Diet Appears to Modulate Alzheimer's Biomarker

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Medscape Today

Results of a new study provide more evidence that diet may modulate the risk for Alzheimer's disease.

In a 4-week diet intervention study, healthy cognitively intact older adults who stuck to a low-saturated-fat, low-glycemic-index diet experienced decreases in cerebrospinal fluid (CSF) levels of β-amyloid 42, a biomarker of Alzheimer's disease risk.

But in a group of older adults with amnestic mild cognitive impairment (aMCI), the healthy diet had the opposite effect, raising CSF levels of this protein.

These observations "made sense to us," Suzanne Craft, PhD, of the Veterans Affairs Puget Sound Health Care System in Seattle, Washington, who worked on the study, told Medscape Medical News.

"That's because in patients with Alzheimer's disease," she explained, "β-amyloid 42 sticks in the brain and so levels are lower in the CSF, and something that is going to reverse that process is going to raise levels in the spinal fluid."

"But for a healthy adult," she said, "it looks like levels get higher and higher over the course of life until, for some people, they reach a tipping point where [β-amyloid 42] begins to stick in the brain. In healthy adults, having levels decrease is actually a healthy pattern."

"It looks like a healthy diet that contains a lot of fruits and vegetables and healthy fats would be important for people who have Alzheimer's disease or conditions that put them at risk for developing Alzheimer's disease," Dr. Craft said.

The study appears in the June issue of the Archives of Neurology.

Mounting Evidence That Diet Matters to the Brain

There is a "fair amount" of evidence starting to accrue in the epidemiologic literature looking at what patterns of diet seem to both be protective and alternatively place someone at greater risk for Alzheimer's disease, Dr. Craft noted.

"That evidence," she said, "is suggesting that a diet like the Mediterranean diet seems to have a protective effect and a diet that has a lot of saturated fat and sugar seems to place you at greater risk."

"Those studies are very important for setting the stage, but what's different about our study is that we actually placed people on a very specific diet and provided every piece of food that they ate for an entire month," the researcher said.

The high-saturated-fat/high-glycemic-index diet included 45% fat (25% saturated fat), 35% to 40% carbohydrates (glycemic index > 70), and 15% to 20% protein. The low-saturated-fat/low-glycemic-index diet included 25% fat (< 7% saturated fat), 55% to 60% carbohydrates (glycemic index < 55), and 15% to 20% protein.

Participants included 20 healthy adults with a mean age of 69.3 years and 29 adults with aMCI and a mean age of 67.6 years. For 4 weeks, 24 participants followed the high-fat diet (9 healthy adults and 15 with aMCI) and 25 followed the low-fat diet (11 healthy adults and 14 with aMCI).

The number of times participants were nonadherent to their assigned diet was "small and comparable among groups," the authors note. The mean nonadherent incidents per week ranged from 1.23 to 1.80 per group.

Effects on β-amyloid "Striking"

As expected, in both groups, the high-fat diet produced unhealthy changes in serum cholesterol and insulin profiles, while the low-fat diet produced healthy changes in these measures.

Notably, the investigators say, the 4-week diet intervention had "striking effects" on β-amyloid 42 concentrations in CSF, the primary outcome measure, and the effects differed by diet and by cognitive status.

In the healthy adults, the high-fat diet increased CSF β-amyloid 42 levels, essentially moving them "in a direction that may characterize a presymptomatic stage of Alzheimer's disease before plaque deposition," the investigators note in their report. The high-fat diet also increased concentrations of the oxidative stress marker F2-isoprostane and lowered insulin levels.

Conversely, in the participants with aMCI, β-amyloid 42 levels were nearly unchanged by the high-fat diet, "possibly because more extreme intervention is needed to exacerbate already-extant pathologic processes," the investigators suggest.

The low-fat diet had beneficial effects in both the healthy participants and the participants with aMCI.

In the aMCI group, it increased β-amyloid 42 concentrations in the CSF, contrary to the pathologic pattern of lowered CSF β-amyloid 42 typically observed in Alzheimer's disease.

