Thursday, September 29, 2011

Alzheimer's disease looks different in people over 80

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Medscape Today

Alzheimer's disease (AD) may be more difficult to detect in people older than 80 years, suggest results of a new study, because disease presentation may be different than that seen in the larger population of patients.

"The typical pattern of AD-related cognitive and morphometric changes seen in the young old appear to be less salient in the very old," first author Nikki H. Stricker, PhD, from the Veterans Affairs Boston Healthcare System and the Department of Psychiatry, Boston University School of Medicine, Boston, Massachusetts, and colleagues report.

"Thus, mild cases of AD in the very old may go undetected if one expects to see the prototypical pattern and severity of cognitive or brain changes that occur in the young old with AD," they conclude.

This study highlights "the importance of paying attention to age when reviewing cognitive test performances and in reviewing other possible biomarkers of Alzheimer's disease such as neuroimaging scans," coauthor Mark W. Bondi, PhD, from the Psychology Service, Veterans Affairs San Diego Healthcare System, San Diego, California, noted in comments to Medscape Medical News.

Their results are published online August 10 in Neurology.

Signs, Symptoms More Subtle in 80-Plus Group

The researchers compared hippocampal volume and cortical gray matter thickness in areas known to be affected by AD in 105 patients with AD and 125 healthy control participants. Participants between 60 and 75 years old made up the "young-old" group, whereas those 80 years and older made up the "very-old" group. Among the 105 participants with AD, 64 were young-old, and 41 were very-old.

Brain morphometric and cognitive scores of the patients with AD were standardized to their respective age-appropriate healthy control subgroup and then compared, the researchers explain.

In the very-old, compared with the young-old, there was less severe cortical thinning in the left posterior cingulate cortex, right lateral temporal cortex, and bilateral parietal cortex, as well as in overall cortical thickness.

This finding is, in part, because these brain areas decrease in thickness as a result of aging. Therefore, there are fewer differences between the healthy very-old brain and the very-old brain with AD, the researchers point out.

"Our results indicate that overlap between normal and AD-related brain changes seen on magnetic resonance imaging (MRI) scans is greater in the very-old than in the young-old," Dr. Bondi said. "For example, the typical pattern of brain changes seen in an 85-year-old person with AD is less salient than in a 70-year old person with AD."

Similarly, several cognitive domains, including executive function, immediate memory, and attention/processing speed, were less abnormal in the very-old patients with AD relative to their young-old peers.

Broad Clinical Implications

"Clarification of how the presentation of AD changes with age may enhance our ability to detect early AD in the very-old, one of the fastest growing segments of the population," Dr. Bondi commented.

"Enhanced detection will be crucial for early application of interventions that may slow the disease process, thus preserving cognitive status, functional independence, and quality of life," he added.

Reached for comment, Rhoda Au, PhD, from the Department of Neurology, Boston University School of Medicine in Boston, Massachusetts, said "the most important broader implications" of this study are "its recognition of the developmental continuum extending to the very last years of life (and) that the elderly population cannot be characterized as a single subset population."

Dr. Au was not involved in the study but authored a linked commentary in the journal.

"As more and more people live into the 8th and 9th decades and beyond, the diagnostic and treatment practices applied to the younger old may not apply or work as effectively with the oldest old," she told Medscape Medical News.

The study was supported primarily by the National Institutes of Health (NIH) and the Dana Foundation. Dr. Stricker receives or has received research support from the Rosalind and Arthur Gilbert Foundation/American Federation for Aging Research and the NIH. Dr. Bondi serves as an associate editor for the Journal of the International Neuropsychological Society and receives research support from the Alzheimer's Association and the NIH. A complete list of author disclosures is listed in the original article. Dr. Au receives research support from the National Institute on Aging, the National Institute of Neurological Disorders and Stroke, and the Fogarty International Center.

Tuesday, September 27, 2011

Sophisticated scan may spot seeds of Alzheimer's risk

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Steve Reinberg HealthDay news

Using an advanced MRI scan, researchers believe they have found changes in the chemistry of the brains of people with no cognitive problems that signal who is at future risk for Alzheimer's disease and other dementias.

And although there is no good treatment or cure for the disease, experts say finding ways to identify those at risk is essential when treatments and possibly a cure become available.

"We found biochemical changes that correlated with cognitive performance," said lead researcher Dr. Kejal Kantarci, a radiologist at Mayo Clinic in Rochester, Minn. "The better people did on tests that measure cognitive abilities, the fewer changes there were."

These biochemical changes were also associated with other changes in the brain that are markers for Alzheimer's disease, Kantarci said.

Kantarci said that people should not be looking at getting scans to detect these changes. "We are just at the early stages of identifying markers," she stressed.

