer's disease and depression and could mean that people with dementia are diagnosed earlier. Currently, up to two-thirds of people with dementia never receive a formal diagnosis and it is often misdiagnosed as depression. Dela Sala's team aims to develop a simple screening test that will help GPs discriminate Alzheimer's from normal ageing and depression," The Scotsman quoted Dr Susanne Sorensen, head of research at the Alzheimer's Society, as saying.


"An early diagnosis is hugely important as it may enable people with dementia to understand their condition, (and] have access to certain drugs that could help relieve some of their symptoms," he added.


The dual task experiment consists of five stages.


First the subject's short-term memory capacity is determined, the outcome called the "digit span".


Then lists of digits are read to the subject who is asked to repeat the lists, which produces a "task list score".


Stage three involves using a pencil to trace a path through a maze, giving a third score.


In stage four, the subject repeats digit lists while tracing a path, the dual task. The final stage is a retest of stage four.


The study has been published in the Journal of Neurology. (ANI)

Drink apple juice 'to stave off Alzheimer's

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DecconChronical

Washington: Want to stave off dementia? Just drink a glass of apple juice daily, says a new study.

Researchers at Massachusetts University have carried out the study and found that fresh apple juice everyday can delay the onset of Alzheimer's disease and various other age-related cognitive decline, the 'Journal of Alzheimer's Disease' reported.

For their study, the researchers carried out a number of laboratory experiments demonstrating that drinking apple juice helped mice perform better than normal in maze trials, and prevented the decline in performance that was otherwise observed as these mice aged.

They found that mice receiving the human equivalent of 2 glasses of apple juice per day for 1 month produced less of a small protein fragment, called "beta-amyloid" that is responsible for forming the "senile plaques" that are commonly found in brains of individuals suffering from Alzheimer's.

"These findings provide further evidence linking nutritional and genetic risk factors for age-related neurodegeneration and suggest that regular consumption of apple juice can not only help to keep one's mind functioning at its best, but may also be able to delay key aspects of Alzheimer's disease and augment therapeutic approaches," lead researcher Thomas Shea said.

Alzheimer's Disease Research Cure

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eHow

At present there is no cure for Alzheimer's disease (AD). Once the disease develops, treatment only slows its progression. By understanding the causes of the disease, lifestyles changes can be made to reduce the risk of developing AD. The diagnosis and treatment of this disease has improved greatly in recent years, and many scientists are convinced that the next 10 years will bring even better treatments and possibly a cure for those just diagnosed with the disease

Alzheimer's Disease
Alzheimer's Disease is an irreversible, progressive brain disease that over time destroys a person's memory and ability to think. As the disease progresses, even everyday tasks are impossible. Over 5.3 million Americans suffer from Alzheimer's disease, and 35 million people worldwide have this mind-robbing disease.
Causes of Alzheimer's Disease
The initial cause of Alzheimer's disease is still unknown, but damage to the brain starts many years before any symptoms appear. According to the Alzheimer's Association, abnormal structures called plaques and tangles develop deep inside the brain, degrading and killing nerve cells. The damage spreads throughout the brain, especially in an area called the hippocampus. This part of the brain is like a file cabinet for new memories. When it is damaged, new memories are lost. As Alzheimer's progresses, more parts of the brain are invaded by plaques and tangles. These affected areas shrink and become non-functional. In the final stage of AD, damage to brain tissue is severe.
Present Treatment
Some drugs are available that help improve the mental action of people with Alzheimer's disease. Mental and physical exercise, eating right, socializing and eliminating unhealthy habits go along way in slowing the progression of Alzheimer's. A tranquil, orderly setting also helps those with AD. Certain supplements seem to help some people with AD, including vitamins A, B, C, D and E. Also, tumeric and fish oil show some promise in the fight against the disease.
Drug Therapies
Aricept is the most commonly used medication for Alzheimer's disease. This drug works by stopping cholinesterase from breaking down acetylcholine in the brain. Acetylcholine helps one part of the brain communicate with another part. This action keeps the brain intact longer. Aricept is the only drug acknowledged by the Food and Drug Administation for all stages of AD. Eventually this drug is not effective in the progression of AD. Also, this drug has side effects intolerable to some individuals such as trouble sleeping, stomach discomfort, muscle cramps and fatigue. Cognex, is similar to Aricept as a cholinesterase blocker, but it has more serious side effects, including abdominal pain, vomiting and liver damage.

