Exercise May Help People With Alzheimer's Avoid Nursing Homes

Study finds regular activity delays physical decline, reduces falls.

Regular exercise slows disability and prevents falls in patients with Alzheimer's disease without increasing overall costs, a new study from Finland says.

The findings suggest that exercise, particularly when tailored to an individual's needs and performed at home, may help Alzheimer's patients maintain their independence and delay the move to a nursing home.

"This is an important study," said Dr. Kostos Lyketsos, Director of the Johns Hopkins Memory and Alzheimer's Treatment Center, in Baltimore. "If we could ever deliver exercise for people with dementia in their homes, I think we could accomplish very substantial benefits for patients and reduce costs, which is a very big deal ... in health care these days." Lyketsos was not involved in the new research.

Mental changes are the first wrenching signs of Alzheimer's disease, and they often are the symptoms that get the most attention.  But physical declines are also a part the disease. Over time, muscles become stiff and uncoordinated, or may start to tremor.  Alzheimer's patients may lose the ability to brush their teeth, climb stairs, and dress, feed and bathe themselves.

"These people are at very high risk of disability. That's one of the reasons they end up in institutional care," said study author Dr. Kaisu Pitkala, a general practitioner at the University of Helsinki. "They need so much help that their caregivers often get very tired, and after a few years they will end up in institutional care, which is very expensive and often not the wish of the patients nor the caregivers."

For the study, published online April 15 in the journal JAMA Internal Medicine, the researchers chose more than 200 patients with moderate to severe Alzheimer's disease who were living at home with a caregiver and showing signs of physical decline. The patients were randomly assigned to one of three groups: home exercise, group exercise at a day care center, or a control group that got usual care through the Finnish national health care system.

Those in the home-exercise group got visits from a physical therapist for one hour twice a week. The physical therapists specialized in dementia care, and they tailored these sessions to each patient's problems with function and mobility.

Patients in the group-exercise classes traveled to an adult care center twice a week, where two physical therapists guided them through exercises to improve endurance, balance, strength and mental function.

The patients in the usual-care group were followed by the study nurses and were given advice on nutrition and exercise.

After one year, all the groups saw declines in physical function, but the groups that exercised regularly fared better than those who got usual care. Those in the home-exercise group did the best. Their physical function declined about half as much as that of the control group. Importantly, they also had half as many falls as those who got usual care.

Group exercisers showed some signs of better health -  their strength improved over the course of the year - but those results were not statistically significant. And although the study found an association between exercise and better health among Alzheimer's patients, it didn't prove a cause-and-effect relationship.

The researchers think one reason the group exercisers didn't see bigger benefits was because they were more likely to skip their sessions than those who exercised at home.

"When the taxi came to the person's home to take them to the group-based exercise, they could say often, 'Today I'm tired; I'm not coming,'" Pitkala said. "When there's a person coming to your home and telling you, 'Let's do a little bit today,' it's much easier to say yes than it is to go outside your home."

During the year they exercised, patients in the home group had fewer hospital admissions and about half as many falls as those in the control group. The money they saved on medical bills more than offset the cost of regular private sessions with a physical therapist. The average annual cost of caring for a patient in the home-exercise group was about $25,000, but it was about $34,000 for patients who received only usual care. The annual cost for group-exercise patients was even lower, at about $22,000.

Another expert who was not involved in the study praised the research and said it offered a practical blueprint to improve the lives of patients and families affected by Alzheimer's disease.

"If you can do something that can improve their physical functioning and mobility and help them stay home and not actually cost anything - or be cost neutral - I think you can make a huge potential impact on a family's quality of life," said Dr. James Galvin, a Professor of Neurology and Psychiatry at NYU Langone School of Medicine, in New York City.

(Source:  HealthDay News, 15 April 2013)

Music Therapy: A Helpful Add-On to Traditional Therapy for Depression

Music has long been known to affect mood - but can it relieve Depression?  According to recent studies, Music Therapy, which typically combines traditional "Talk Therapy" with listening to music or creating it, may work to alleviate Depression in several ways.

·       Playing an instrument allows depressed people to express themselves non verbally when they  can't easily talk about how they feel.

·       Listening to soothing music helps others relax so they're better able to let go of feelings that are troubling.

·        Still others may find that sharing a musical experience with a Therapist - playing or listening -  help them feel more comfortable discussing their problems and feelings.

Music Therapy is either active or receptive and does not require prior musical background or abilities.

·         In Active Music Therapy, the Therapist and the patient improvise, recreate, or compose music using a drum, mallet instrument or the voice. The goal is for the patient to share thoughts and feelings that arise with the music making and, as a result, develop insight into his or her problems.

·         In Receptive Music Therapy, patients listen to music while meditating, drawing or reminiscing. This process allows patients to improve their mood and develop coping and relaxation skills.

The duration and frequency of Music Therapy Sessions vary, but they typically last 20 minutes to one hour. Patients may undergo sessions daily, weekly or monthly. Music Therapy Sessions can take place in a group or individually in a hospital, therapist's office or patient's home.