However, finding these biomarkers is important, Kantarci added. "When possibilities for preventive intervention come about, then we will have a marker which will help us identify those individuals who would benefit from these preventive interventions," she said.

The report was published in the Aug. 24 online edition of Neurology.

For the study, Kantarci's group used a technique called proton magnetic resonance spectroscopy to see if they could identify changes in brain chemistry in 311 men and women in their 70s and 80s who had no apparent cognitive problems.

The participants also underwent PET scans to see if there were any amyloid-beta deposits, or plaques, in the brain. These plaques are the first signs of Alzheimer's disease, the researchers noted.

In addition, participants took tests that evaluated memory, language and other skills.

Kantarci's team found that 33 percent of the people had significantly high levels of amyloid-beta deposits in their brains. These people also had high levels of two chemicals: myoinositol/creatine and choline/creatine.

Those with high levels of these so-called brain metabolites also were more likely to have lower scores on several of the cognitive tests, regardless of the amount of amyloid-beta deposits in their brains, the researchers added.

Kantarci said these biochemical changes start years before people show signs of cognitive problems. Whether these markers are a cause of dementia or only a signal for other changes isn't known, she said. "What we are seeing is a marker of a pathological process rather than a cause," she explained.

Heather M. Snyder, senior associate director of medical & scientific relations at the Alzheimer's Association, said "there is a growing body of evidence that biological changes associated with Alzheimer's disease are occurring maybe even 20 years prior to any individual having any cognitive issues."

"The goal is that we would like people to live a healthy life as long as possible, so if we can diagnose people with these changes as early as possible, when a treatment is available we can intervene -- that's really our ultimate goal," she said.

That's why finding ways to identify people at risk early is important while the search for treatments and cures continues, Snyder said.

Identifying people at risk for dementia is also important for research, said Dr. Marc L. Gordon, a neurologist and Alzheimer's researcher at The Feinstein Institute for Medical Research in Manhasset, N.Y.

"It is important to identify people at risk of dementia, particularly if we want to test therapies that have the potential to alter the process to try to prevent people from converting to dementia," he said.

Greg M. Cole, a neuroscientist at the Greater Los Angeles VA Healthcare System and associate director of the Alzheimer's Disease Research Center at the University of California Los Angeles David Geffen School of Medicine, said that "these results show that more and more specific biochemical changes that presage Alzheimer's disease can be detected in our normal aging population using sophisticated imaging technology."

But, Cole added, "The question now is whether we can find a way to intervene in people where these very early steps in the disease process are measurable by suppressing the pathological process until we normalize the disease indices and show that they don't go on to develop dementia."



Sunday, September 25, 2011

Calcified Plaque in Arteries May Pose Stroke, Dementia Risk

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American Heart Association
Calcified Plaque in Arteries May Pose Stroke, Dementia Risk
American Heart Association Rapid Access Journal Report
Study Highlights:

Calcium build-up in blood vessels outside the brain may be associated with brain changes linked to future risk of dementia and stroke.
The results may help understand how atherosclerosis affects brain function and ultimately the risk of developing dementia and stroke.

Greater calcium build-up in blood vessels outside the brain may be associated with brain changes linked to future risk of dementia and stroke, according to new research in Arteriosclerosis, Thrombosis and Vascular Biology: Journal of the American Heart Association.

"The relationship between calcium in atherosclerotic plaque and brain changes exists on top of the effect of classic cardiovascular risk factors such as high blood pressure, smoking and diabetes," said Meike W. Vernooij, M.D., Ph.D., senior study author and assistant professor of epidemiology and radiology at the Erasmus Medical Center in Rotterdam, the Netherlands.

Furthermore, the amount of hardened, calcified plaque provided more information about the extent of brain changes than traditional ultrasound measures of the presence of plaque in the carotid artery.

The researchers studied 885 people, average age 67, participating in the Rotterdam Study, which includes varying types of imaging to better understand the causes and predictors of dementia and stroke. They used computed X-ray tomography (CT) scans to measure calcification in four blood vessel areas: the coronary arteries that feed the heart; the aortic arch (part of the body's largest artery that delivers blood from the heart into the general circulation); and the extracranial and intracranial carotid arteries that carry blood through the neck into the brain.

Researchers used magnetic resonance imaging or MRI of the brain to visualize small brain infarctions, microbleeds (tiny brain bleeds) and bright areas called white matter lesions. White matter in the brain refers to the fiber tracts that carry information to and from the brain. White matter lesions are more commonly seen in patients who have risk factors such as a history of hypertension, diabetes and high cholesterol.