In the healthy adults, the healthy diet decreased CSF β-amyloid 42 levels, which may help move them away from the "tipping point" that corresponds with the start of β-amyloid brain deposition, leading eventually to cognitive impairment.

In both groups, the low-fat diet reduced F2-isoprostane concentrations; increased apolipoprotein E, which aids with β-amyloid clearance; and was associated with improved delayed memory, a hallmark cognitive deficit in aMCI and Alzheimer's disease.

In their paper, the researchers say their study provides "converging support" for recent epidemiologic investigations of dietary patterns and Alzheimer's disease risk.

The results, they conclude, support further investigation into the "possibility that consumption of a diet high in saturated fat and simple carbohydrates may contribute to pathologic processes in the brain that increase the risk of Alzheimer's disease, while a diet low in saturated fat and simple carbohydrates may offer protection against dementia and enhance brain health."

The study was supported by grants from the National Institute on Aging and by funding from the Nancy and Buster Alvord Endowment. The authors have no disclosed no relevant financial relationships.

New Research Calls For Pre-Alzheimer's Intervention To Maximize Benefits

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Inventorsspot
by T Goodman

Every month more studies are published that demonstrate that if there is to be successful avoidance of, or limitation to, the ravages of Alzheimer's disease, intervention needs to begin as early as possible. Several suggest that treatments begin before Alzheimer's symptoms appear. One study, published online just yesterday in the Archives of Neurology, shows the benefits of doing such.

Longitudinal Change of Biomarkers in Cognitive Decline, was conducted at 59 sites of the Alzheimer's Disease Neuroimaging Initiative, with 819 participants 55 to 90 years old. The study measured levels of amyloid beta peptide Aβ42 in cerebrospinal fluid (CSF), fludeoxyglucose F18 (FDG), and hippocampal volume, all known biomarkers of Alzheimer's disease. The researchers compared the development of these biomarkers with their subjects' cognitive changes at different ages and stages of Alzheimer's disease.

Findings reveal that the depth of the tracks left by the biomarkers become more and more prominent as the symptoms of Alzheimer's appear, but that the levels of CSF Aβ42, in particular, decline prior to cognitive loss. This information strongly calls for an intervention as soon as the CSF Aβ42 marker begins to decline, thus very possibly altering the course of the disease.

Roger N. Rosenberg, MD and editor of the Archives, cites the above study as well as others in his editorial published June 13, 2011 online edition of the Archives, in which he argues for the treatment of Alzheimer's before it is diagnosed. But, he writes, "In our research to develop a DNA anti-Aβ42 vaccine as preventive therapy for AD, we have encountered the idea that it should be clinically tested only after the diagnosis of AD has been made."

"It is incumbent on the AD research community," Rosenberg continues, "to educate our colleagues, the public, and regulatory agencies to accept that it is necessary to treat AD before it is symptomatic. Alzheimer's disease therapies must be allowed to be given in rigorous, phase-1 clinical trials to individuals who have progressive memory loss or mild cognitive impairment, before they are diagnosed with dementia due to AD, when preventive therapy has a chance to succeed."




Low fat, low glycemic index diet appears to help memoryIn an unrelated study, also published in the Archives of Neurology, researchers from the Veterans Administration Medical Center in Seattle compared levels of CSF Aβ42 in healthy adults and adults with mild cognitive impairment before and after a 4-week diet. Two diets, one a high fat, high glycemic index diet, and the second a low fat, low glycemic index diet, were randomly assigned to the groups.

After four weeks, CSF testing showed that the healthy group on the low fat diet reduced their CSF biomarkers for the disease, and they also performed better on memory tests than they did prior to the diet. Healthy persons on the high fat diet increased their biomarkers for Alzheimer's disease, characteristic of "a pre-symptomatic state of Alzheimer's Disease."