Exelon and Razadyne are newer drugs that stop the breakdown of acetylcholine. The best results occur when they are taken in earlier stages of Alzheimer's. They also have side effects, including severe allergic reactions, depression, tremors and irregular heartbeat.

Namenda is effective for some people with moderate-to-severe Alzheimer's. Its action appears to restore function to damaged nerve cells. This drug only works for some individuals and has several unwanted side effects like increased agitation, severe fatigue, changes in eyesight and severe allergic reactions.
Finding a Cure
From 1999 to 2009 scientists formulated new technologies that will speed up Alzheimer's research. The government and drug companies are putting money into research and new treatments are developed each year.

On April 29, 2009, neuroscientists Frank LaFerla and Mathew Blurton-Jones received $3.6 million for the advancement of AD therapy employing human neural stem cells. Research into a vaccine for protection against Alzheimer's will be started again and researchers from Southampton University will be re-evaluating 80 participants in a trial of a vaccine. Initially the vaccine had some deadly side effects. Hormone replacement therapy also appears to have some promise in lowering the risk of developing AD. The results among oestrogen users in a cohort study of Paganini-Hill and Henderson showed that the relative risk of developing Alzheimer's decreased with increasing doses of this hormone.

Research is also being........read all of Alzheimer's Disease Research Cure

Alzheimer's disease mysteries

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redOrbit



One of the many mysteries of Alzheimer's disease is how protein-like snippets called amyloid-beta peptides, which clump together to form plaques in the brain, may cause cell death, leading to the disease's devastating symptoms of memory loss and other mental difficulties. In order to answer that key question and develop new approaches to preventing the damage, scientists must first understand how amyloid-beta forms the telltale clumps

One of the many mysteries of Alzheimer's disease is how protein-like snippets called amyloid-beta peptides, which clump together to form plaques in the brain, may cause cell death, leading to the disease's devastating symptoms of memory loss and other mental difficulties.

In order to answer that key question and develop new approaches to preventing the damage, scientists must first understand how amyloid-beta forms the telltale clumps.

University of Michigan researchers have developed new molecular tools that can be used to investigate the process. The molecules also hold promise in Alzheimer's disease treatment. The research, led by assistant professor Mi Hee Lim, was published online this week in the Journal of the American Chemical Society.

Though the exact mechanism for amyloid-beta clump formation isn't known, scientists do know that copper and zinc ions are somehow involved, not only in the aggregation process, but apparently also in the resulting injury. Copper, in particular, has been implicated in generating reactive oxygen species, which can cause cell damage.

One way of studying the role of metals in the process is by sopping up the metal ions with molecules called chelators and then seeing what happens when the metal ions are out of the picture. When other scientists have done this they've found that chelators, by removing metals, hamper both amyloid beta clumping and the production of those harmful reactive oxygen species, suggesting that chelators could be useful in treating Alzheimer's disease.

However, most known chelators can't cross the blood-brain barrier, the barricade of cells that separates brain tissue from circulating blood, protecting the brain from harmful substances in the bloodstream. What's more, most chelators aren't precise enough to target only the metal ions in amyloid-beta; they're just as likely to grab and disable metals performing vital roles in other biological systems.

Lim and coworkers used a new strategy to develop "bi-functional" small molecules that not only grab metal ions, but also interact with amyloid-beta.

"The idea is simple," said Lim, who has joint appointments in the Department of Chemistry and the Life Sciences Institute. "We found molecules known for amyloid-beta recognition and then attached metal binding sites to them." In collaboration with Ayyalusamy Ramamoorthy, professor of chemistry and associate professor of biophysics, Lim then used NMR spectroscopy to confirm that the new, hybrid molecules still interacted with amyloid-beta.