"These subclinical brain changes, apparent on MRI, do not necessarily cause symptoms right away but are frequently seen in patients with stroke or dementia and over the long term may be associated with worse cognitive performance," Vernooij said.

Among the results:

Calcium build-up in each of the four arteries scanned was associated with the presence of small brain infarctions and white matter lesions in the brain.
No associations were found between microbleeds in the brain and calcification in any of the arteries studied.
As predicted, the amount of calcification in vessels closer to the brain — the extracranial and intracranial carotids — had the strongest relationship to MRI markers of vascular brain disease.
The most prominent associations were found between intracranial carotid calcification and the volume of white matter lesions, and extracranial carotid calcification and brain infarctions.
"The distinction between the impact of calcification in the extracranial and intracranial carotids adds to the current belief that white matter lesions mainly result from disease in smaller intracranial vessels, while brain infarctions are thought to be mainly caused by larger vessel disease," Vernooij said.

The results will be used to advance the understanding of how atherosclerosis affects brain function and ultimately the risk of developing dementia and stroke.

"We are a long way from using CT-assessed calcification to screen individuals for brain lesions and dementia risk," Vernooij said.

Unanswered questions include whether treatment can reduce calcification in blood vessels and whether doing so would improve cognitive health or lower the risk of dementia and stroke.

However, if a physician has performed a heart CT scan to assess heart attack risk, the results may provide information that extends beyond the reason for the examination.

"Though far away from the brain, calcification in coronary arteries may indicate the presence of subclinical brain disease as well," Vernooij said.

Co-authors are: Daniel Bos, M.D.; M. Arfan Ikram, M.D., Ph.D..; Suzette E. Elias-Smale, M.D., M.Sc.; Gabriel P. Krestin, M.D., Ph.D.; Albert Hofman, M.D., Ph.D.; Jacqueline C.M. Witteman, Ph.D.; and Aad van der Lugt, M.D., Ph.D. Author disclosures and funding sources are on the manuscript




Friday, September 23, 2011

Atypical psychotics may hasten dementia decline (part 2)

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Medscape Today
Deborah Brauser

great deal of care," said Dr. Schneider.

He added that the meta-analysis showing a link between atypical antipsychotics and increased mortality risk in an elderly population with dementia helped support the Food and Drug Administration's (FDA's) subsequent black box warning in 2005.

A recent study published in the Archives of General Psychiatry and reported by Medscape Medical News at that timeshowed use of atypicals to treat behavioral symptoms has decreased significantly since the FDA warning was issued. However, other studies have shown that the overall prescription rate has not decreased ( Arch Intern Med. 2010;170:89-95 and CMAJ. 2008;179:438-446).

In the current study, investigators evaluated data on the 421 outpatients with AD and psychosis or aggressive behavior from CATIE-AD, which was conducted at 45 sites in the United States between April 2001 and November 2004.

Significant Decline

During the first phase of the trial all participants were randomized to receive flexible doses of either olanzapine (n = 100; mean dose, 5.5 mg/day), quetiapine (n = 94; mean dose, 56.5 mg/day), risperidone (n = 85; mean dose, 1.0 mg/day), or placebo (n = 142).

After 2 weeks, they could discontinue their allocated treatment and switch to another randomly assigned medication, on their clinicians' request. If they discontinued use of that medication, patients could move into phase 3 of the study, which consisted of open-label treatment with one of the other randomly assigned study drugs.

"At any time, the clinician could choose to enter the patient into phase 4, where data collection continued but the physician prescribed medication," explain the researchers.

The subjects were followed up for 9 months and scheduled to undergo cognitive assessments at the 12-, 24-, and 36-week timepoints. This new analysis assessed the 357 patients (54% male; mean age, 77.6 years) who participated in at least 1 baseline and 1 follow-up cognitive measure.

Measurements included the Mini-Mental State Examination (MMSE), the cognitive subscales of the AD Assessment Scale (ADAS-Cog) and of the Brief Psychiatric Rating Scale (BPRS), a cognitive summary score that combined changes on 18 cognitive tests, and the Clinical Global Impression of Change (CGIC).

Results showed that at 36-week follow-up all of the patients had declined significantly in most cognitive areas, including worsening scores on the MMSE (−2.4 points) and ADAS-Cog (−4.4 points).

The only statistically significant difference between individual antipsychotic groups and the placebo group were greater cognitive decline in the following:

•the cognition summary for those taking olanzapine or risperidone (P = .04 and P = .001, respectively);
•the MMSE for those taking olanzapine (P = .05); and
•BPRS for those taking quetiapine (P = .05).
When all 3 atypical groups were combined, participants' cognitive function decreased significantly more than their counterparts who were taking placebo on the MMSE (P = .004), BPRS (P = .05), and cognitive summary (P = .004).