The early stage Alzheimer's subjects, those with mild cognitive impairments, did not experience a reduction in CSF biomarkers after the 4 week low fat diet, unfortunately. But the study certainly does force the issue of early intervention. Whether it's drugs or diet, these conclusions regarding the timing of Alzheimer's intervention should not be ignored.

Testosterone Therapy Improves Memory in Post-menopausal Women

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Newswise — Post-menopausal women have better memory after daily treatment with a testosterone spray for six months, a new preliminary study finds. The results will be presented Saturday at The Endocrine Society’s 93rd Annual Meeting in Boston.

“Women have a higher risk of developing dementia compared to men,” said Sonia Davison, MD, PhD, the study’s lead investigator and a postdoctoral research fellow at Monash University, Melbourne. “These results offer a potential therapy, where none currently exists, to slow cognitive decline in women.”

The researchers compared a control group of 30 women who received no treatment with a group of nine healthy women in early menopause (ages 47 to 60) who knowingly received the testosterone spray on their skin. The spray dose returned testosterone levels in the blood to those typical of young women of childbearing age, according to Davison. All of the treated women were receiving a stable dose of non-oral hormone replacement therapy.

All women underwent testing of cognitive function with a battery of computerized tests that can detect even small changes in cognitive performance, Davison said. The researchers tested subjects’ memory through their ability to recall items from a grocery list read aloud to them—a test of verbal learning and memory—and through their performance on tests of visual learning and memory. Cognitive testing occurred at the beginning and end (week 26) of the study.

At the start of the study the two groups did not differ significantly in their cognitive test results. After 26 weeks the untreated controls showed no significant differences between their initial and final test results, the authors found. The testosterone-treated group, however, improved their verbal learning and memory, as found on the shopping list test, Davison reported.

“This is exciting in that the testosterone-treated women were all healthy, with no cognitive impairment, and there was a definite treatment effect of the testosterone spray,” Davison said. “Testosterone may play a protective role against dementia.”

She said their results need confirmation in a randomized, controlled clinical trial.

The following organizations helped finance this study: the National Health and Medical Research Council of Australia, the Royal Australasian College of Physicians Research and Education Foundation (Vincent Fairfax Family Foundation fellowship) and FemPharm in Australia, which makes the testosterone spray for women.

Make Managing Mild Dementia Easier

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Caring.com

Paula Spencer

By "problem-proofing" your loved one's closet in the earliest stage of dementia, you can make dressing easier, prolong independence, and help avoid later embarrassing goofs.

Five easy ideas:

1. Conform the sock drawer.

Switch to socks that are all identical -- same style and color. No more searching for matches, or not realizing that brown and black aren't the same.

2. Go solid.

Pare down tops and sweaters so they all color-coordinate easily. Better still, eliminate prints so outfits never clash.

3. Adopt a uniform.

Some people with mild dementia choose to adopt a uniform look they're known for -- say, a white t-shirt and black cardigan with slacks, or a turtleneck a la Steve Jobs. A signature look becomes a stylish brain aid.

4. Enlarge the fasteners.

Go on a hunt for wee buttons and tiny zipper pulls. They can befuddle any pair of aging hands, but combined with the physical limitations dementia can bring, they can be utterly impossible. Best to weed them from the closet now.

5. Simplify the shoes.

Fussy buckles and challenging laces will become increasingly frustrating. Slip-on loafers, Velcro-style closures, or very simple styles are better.

Daffodil Drug Improves Dementia

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Worldhealth.net |

A new drug designed to treat Alzheimer's disease looks set to be an effective treatment for vascular dementia. A recent 12-month clinical trial of the drug Galantamine (Reminyl), which is derived from the daffodil, revealed that the drug improved cognitive function, delayed the effects of dementia, and prevented behavioral decline.