In experiments in solutions with or without living cells, the researchers showed that the bi-functional molecules were able to regulate copper-induced amyloid-beta aggregation, not only disrupting the formation of clumps, but also breaking up clumps that already had formed. In fact, their molecules performed better than clioquinol, a clinically-available metal chelator that showed promise in early trials with Alzheimer's patients, but has side effects that limit its long-term use.

"Based on their small size and other properties, we believe our compounds will be able to cross the blood-brain barrier, but we want to confirm that using mouse models," Lim said. The researchers also plan experiments to see if their new chelators are as good at preventing and breaking up amyloid-beta plaques in the brains of mice as they are in solutions and cultured cells.

Blood Test Identifies Women At Risk From Alzheimer's

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redOrbit


Middle-aged women with high levels of a specific amino acid in their blood are twice as likely to suffer from Alzheimer's many years later, reveals a thesis from the Sahlgrenska Academy at the University of Gothenburg, Sweden. This discovery this could lead to a new and simple way of determining who is at risk long before there are any signs of the illness.

The thesis is based on the Prospective Population Study of Women in Gothenburg, which was started at the end of the 1960s when almost 1,500 women between the ages of 38 and 60 were examined, asked questions about their health and had blood samples taken. Nearly all of the samples have now been analysed and compared with information on who went on to suffer from Alzheimer's and dementia much later.

"Alzheimer's disease was more than twice as common among the women with the highest levels of homocysteine than among those with the lowest, and the risk for any kind of dementia was 70 per cent higher,"

Homocysteine is an amino acid that is important for the body's metabolism. It is known that high levels of homocysteine can damage the blood vessels and increase the risk of blood clots. Previous longitudinal studies linking homocysteine and dementia had 8 years of follow-up at most. The present study is by far the longest one with follow-up time of 35 years. The study is also the first to show association between homocysteine levels in middle aged women and dementia development several decades later. The researchers do not yet know whether it is the homocysteine itself that damages the brain, or whether there is some other underlying factor that both increases levels of the homocysteine and causes dementia.

Historically elevated homocysteine levels were related to certain vitamin defficiencies (B12 anf folate). Today we know that high homocysteine levels might be present even with perfectly normal vitamin status. "These days we in our clinical practice use homocysteine analyses mainly for assessment of vitamin status. However, our results mean that we could use the very same analysis för assessment of individual's risk profile for dementia development. This opens the possibility for future preventive treatment at a very early stage", says Zylberstein.

The thesis also looks at a gene which, in some variants, appears to offer protection against dementia. This gene variant reduces the risk of dementia by no less than 65 percent when present doubled (homozygous) which occures in just one in ten Swedes and by 40 percent when present in mixed form (heterozygous) i additional four of ten Swedes.

"We have only been able to carry out a genetic analysis on just over 550 of the blood samples from the Prospective Population Study of Women, and want to undertake bigger studies before we can say for sure that the gene really does protect against dementia," says professor Lauren Lissner who supervised the thesis. "We hope to be able to perform the same analysis on more samples from the study."

Read more about blood test for Alzheimer's

Judicious Drinking Associated with Reduced Risk of Dementia

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medpageToday

By John Gever, Senior Editor, MedPage Today

Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco .

MAYWOOD, Ill., Having a drink only occasionally may reduce the risk of dementia, perhaps because long exposure to low alcohol levels help brain cells survive other stresses, researchers here said.

Most studies that have sought to compare drinking patterns with risk factors associated with dementia have found that moderate drinkers generally have a lower risk, according to Michael A. Collins, Ph.D., of Loyola University Chicago, and colleagues.


Yet their literature review of cardiovascular and neurological effects of ethanol, published online in Alcoholism: Clinical and Experimental Research, outlined a potential neuroprotective mechanism that light-to-moderate drinking could induce.


It was derived from a variety of preclinical studies of a phenomenon known as alcohol preconditioning.


In an interview, Dr. Collins said it was analogous to ischemic preconditioning, in which exposing brain neurons to a brief period of hypoxia helps them survive later bouts of more severe ischemia, such as would occur in a stroke.


These studies have shown that neurons in vitro temporarily dosed with low levels of ethanol can survive stresses that kill untreated neurons.