"Over the 36-week trial period, patients receiving any antipsychotic had an average decline 2.46 points greater on the MMSE than placebo patients, a difference both statistically significant and clinically relevant," write the researchers.

The average CGIC scores for all 4 groups indicated minimal improvement and did not differ significantly (placebo, 3.13; olanzapine, 3.11; quetiapine, 2.83; risperidone, 2.81).

Permanent Effect?

"Because we did not measure differences in the rates of cognitive decline over longer exposure periods, we cannot address the question of whether these drugs would accelerate [the] decline permanently or merely impair cognition during acute administration," the investigators write.

They note that they also do not know whether the decrease in cognition was due to a worsening of Alzheimer's pathology or if it was an independent effect.

Much of medication use is due to the lack of interest, willingness, funding, or ability to provide psychosocial or environmental interventions to patients with agitation, aggression, and psychosis who have dementia.
Although the investigators write that the declines found in this study reached "at least as great a magnitude as the effect of cholinesterase inhibitors but in the negative direction," they add that use of atypicals may still be warranted in individual cases.

"The relative adverse effects on cognitive function within the class of medication need to be addressed in further studies that include assessment of attention, psychomotor function, and executive function," they write.

Dr. Schneider noted that nonpharmacologic treatments should also be investigated.

"Much of medication use is due to the lack of interest, willingness, funding, or ability to provide psychosocial or environmental interventions to patients with agitation, aggression, and psychosis who have dementia."

He explained that much agitation can be redirected and that aggression often comes about due to cognitive impairment — and can be mitigated by the way caregivers react to or communicate with patients.

"These approaches have limits too, but certainly they are not applied enough because they involve significant amounts of time and training," said Dr. Schneider.

Few Alternative Treatments

"Risk-benefit analysis is always part of the decision to use psychotropic medication. The aged are a particularly vulnerable group, and this study strongly underscores that vulnerability," write D. P. Devanand, MD, from the Division of Geriatric Psychiatry at the College of Physicians and Surgeons at Columbia University in New York City, and Susan K. Schultz, MD, from the Department of Psychiatry at the University of Iowa College of Medicine in Iowa City, in an accompanying editorial.

"Neuropsychological testing across a range of domains in this study offers a powerful look at the progression of AD in the context of treating neuropsychiatric symptoms," they add.

However, they caution that several caveats should be considered "when interpreting the findings and their potential impact on clinical practice," including that the investigators had to combine the 3 treatment groups to find statistical differences from placebo on the MMSE and the summary scores.

"It is likely that individual vulnerabilities to specific antipsychotics are mediated by a variety of factors, including concomitant medications, medical comorbidity, and underlying frailty, that are beyond the scope of this analysis."

Despite the widespread awareness of adverse consequences, we can only infer that atypical antipsychotics continue to be prescribed for dementia treatment because there is a lack of alternatives and there is a perceived clinical benefit by care providers.
In addition, the editorialists note that "while dose effects were not addressed in this analysis, adverse events in this population are dose related, and treatment dropouts occur more frequently with risperidone doses above 2 mg and olanzapine doses above 5 mg."

Other concerns cited include that data for any patient receiving an antipsychotic for at least 2 weeks was included, whether they had switched medications or not, which may result in short-term harmful effects that may not continue with longer treatment exposure.

Dr. Devanand and Dr. Schultz note that alternative pharmacologic treatments, such as benzodiazepines, also provide risky cognitive liabilities.

"Despite the widespread awareness of adverse consequences, we can only infer that atypical antipsychotics continue to be prescribed for dementia treatment because there is a lack of alternatives and there is a perceived clinical benefit by care providers," they write.

"These complex issues will require a thoughtful and balanced evaluation with an appreciation of the care setting, individual patient vulnerabilities, and goals of care."

The study was supported by the National Institute of Mental Health, the USC Alzheimer's Disease Research Center, and the Department of Veterans Affairs. Medications were provided by AstraZeneca, Forest, Janssen, and Eli Lilly. The study authors report several disclosures, which are listed in the original article. The editorialists report having received research support from Eli Lilly and Novartis and are currently consultants for Bristol-Myers Squibb and Sanofi-Aventis.




Wednesday, September 21, 2011

Atypical antipsychotic drugs may hasten dementia decline

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Medscape Today
Deborah Brauser

Use of atypical antipsychotics to treat agitation or psychosis in patients with Alzheimer's disease (AD) may lead to severe cognitive impairment, according to new findings from the Clinical Antipsychotic Trials of Intervention Effectiveness–Alzheimer's Disease (CATIE-AD) study.