SOURCE/REFERENCE: Reported by www.health-news.co.uk

Study: Obesity in elderly boosts risk of dementia 300%

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Jerusalem Post

By JUDY SIEGEL-ITZKOVICH

Now there is another reason to control your weight: The journal Neurology has published Swedish research that has found that long-term obesity in older people raises the risk of developing dementia by 300 percent. Prof. Andrei Keidar, who is responsible for bariatric (stomach shortening) surgery at the Rabin Medical Center-Beilinson Campus in Petah Tikva, says the new findings are very important, and show that being overweight even in the elderly should be treated.

Eight thousand five hundred pairs of identical twins over 65 participated in the study; 350 were diagnosed as having vascular dementia (from blood vessel constriction), while 114 were suspected of having regular dementia. The researchers concluded that there is a significant connection between dementia and obesity.

Keidar explained that it has been known that metabolic diseases of the overweight, such as type 2 diabetes, involve excess sugar – the primary “fuel” of brain tissue. It may be that the disruption of normal metabolism contributes to the increase in the prevalence of dementia beyond the damage caused to the blood vessels, he suggested. Thus he concludes that preventing obesity and treating it at a younger age could reduce the amount of Alzheimer’s disease and other dementias. Alzheimer’s affects some 100,000 Israelis – more than 6% of people aged 65, and up to half of those over 85.

Health Ministry statistics show that 44.6% of Israeli adult men and 31.7% of women are overweight.

In the US and Europe, some 50% of older people are overweight or obese.

Keidar suggested that the amount of time for which people were heavy could affect their risk of dementia.

Exercise, diets, medical treatment and – as a last resort – bariatric surgery can help people avoid a series of diseases that can harm the quality and length of their lives, said Keidar. Some 5,000 bariatric operations were conducted (it is included in the basket of health services for those qualified) last year, compared to only 1,500 in 2006. After extensive study, two international medical societies recently stated that the efficacy of bariatric surgery in improving the health of the obese has been proven.

New Direction in Alzheimer's Research Discovered

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Santa Barbara, CA (Scicasts) – According to a report from the University of California - Santa Barbara, scientists from the Institue have made an important finding about what happens to brain cells that are destroyed in Alzheimer's disease and related dementias.

The results are published in the online version of The Journal of Biological Chemistry.

Stuart Feinstein, professor of Molecular, Cellular and Developmental Biology, senior author, and co-director of UCSB's Neuroscience Research Institute, explained: "With dementia, the brain cells, or neurons, that you need for cognitive skills are no longer working properly. Then, they're not even there anymore because they die. That's what leads to dementia; you're losing neuronal capacity."

Feinstein has studied the protein called "tau" for about 30 years, using test tube biochemistry and a variety of cultured cells as models. Under normal conditions, tau is found in the long axons of neurons that serve to connect neurons with their targets, often far from the cell body itself. Among tau's major functions is to stabilize microtubules, which are an integral part of the cellular cytoskeleton that is essential for many aspects of neuronal cell structure and function.

It has been known for many years that a small peptide named amyloid beta can cause neuronal cell death and Alzheimer's disease, although the mechanism for how it works has been poorly understood. Recently, genetic evidence has demonstrated that the ability of amyloid beta to kill neurons requires tau; however, what it does to tau has been enigmatic. "We know amyloid beta is a bad guy," said Feinstein. "Amyloid beta causes disease; amyloid beta causes Alzheimer's. The question is how does it do it?"

He explained that most Alzheimer's researchers would argue that amyloid beta causes tau to become abnormally and excessively phosphorylated. This means that the tau proteins get inappropriately chemically modified with phosphate groups. "Many of our proteins get phosphorylated," said Feinstein. "It can be done properly or improperly."

Feinstein added that he and his students wanted to determine the precise details of the presumed abnormal phosphorylation of tau in order to gain a better understanding of what goes wrong. "That would provide clues for drug companies; they would have a more precise target to work on," said Feinstein. "The more precisely they understand the biochemistry of the target, the better attack a pharmaceutical company can make on a problem."

Feinstein said that the team's initial hypothesis suggesting that amyloid beta leads to extensive abnormal tau phosphorylation turned out not to be true. "We all like to get a curve ball tossed our way once in a while, right?" said Feinstein. "You like to see something different and unexpected."