What the Research shows

Some studies of music therapy for depression have been encouraging. A review of five small randomized, controlled trials found that in four of the studies, depressive symptoms were reduced more in patients who participated in music therapy than in those who received standard treatment. However, the methodological quality of these studies was moderate to poor, and the types of music therapy and standard treatments used and patients studied varied considerably.

Is Music Therapy right for you? 

Although Music Therapy appears to be helpful, it's likely most suitable as an add-on to traditional therapies such as medication and other forms of psychotherapy. Anyone receiving treatment for depression should first discuss the use of Music Therapy with his or her health care provider.

(Source: John Hopkins Health Alert, posted in Depression and Anxiety on April 2, 2013) 

OLIVE OIL FOUND TO PROTECT AGAINST ALZHEIMER'S DISEASE

Want to keep Alzheimer’s disease at bay? A new study suggests upping your intake of olive oil.

Scientists have found a 

substance in Olive Oil that
protects nerve cells from 
damage that  brought on 
by Alzheimer's Disease

©shutterstock/ilker canikligil/shutterstock.com

While the Mediterranean liquid gold has long been touted for its multiple health benefits, a team of US scientists from the University of Louisiana has identified a specific component in olive oil that they say protects nerve cells from damage brought on by Alzheimer’s disease.

Their research stems from a larger trend observed in the worldwide prevalence of the cognitive illness: While it's estimated that 30 million people suffer from the disease around the world, rates are notably lower in Mediterranean countries.

And though scientists had long attributed the trend to the high consumption of healthy, monounsaturated fats found in olive oil, the latest study, released by the American Chemical Society last week, identifies a substance called oleocanthal that was observed to protect against the leading cause of Alzheimer’s in the brain: the accumulation of peptide beta-amyloid.

The findings were published in the journal ACS Chemical Neuroscience.

In animal studies, scientists found that oleocanthal worked by boosting the production of proteins and key enzymes believed to be critical in removing the beta-amyloid in the brain.

“Extra-virgin olive oil-derived oleocanthal associated with the consumption of Mediterranean diet has the potential to reduce the risk of AD or related neurodegenerative dementias," the report concludes.

Meanwhile, earlier this month, another study found that olive oil is an effective way of satiating hunger pangs and curbing the munchies. For their research, Austrian researchers fed participants yogurt enriched with lard, butterfat, rapeseed oil or olive oil.

The result?  Olive oil had the biggest satiety effect.

(Source: The Star, 26 March 2013 - AFPRelaxnews)

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Alzheimer's Association 2013 Alzheimer's Disease Facts and Figures

The Alzheimer's Association 2013 Alzheimer's Disease Facts and Figures released on 14 March 2013 reveals new statistics on the ever-growing weight of Alzheimer's disease on our nation. The report uncovers new information on growing death rates, the cost of the disease, and the burden placed on long-distance caregivers.

"Unfortunately today there are no Alzheimer's survivors. If you have Alzheimer's disease, you either die from it or die with it. Now we know that 1 in every 3 seniors dies with Alzheimer's disease or another dementia. Urgent, meaningful action is necessary, particularly as more and more people age into greater risk for developing a disease that has no cure and no way to slow or stop its progression," said Harry Johns, president and CEO of the Alzheimer's Association.

By 2025, the number of people 65 and older with Alzheimer's disease is estimated to reach 7.1 million – a 40 percent increase from 5 million aged 65 and older currently affected. Startling facts include:

·  1 in 3 seniors dies with Alzheimer's or another dementia.

·  Deaths from Alzheimer's increased 68 percent between 2000 and 2010, while deaths from other major diseases, including the number one cause of death (heart disease), decreased.

·  In 2012, the direct costs of caring for those with Alzheimer's or other dementias to American society will total an estimated $203 billion, including $142 billion in costs to Medicare and Medicaid.

The face of Alzheimer's is changing, affecting more of our friends and family every day.

The 2013 Alzheimer's Disease Facts and Figures is a statistical resource for      U.S. data related to Alzheimer’s disease, the most common type of Dementia, as well as other Dementias. Background and context for interpretation of the data are contained in the Overview. This information includes definitions of the various types of dementia and a summary of current knowledge about Alzheimer’s disease. Additional sections address prevalence, mortality, caregiving and use and costs of care and services. The Special Report focuses on long-distance caregivers of people with Alzheimer's disease and other dementias.

View -> VIDEO

(Source: Alzheimer's Association, 14 March 2013) 

Dementia Drugs Slow Heart Rate, Provoke Fainting

Memory drugs for dementias such as Alzheimer's appear to provoke slower heart rates and fainting. However, the magnitude of these risks has not been clear until now. Learn about these side-effects. Avoid needless pacemaker surgery or injuries from falls.

Side effects associated with several commonly-prescribed dementia drugs may be putting elderly Canadians at risk, says Queen's University Geriatrics Professor Sudeep Gill.

Cholinesterase inhibitors (Aricept®, Exelon® and Reminyl) are often prescribed for people with Alzheimer's disease and related dementias because they increase the level of a chemical in the brain that seems to help memory. Although such drugs are known to provoke slower heart rates and fainting episodes, the magnitude of these risks has not been clear until now.