In the analysis, investigators found that patients with AD randomly assigned to olanzapine, quetiapine, or risperidone showed a significant decrement in neuropsychological functioning, as seen on several cognition measurements, compared with those receiving placebo.

"We found that the atypical antipsychotics used in this study were as a group associated with worsening cognitive function and that the magnitude of this impairment was, on average, the rough equivalent of 1 year's progression of illness," principal investigator of the CATIE-AD studies Lon S. Schneider, MD, professor of psychiatry, neurology, and gerontology at the University of California (USC) Keck School of Medicine in Los Angeles, told Medscape Medical News.

"It really comes down to the fact that the current medications aren't very effective in treating agitation, aggression, or psychosis in dementia. So maybe we should be trying to address these problems in different ways than merely prescribing the medications that have been licensed for treating patients with schizophrenia or major depression."

The study is published in the August issue of the American Journal of Psychiatry.

Efficacy Offset by Adverse Effects

"Delusions or hallucinations appear in 30% to 50% of patients with AD, and up to 70% demonstrate agitated or aggressive behaviors," report the researchers.

In a meta-analysis conducted the same year, Dr. Schneider's team found small effect sizes on symptom rating scales for aripiprazole and risperidone along with significant adverse events, including cerebrovascular events and worsening cognitive test scores, in older patients with AD.

"Any advantages of efficacy found for these drugs were offset in general by lack of tolerability and by adverse effects. So they should be used with a

Monday, September 19, 2011

New way for treating Alzheimer's disease

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Examiner.com
Ruben Dagda, Pittsburgh Medical Technology Examiner

Making the blood brain barrier more permeable may be the answer

Although there is currently no cure for treating Parkinson's and Alzheimer's disease, a preclinical study published yesterday at the prestigious Journal of Neuroscience may revolutionize the way patients will be treated in the US. Currently, one of the major impediments for treating many neurodegenerative diseases is the fact that the blood brain barrier is highly impermeable to most FDA approved and experimental drugs. Therefore, only a small fraction of the drug reaches the brain and has a therapeutic effect.

However, scientists from Cornell University discovered a way to make the blood brain barrier more permeable so that the brain absorbs a higher amount of therapeutic drugs: by using adenosine agonists. In brief, scientists discovered that mice intravenously injected with drugs that stimulate adenosine receptors (NECA) were able to accumulate a higher amount of an experimental sugar molecule (dextran) in the brain upto three times more compared to untreated animals. The modified sugar stayed in the brain upto 24 hrs. following a single intravenous injection of the adenosine receptor agonist drug. The effect of the drugs on the blood brain barrier is specific for adenosine receptors since mice that lacked adenosine receptors did not accumulate the dextran in the brain.

What is the medical relevance of this study?

A pathological hallmark of Alzheimer's disease is that patients accumulate protein garbage in neurons called beta-amyloid and tau protein which is associated with the destruction of memory neurons. Using a mouse model of Alzheimer's disease, the scientists showed that mice co-injected with adenosine agonists and with beta amyloid busters (a monoclonal antibody called 6E10) were able to bind to beta amyloid deposits in mice. This experiment is a proof of principle for using drugs that can make the blood brain barrier and with FDA approved drugs for Alzheimer's disease such as acetycholinesterase inhibitors. This study is promising and can lead to the creation of new revolutionary therapies for treating Alzheimer's disease.

Final remarks-

Approximately about 5.5 million people are afflicted with Alzheimer's and Parkinson's disease in the US. Many patients over 65 years of age are relegated to spending their final days of life in nursing homes or are cared by family members which can be a great economic and emotional burden.

There is a great need for finding safe and efficient techniques to administer drugs that can penetrate the blood brain barrier in high concentrations. Nowadays, some patients undergo highly invasive techniques such as direct injections of drugs into the ventricles of the brain, epidural injections or installing intracranial pumps to treat neurodegenerative diseases. Also, most drugs need to be chemically modified so that it can reach the blood brain barrier but renders the drug also capable to concentrate in unwanted tissues.

But what if we can avoid all this hassle and inconvenience of undergoing painful surgical procedures or spending a high amount of money on drugs that do not reach the brain? For instance about less than 10% of Parkinson's disease drugs such as Levodopa in combination with Carbidopa reach the brain while the rest is metabolized and wasted in Parkinson's disease patients. The solution proposed by the authors could bring down the costs of anti-neurodegenerative drugs and increase patient compliance.

The only downside is that patients will not be able to drink coffee or other caffeinated products if adenosine analogues or the FDA approved Lexiscan is used as treatment for Parkinson's and Alzheimer's.


References:

Carman, A., Mills, J. Krenz, A., Kim, D. Bynoe, M. Adenosine receptor signaling modulates permeability of the blood-brain barrier, 2011, The Journal of Neuroscience 31(37): 13272-13280.