The research team found that when they added amyloid beta to neuronal cells, the tau in those cells did not get massively phosphorylated, as predicted. Rather, the surprising observation was the complete fragmentation of tau within one to two hours of exposure of the cells to amyloid beta. Within 24 hours, the cells were dead.

Feinstein explained that tau has many jobs, but its best-understood job is to regulate the cellular cytoskeleton. Cells have a skeleton much like humans have a skeleton. The major difference is that human skeletons don't change shape very abruptly, whereas a cell's skeleton is constantly growing, shortening, and moving. It does this in order to help the cell perform many of its essential functions. The cytoskeleton is especially important to neurons because of their great length.

Feinstein argues that neurons die in Alzheimer's disease because their cytoskeleton is not working properly. "If you destroy tau, which is an important regulator of the microtubules, one could easily see how that could also cause cell death," said Feinstein. "We know from cancer drugs that if you treat cells with drugs that disrupt the cytoskeleton, the cells die," he said. "In my mind, the same thing could be happening here."

Cinnamon for dementia?

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JERUSALEM, (Xinhua) -- Cinnamon, a spice usually associated with sweet foods, contains properties that may delay the onset of Alzheimer's disease, and possibly offer a cure, according to a new Israeli study.

The neurodegenerative illness is characterized by gradual memory loss, which doctors attribute to an accumulation of beta amyloid, a fibrous protein aggregate, outside the brain's nerve cells. The World Health Organization says some 70,000 Israelis are currently diagnosed with the disease, out of 18 million worldwide.

A research team, headed by Michael Ovadia from Tel Aviv University's Zoology Department, recently isolated one of the ingredients in cinnamon, CEppt, and used it in a series of tests conducted on two-month-old lab mice that were raised with five aggressive strains of Alzheimer's-inducing genes.

The experiment's results, recently published in the PLoS ONE scientific journal, were impressive. Fed drinking water containing a CEppt solution over four months, researchers found that the disease's development was delayed, with additional trials showing that existing amyloids has been dissolved.

"The finding points at the possibility that the material found may not only prevent Alzheimer's but may also contain therapeutic qualities," Ovadia told the Ha'aretz newspaper.

"The discovery is exciting," Ovadia said. He said that while some companies are developing synthetic materials to combat Alzheimer's, CEppt is a "natural and safe" material with no side effects.

Testing on humans, he said, may prove difficult owing to the disease's slow progression. The research team is now considering trying out the recent discovery on other animals.

Despite the optimistic news, Ovadia cautioned against excessive consumption of cinnamon, which can damage liver functions, and recommends consuming no more than 10 gram a day.

Meanwhile, the professor said that he and his students have begun implementing the study's findings with a daily cup of tea mixed with a cinnamon stick.

New Insight on Cause of Alzheimer's

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Laboratory Equipment


For years researchers have known that a small peptide named amyloid beta can cause neuronal cell death and Alzheimer’s disease, although the mechanism for how it works has been poorly understood. Recently, genetic evidence has demonstrated that the ability of amyloid beta to kill neurons requires a protein called “tau”; however, what it does to tau has been enigmatic.

Under normal conditions, tau is found in the long axons of neurons that serve to connect neurons with their targets, often far from the cell body itself.

“We know amyloid beta is a bad guy,” says study leader Stuart Feinstein, professor of molecular, cellular and developmental biology at Univ. of California, Santa Barbara. “Amyloid beta causes disease; amyloid beta causes Alzheimer’s. The question is how does it do it?”

Most Alzheimer’s researchers would argue that amyloid beta causes tau to become abnormally and excessively phosphorylated, says Feinstein. This means that the tau proteins get inappropriately chemically modified with phosphate groups. “Many of our proteins get phosphorylated,” adds Feinstein. “It can be done properly or improperly.”