Dr. Collins said the mechanism appears to involve a sensor-transducer pathway, in which focal adhesion kinase and certain protein kinase C species are activated following low-dose alcohol exposure, which in turn generates two heat shock proteins, Hsp27 and Hsp70.


These latter proteins are well-known to protect cells from stress.


The likelihood of a direct neuroprotective mechanism is boosted by laboratory studies with two known neurotoxic agents, gp120 and beta-amyloid protein. The latter is believed to play a role in Alzheimer's disease, while gp120 is responsible for HIV dementia.


Pretreatment with alcohol protected brain neurons from these agents in vitro, Dr. Collins said.


Whether the preconditioning model accurately reflects what goes on in the brains of human drinkers is uncertain, Dr. Collins acknowledged.


"It is nonetheless conceivable that light-to-moderate, stable alcohol ingestion over years exerts 'preconditioning-like' effects on glia and neurons," he and his colleagues wrote in their review.


Noting that millions of new cases of dementia are diagnosed annually, they added, "it seems imperative that as much as possible is learned about the apparent cytoprotective mechanisms engendered by low-moderate alcohol intake and levels."


The review covered more than 100 studies of the cardiovascular and neurological effects of ethanol. It summarized and updated the proceedings of a roundtable meeting organized and chaired by Dr. Collins in 2007.


Dr. Collins and colleagues noted that not all studies showed a decreased risk. Moreover, they said, many of the investigators who did find reduced risk factors attributed their findings to the hematologic and cardiovascular effects of alcohol, or of other components of alcoholic drinks such as resveratrol.


But the review also included a number of in vitro and animal studies suggesting that low-dose ethanol has direct neuroprotective effects.


"Light to moderate, non-binge alcohol intake . . . does no apparent harm to cognition during aging, even possibly reducing the risk of cognitive decline [and] dementia," Dr. Collins and colleagues said.


"Alcohol-related anti-inflammatory heat shock protein and protein kinase changes in the brain bear similarities to those elucidated in the heart, particularly with respect to protein kinase C and quite likely other signal transduction kinases," they added

Older adults with dementia at increased flu mortality risk

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Newsport onlone
Older patients with dementia are diagnosed with flu less frequently, have shorter hospital stays, and have a fifty percent higher rate of death than those without the disorder, a new study has revealed.

“The increased mortality of older patients with dementia hospitalized for flu may be indicative of inadequacies in health care quality and accessibility. It could be beneficial to refine guidelines for the immunization, testing, and treatment of flu in older patients with dementia when planning for the possibility of a flu pandemic,” said first and senior author Elena Naumova, PhD, professor of public health and community medicine at Tufts University School of Medicine.

Dementia, defined by the authors as cognitive impairment to the extent that normal activity is impaired, causes unique obstacles to the early diagnosis and treatment of flu.

Patients may have difficulty communicating symptoms and medical complications due to poor oral hygiene or impaired swallowing.

Additionally, the researchers believe that limited access to health care services and inadequate testing practices may contribute to the higher rates of mortality and lower rates of diagnosis of flu seen in older patients with dementia.

A geographic analysis of the data showed that pneumonia and influenza (P&I) rates were highest among older adults in poor and rural areas, where there is a lower concentration of health care facilities.

“Limited access to specialized health care services can delay diagnosis and treatment of the flu, causing it to progress to pneumonia, the fifth leading cause of death among the elderly. This study has helped us identify this vulnerable population, and now further study is needed to confirm the findings and assess the testing and vaccination policies for older patients with dementia,” said Naumova.

Study data were obtained from the Centers for Medicaid and Medicare Services (CMS), and covered a span Of the 36 million hospitalization records for adults aged 65 and older, more than six million records documented a P&I diagnosis.

Of these records showing a P&I diagnosis, over 800,000 (13 percent) also showed dementia.

The demographic and geographic patterns of P&I hospitalizations and their links with hospital accessibility were explored.

Pneumonia and influenza admissions, length of stay in a hospital, and mortality rates among elderly with dementia were compared to national estimates.

The study was published online in advance of print in Journal of the American Geriatrics Society. (ANI)