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Saturday, September 17, 2011

Intranasal insulin treatment for Alzheimer's disease

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Alzheimer's Association

Currently, there is no cure for Alzheimer's disease. But drug and non-drug treatments may help with both cognitive and behavioral symptoms. Researchers are looking for new treatments to alter the course of the disease and improve the quality of life for people with dementia.

In an article published September 13, 2011, in the Archives of Neurology, results from a small, short-term treatment trial (four months) of intranasal insulin in Alzheimer's disease and mild cognitive impairment (MCI) showed statistically significant benefits on certain tests of memory and functioning, but no changes on some others. In those people who showed benefits on memory tests, the researchers also measured changes in chemicals in participants' spinal fluid that may indicate a beneficial effect of the treatment on Alzheimer's.

It is important to note that, quite often, preliminary studies like this generate positive results but fail to show long-term benefit in larger trials. That said, these findings are very encouraging, and further research — longer trials with larger numbers of participants — of intranasal insulin as a therapy for Alzheimer's and MCI is warranted.

We urgently need earlier detection and better treatments for Alzheimer's, which is a devastating, heartbreaking and fatal disease, and a growing epidemic. This requires a greater commitment to research — increasing funding for Alzheimer's research and recruiting more volunteers for Alzheimer's clinical trials.



























































































































































Researchers selected 104 men and women for the study. All had either mild to moderate Alzheimer's or mild cognitive impairment, a condition that increases the risk of developing Alzheimer's, especially when memory is affected. The participants were divided into three groups. Using a nasal spray, each group received twice-daily doses of either lower or higher doses of insulin or a placebo.

The study found that men and women who used the lower dose of insulin nasal spray tended to score better on memory tests than those who used the placebo. No improvement was seen in those receiving the higher insulin dose. Both groups receiving insulin preserved their level of daily functioning, according to reports from their caregivers, while participants in the placebo group showed an overall decline in function. Few side effects occurred among those treated with the insulin spray, other than occasional light-headedness and dizziness or stuffy nose.

Related
•Minor ailments linked to Alzheimer's. Read
•Can you walk away from dementia? Read
•Eating berries may protect against dementia, Alzheimer's. Read
•Do drugs for treating early-stage Alzheimer's work? Read

The brain needs insulin

Over the past 10 years scientists have come to learn that insulin plays an important role in the brain, says clinical neuroscientist Suzanne Craft, of the Veterans Affairs Puget Sound Health Care System and the University of Washington School of Medicine. It helps the brain form memories, allows brain cells to communicate with one another and manages levels of brain chemicals.

All cells, including those that make up the brain, use glucose for energy. The hormone insulin makes it possible for glucose, aka blood sugar, to enter cells, enabling them to work properly. With age, however, many people develop a problem called insulin resistance, a condition in which the body and the brain do not use insulin effectively.

If glucose cannot enter brain cells, the cells won't carry out their tasks related to memory and thinking. "This sets the stage for problems in brain function that may develop into conditions like Alzheimer's disease," says Craft, lead author of the study. She and her colleagues set out to determine whether providing insulin directly to the brain could improve the cell's ability to use insulin.

Tuesday, September 13, 2011

Why you should celebrate World Alzheimer's Day on September 21

World Alzheimer's Day


Caregivers, and healthcare professionals,here is interesting information
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Here are more interesting dementia brain boosting activities

Healthnews-stat.com



Author Susan Berg says "It is everyone’s duty to embrace this day because there is no time to lose when fighting the battle of preventing this terrible disease." Here are some simple things you can do

What do you know about Alzheimer’s disease and related dementias?

How can you decrease your chances of getting these disease?

How can you help someone with Alzheimer’s disease or a related dementia?

This year’s theme is 'Faces of dementia'
'
Yes, there is an urgency for all to learn about these diseases and do what they can to prevent them in themselves. Also legislators need to contacted so more funds can be allocated for research. World Alzheimer’s day, on Sept 21, is the perfect time to do this.

Approximately 5.5 million people in the United States already have Alzheimer’s disease or a related dementia. The number will continue to grow as the baby boomers reach the age of retirement.

What can you do right now to lessen your chances of getting these diseases?

1. Stop smoking! There is nothing positive about smoking. Studies have shown that smoking not only raises your chances of developing dementia, but it also increases your chances of getting other diseases.

2. Eat a healthy diet. Research suggests that the Mediterranean diet staves off the onset of dementia

3. Keep mentally active. Again studies have shown this, to be a way to delay the onset of dementia.

4. Keep physically active. Research indicates that moderate exercise at least a half an hour three times a week is another way to keep dementia from affecting you.