Feinstein’s research team wanted to determine the precise details of the presumed abnormal phosphorylation of tau in order to gain a better understanding of what goes wrong. “That would provide clues for drug companies; they would have a more precise target to work on,” says Feinstein. “The more precisely they understand the biochemistry of the target, the better attack a pharmaceutical company can make on a problem.”

The team’s initial hypothesis suggesting that amyloid beta leads to extensive abnormal tau phosphorylation turned out not to be true. “We all like to get a curve ball tossed our way once in a while, right?” says Feinstein. “You like to see something different and unexpected.”

They found that when they added amyloid beta to neuronal cells, the tau in those cells did not get massively phosphorylated, as predicted. Rather, the surprising observation was the complete fragmentation of tau within one to two hours of exposure of the cells to amyloid beta. Within 24 hours, the cells were dead.

The findings are reported in the Journal of Biological Chemistry.

In defense of Antipsychotic drugs for dementia

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By Daniel Carlat CNN

Although it's true that a prescription for antipsychotics to treat agitation in dementia is "off-label," this hardly means they are ineffective or that Medicare claims for these drugs are "erroneous." In fact, large placebo-controlled trials have shown that antipsychotics are the most effective medications for the agitation that often bedevils patients with dementia.

When these drugs are successful, they soothe the inner turmoil that makes life intolerable for these patients, improving their quality of life dramatically.

Off-label prescribing simply means the medicine has not undergone the vastly expensive process of gaining FDA approval. Doctors are allowed to prescribe medications off-label; indeed, without this prerogative, much of medical care would grind to a halt. More than 60% of drugs prescribed by both pediatricians and oncologists are "off-label," and almost all drugs prescribed by obstetricians fall into that category. Has your doctor every given you Valium to help you sleep? If so, your doctor was "erroneously" billing your insurance, according to the Office of the Inspector General, because Valium is FDA approved for anxiety, not for insomnia.

The unfortunate fact is that not a single medication is FDA-approved for the agitation of dementia, and yet the condition is common. About 15% of people over 65 have dementia, and half of them will develop agitation at some point. Anybody who has visited a loved one in the Alzheimer's unit of a nursing home understands agitation only too well; it includes combativeness, shouting, verbal abuse, extreme hyperactivity and sometimes outright violence to caregivers and family.

Agitation is often due to psychosis. For example, I recall one unfortunate gentleman with Alzheimer's disease who ripped an IV line out of his arm because he woke up in a strange room and believed his wife was in the next room calling his name. The room that seemed strange to him was a nursing home room he had occupied for three years, and his wife had died 15 years earlier.

This kind of agitation is dangerous for the patient, for staff and very upsetting for family members. When geriatric psychiatrists are asked to treat agitation, they look first for potential triggers that can be solved without resorting to behavioral drugs. Infections, drugs interacting with drugs, or pain are sometimes the culprits. At times, changes in the environment can help, such as increasing contact with a caregiver, changing roommates, or even adjusting the room's temperature.

But in many cases, such measures don't help enough.

Antipsychotics, such as Risperdal, Seroquel, and Zyprexa, have all been shown to be convincingly more effective than placebos in quelling agitation in the elderly. Their vaunted "lethal" risks are based on data that is surprisingly unimpressive. When each antipsychotic was studied separately, no significant difference in mortality was found between patients on drugs or on placebos. But when data on thousands of patients were combined, the mortality rate with four specific drugs was 4.5% in the medication group vs. 2.6% in the placebo group. The most common causes of death? Heart failure and pneumonia, which are the most common causes of death for all patients with dementia.

Physicians are not prescribing these medications in order to do harm to their patients. They are using them because there are no better options. Antipsychotics, by helping patients to be calm, are humane treatments for patients who are reaching the end of their days.

The solution is to expand research on safer and more effective treatments of dementia. It is not, as proposed by Levinson, to hire government auditors to decide whether doctors are prescribing drugs "appropriately." God help us if they do.

Another Reason to Have Weight Loss Surgery

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ac content

A new study points to evidence that weight-loss surgery in obese diabetics could lower their risk of developing Alzheimer's disease.
Researchers discovered that those who had gastric bypass, when they were tested six months after their weight-loss surgeries, had less evidence of genes that are thought to be precursors of the abnormal proteins that clogs the brains of people with Alzheimer's disease.

The study’s author is Dr. Paresh Dandona, a professor at State University of New York at Buffalo. The study was presented at the Endocrine society's annual meeting in Boston.

The researchers analyzed read all of Another Reason to Have Weight Loss Surgery

Treatment for Dementia May Be a Cancer Drug

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ac content

Reseachers at the University of Texas (UT) Southwestern Medical Center's Alzheimer's and Neurodegenerative Diseases Unit have made a remarkable discovery. The drug Suberoylanilide hydroxamic acid (SAHA) could be
used therapeutically for familial frontotemporal dementia (FTD). There is no treatment for the FTD, a neurological disease as of yet. FTD is the second most common form of non-elderly dementia.

People with FTD are usually diagnosed around the age of 60 though its symptoms may appear much earlier. Its onset is followed by a decline in decision-making ability, behavioral control, and/or language skills. About 25 percent of FTD patients have the familial or inherited form of the disease, in which one copy of the granulin (GRN) gene is normal and one is mutated, thus limiting the reproduction of GRN - a gene that is essential for the survival of nerve cells.

In studies performed by members of the UT Center, UCL A, UCSF, and the University of Massachusetts Medical School , SAHA...read all of Treatment for Dementia May Be a Cancer Drug

Is it Delirium or Dementia

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ac content

People with either or both dementia and delirium are unable to increase, retain, and use knowledge in the normal fashion. Delirium and dementia may occur together, but their medical definitions are quite different.

Delirium starts quite suddenly, causes changes in mental functioning, and is often reversible according to the medical definition. Delirium affects mainly attention. People with delirium are often disoriented, unable
to think clearly, and may be hyper one minute and in a sleep-like state the next. There are many causes of delirium. It may occur at any age. It is more common in older people because of changes in the brain that occur with age. Delirium affects 15 percent to 50 percent of hospitalized people who are 70 or older, according to the Merck Manual. It is common among nursing home residents.

A person with dementia gets worse over time. The disease slowly progresses and is most often irreversible. Dementia usually affects a person's short-term memory first. The other problems that a person with dementia may have include difficulty with language, planning ahead and judgment, simple mathematical calculations, and movement according to the medical definition. Age is a common risk factor for dementia. As the disease progresses, mental functions deteriorate depending on what part of the brain is affected.

To make a diagnosis of dementia, delirium must be .....read all of Is it Delirium or Dementia

Eye Test to Detect Alzheimer's Disease

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The eye test that may help diagnose Alzheimer's dsease detects dying nerve cells within the eye's retina. Dying nerve cells are one of the early signs of Alzheimer's disease.

Alzheimer's disease is a devastating mind robbing disease. At present, there is no cure. Usually the first sign of this disease is short tem memory loss. There are other thinking, speech and behavior problems as
Alzheimer's disease progresses. These problems are caused by brain cell death. Unfortunetaly, by the time the first outward memory problems occur, many brain cells have already died.

The new research which uses eye tests to detect dying nerve cells in the eye's retina were done in laboratories at the University College of London by Professor Francesca Cordeiro and other scientists Other research centers in Italy and the United States also studied this eye test. The research detected whether the technique could spot retinal cell death in the retinas of mice. The study was published in the journal, Cell Death and Disease.

Making a diagnosis of Alzheimer's disease is difficult so another test to help identify this condition would be helpful. Right now it is too early to say how soon this eye test might be available. Also it is not clear as to whether it would be safe, useful, or even able to be done in humans.

In this study scientists used a system to test nerve-cell death in the retina of the eyes of.mice. Because of similarities between nerve-cell death in the eye and in the brain, they hoped that this technique might give insight into brain nerve-cell death.

The researchers tracked...read all of...Eye Test to Detect Alzheimer's Disease