How can you help others?

Donate to the Alzheimer’s Association. Give your time and/ or money. Help with special events. Organize fund raisers.

Susan Berg has written a book called, Adorable Photographs of Our Baby, for those with dementia, their caregivers, and interested professionals.
She is donating money to the Alzheimer’s Association for each book she sells. She is passionate about educating others on these diseases. Visit her blog at http://dementiaviews.blogspot.com.

You or someone you know could develop symptoms tomorrow. The cost of caring for those with Alzheimer’s disease or a related dementia is expensive monetarily, physically, emotionally, and psychologically.

So please acknowledge World Alzheimer’s Day, this Tuesday, September 21

Sunday, September 11, 2011

Heart's Pumping Ability May Hold Key to Dementia

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By Kristina Fiore, Staff Writer, MedPage Today
Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner

Left ventricular ejection fraction (LVEF) may play a role in cognitive aging, but that role is not a simple matter of impaired LVEF, researchers found.

Patients in lowest quartile of LVEF performed significantly worse on several cognitive tests than patients in middle quintiles, but there was no linear association since U-shaped curves also showing an association between the highest LVEF levels and cognitive aging, Angela Jefferson, PhD, of Boston University, and colleagues reported online in the American Journal of Cardiology.

Jefferson and colleagues called these findings "unexpected."

Heart failure is a known risk factor for Alzheimer's disease and cerebrovascular disease. But even in the absence of end-stage heart disease, it's thought that LVEF may have an affect on brain aging.

To test their hypothesis that lower LVEF was associated with cognitive and neuroimaging markers of preclinical Alzheimer's disease, Jefferson and colleagues looked at data from the Framingham Offspring Study, an offshoot of the Heart study.

They analyzed brain MRI and cardiac MRI studies as well as the results of neuropsychological examinations for 1,114 patients -- mean age 67 -- who didn't have stroke or dementia.

Multivariate analyses revealed overall that LVEF wasn't associated with any brain variable.

However, there were several U-shaped associations when LVEF levels were separated into quintiles.

Patients in the first quintile, or those with the lowest LVEF values, had lower mean cognitive performance on several cognitive tests, including the Visual Reproduction Delayed Recall and the Hooper Visual Organization Test, compared with patients in the middle quintiles (P<0.001 for both).

But the researchers noted that there were no differences among groups on any of the brain MRI variables.

Unexpectedly, they said, patients in the highest quintile of LVEF values also had lower mean performance on cognitive tests, including the Logical Memory Delayed Recall (P=0.03), the Visual Reproduction Delayed Recall (P=0.03), the Trail Making Test (P=0.02), and the Hooper Visual Organization Test (P=0.02).

Jefferson and colleagues reported that the associations were similar even after excluding prevalent cardiovascular disease.

"The observation that a lower LVEF is associated with abnormal brain changes extends previous research examining patients with severe cardiomyopathies, which reported that a reduced LVEF was associated with memory, reasoning, and sequencing impairments," they wrote.

"While healthy LVEFs may be good for brain health, very high LVEFs may correspond to subtle cognitive impairment," they wrote, adding that the finding may also be a sign of another pathologic process such as anemia or thyroid disease.

The study was limited by its use of observational, cross-sectional data, which cannot establish causality. The study may also be limited in generalizability, because the cohort was predominantly white and middle-aged to elderly.

Still, they concluded that "in the absence of clinical heart failure and prevalent cardiovascular disease, our findings suggest that lower LVEFs are also related to abnormal brain aging."

Friday, September 9, 2011

The danger of your aging parent covering up dementia (part 2)

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Forbes

Carolyn Rosenblatt

Mom just steps in and does what Dad is forgetting. He forgot, for instance, how to make coffee. He’s been making coffee for decades. He forgot the steps. He didn’t remember them later. He got lost driving home. Is that “normal” because he’s 86? It isn’t. Both of these memory issues are signs of trouble brewing.

Dad refused to try a new card game, something he’s always loved to do in the past. He is having more and more trouble learning any new information, say nothing of keeping track of the information he already knows.

Jaclyn wants to help, but is afraid to bring up the subject of what she sees. Mom will just deny a problem and say Dad is fine, just getting old.

Does it matter whether Dad goes to see a neurologist? Yes. At least that can help sort out the behavior that is not what the family is used to seeing and rule out various causes. Medication interactions, infections, stroke, and even dehydration can cause changes in brain function and behavior. It’s good to find out possible reasons for the memory problems and learn whether they can be treated.

A doctor generally won’t diagnose Alzheimer’s Disease unless there is enough evidence from testing and examining a patient to give the physician reasons to do so. There’s no one test to tell you if your aging parent has it or not. We get clues and doctors draw reasonable conclusions from them, but it’s not a precise thing.

Regardless, if your aging parent is showing the signs Jaclyn’s father is showing, you can take better control of how you handle the problem by acting on the signs rather than ignoring them. You can be sure that if Dad gets lost driving home, his driving days should come to an end. That is definitely worth talking to the doctor about, as Dad may need help facing the enormous consequences of losing the ability to drive.

If there is no official diagnosis other than “early dementia” or “mild cognitive impairment”, it’s not a signal to the family that everything is ok and no one needs to plan ahead. Rather, it’s time to take a look at Dad’s future. In advising Jaclyn, I gave her a list of a few things to check into now, rather than wait for a crisis.

Here’s Jaclyn’s 4-item beginning “to do” list:

Wednesday, September 7, 2011

The Danger Of Your Aging Parent Covering Up Dementia

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Carolyn Rosenblatt

The signs are subtle at first. The brain-destroying disease that creeps up unannounced and steals your loved one comes in disguise. “Maybe he’s just getting old”, you tell yourself.

Your aging parent may have noticed being unable to remember things for some time. Dad will compensate by changing the subject, or finding some other words to replace the ones he can’t find. But he might just stop in the middle of a sentence. He works at covering up the problem.

Mom will insist she’s fine. She knows she isn’t but doesn’t want you to find out. She’ll do anything to keep her memory loss a secret. She fears you’ll put her in a home. To her, that’s a death sentence.

No one has yet developed a simple test for Alzheimer’s or other dementias. Brain scans and MRI’s don’t tell us exactly who has Alzheimer’s and who doesn’t. They only give some clues. Neurologists and primary care physicians make educated guesses. Your aging parent can fool others for a while before the symptoms are unmistakable.

Here’s what’s important: it doesn’t matter if you have a diagnosis for your aging parent or not. It matters how your aging parent functions. It matters how you deal with what you see.

If your aging parent or loved one is showing persistent memory loss and starting to mess up the basics of life, it’s a warning you should not ignore. It’s more than a “senior moment”.

Here’s an example. A friend, Jaclyn, asked me for some information about her father, age 86. Aging is my field and advising is what I do for a living.

Jaclyn’s dad is a brainy guy, a mathematician in his pre-retirement years. She’s noticing changes, which her mom is covering up. He can’t keep track of their finances any longer. Jaclyn knows this isn’t the Dad she’s used to.

Monday, September 5, 2011

How to celebrate Grandparents day with those who have dementia

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be



Folks with dementia love children, especially babies. Take advantage of Grandparent’s day to allow these two groups of people to connect. Kids make most people smile especially those with dementia

Over 5.4 million Americans have dementia. Most of them are grandparents. Folks with dementia love children, especially babies. Take advantage of Grandparent’s day to allow these two groups of people to connect. Kids make most people smile especially those with dementia

Even though Grandparent’s day is Sept 11, extend it to Grandparent’s week if you are dealing with someone who has dementia. If too many grand kids visit at once, the excitement and confusion might be too much for a dementia person. Have the grandchildren visit one or two at a time. That way quality time is exchanged and the level of confusion is kept at a minimum.

Keep visits short. Discuss dementia with the children before the visit. There are many good books to assist you in helping a child to understand dementia. One such book is The Magic Tape Recorder by Joyce Simard. This is a thoughtful and well written book that explains the effects of Alzheimer's disease and related dementias to children in a light and entertaining way. If the youngsters are familiar with the disease, the time spent together will be more meaningful for all.

What should you do during the visit?
There are many activities that both the dementia person and children enjoy.
*Look at family pictures and recall the stories that go with them. Of course, you would have told the child that he may hear the same story several times. If you do not have old family photos or have not organized them yet, use this book, Adorable Photographs of Our Baby-Meaningful, Mind Stimulating Activities and More for the Memory Challenged, their Loved Ones and Involved Professionals, by Susan Berg. It not only has cute conversation stimulating baby pictures, but activity ideas related to the photos are suggested.
*Sing familiar songs together. Patriotic songs are ideal because most people, young and old, know them. Some good songs are: America, America the Beautiful, and God Bless America
*Watch a portion of a classic musical movie. Do not try to watch too long because the dementia person or child may lose interest. Movie suggestions are: any Shirley Temple movie, Judy Garland movies including, The Wizard of Oz, and The Sound of Music.
*Have a snack or meal together. Everyone loves ice cream.
*Make an old family favorite recipe together. Then eat it
*Go for a ride. Because gasoline prices are high and attention spans are short, a short trip is best.

So this Grandparents day, September 11, include a loved one with dementia and a grandchild in a lovely experience for both.

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