"This is very troubling, because the drugs are marketed as helping to preserve memory and improve function," says Dr. Gill, who is an Ontario Ministry of Health and Long-term Care Career Scientist, working at Providence Care's St. Mary's of the Lake Hospital in Kingston. "But for a subset of people, the effect appears to be the exact opposite."

In a large study using province-wide data, Dr. Gill and his colleagues discovered that people who used cholinesterase inhibitors were hospitalized for fainting almost twice as often as people with dementia who did not receive these drugs. Experiencing a slowed heart-rate was 69 per cent more common amongst cholinesterase inhibitor users. In addition, people taking the dementia drugs had a 49 per cent increased chance of having permanent pacemakers implanted and an 18 per cent increased risk of hip fractures.

Unfortunately, Dr. Gill continues, this class of drugs is one of the few effective dementia treatments available today. Acknowledging that these drugs do have an important role in the management of dementia, he suggests that people who are already at a higher risk (for example, those who have had previous episodes of fainting or slowed heart rate) may want to ask their doctors to reassess the value of taking the drugs.

Slowing of the heart rate from cholinesterase inhibitors, if significant, may cause a person to faint and suffer fall-related injuries such as a broken hip - often debilitating and sometimes fatal for seniors. However, many physicians aren't aware of the connection between these problems and the dementia drugs, Dr. Gill notes.

If the association with dementia drugs is not identified, people who faint may be prescribed a permanent pacemaker: an invasive procedure that can involve serious complications for seniors. Both the injuries incurred from falling and the risks from pacemaker implants are "downstream consequences" of not recognizing this drug-induced phenomenon.

"This study does not suggest that dementia patients shouldn't take these drugs," says Dr. Gill. "What's critical is that patients, caregivers and physicians be aware of the potential side effects, and weigh these risks carefully against the potential for beneficial effects."

(Source: Alzheimer’s Weekly & Dementia Weekly, 10 March 2013)

Diagnosing Dementia: Alzheimer's May Really Be Mini-Strokes

What causes memory problems?  Often, it's plaque in the brain, which leads to Alzheimer's. Now, new research shows a more common culprit may be vascular brain injury. Find out about this type of cognitive decline from stroke, mini-stroke and high blood pressure. Learn why diagnosing the right cause effects therapy and treatment.

Alzheimer's is connected to sticky plaques made of beta-amyloid that choke brain cells, thereby causing dementia. People may act like they have Alzheimer's when they really have vascular dementia. Vascular dementia is caused by vascular events (related to blood vessels) such as strokes and mini-strokes, so treatment is different. (Mini-strokes occur in the brain when blood vessels clog up or burst. They can accumulate slowly and can go unnoticed for years.)

For example, the damage caused by plaque is typically treated with acetylcholinesterase inhibitors like Aricept®. These drugs target the nervous system. Vascular problems like mini-strokes are treated with blood-targeting medications and therapies.

Alzheimer's disease and vascular dementia are two types of dementia that are common in the elderly. A person's dementia can even be caused by a combination of the two, called "Mixed Dementia."

With today's technology, both vascular brain injury as well as beta-amyloid plaque can be detected in the brain. They both cause memory and thinking problems, called "cognitive impairment". If the cognitive impairment is strong and interferes with a typical person's day, it is called dementia. If it is mild, it is called MCI (Mild Cognitive Impairment).

Until now, doctors generally assumed that when they saw cognitive impairment, it was probably from plaque building up in the brain. Treatment and therapy were given accordingly. New research is showing that vascular brain injury from strokes or the mini-strokes often caused by high blood pressure may deserve the greater part of their attention.

A study at the Alzheimer’s Disease Research Center at UC Davis has found that vascular brain injury from conditions such as high blood pressure and stroke are greater risk factors for cognitive impairment among non-demented older people than is the deposition of the amyloid plaques in the brain that long have been implicated in conditions such as Alzheimer’s disease.

Published online early today in JAMA Neurology (formerly Archives of Neurology), the study found that vascular brain injury had by far the greatest influence across a range of cognitive domains, including higher-level thinking and the forgetfulness of mild cognitive decline.

The researchers also sought to determine whether there was a correlation between vascular brain injury and the deposition of beta amyloid (Αβ) plaques, thought to be an early and important marker of Alzheimer’s disease, said Bruce Reed, associate director of the UC Davis Alzheimer’s Disease Research Center in Martinez, Calif. They also sought to decipher what effect each has on memory and executive functioning.

“We looked at two questions,” said Bruce Reed, Professor in the Department of Neurology at UC Davis. “The first question was whether those two pathologies correlate to each other, and the simple answer is ‘no.’

Earlier research, conducted in animals, has suggested that having a stroke causes more beta amyloid deposition in the brain. If that were the case, people who had more vascular brain injury should have higher levels of beta amyloid. We found no evidence to support that.”

"The second,” Reed continued, “was whether higher levels of cerebrovascular disease or amyloid plaques have a greater impact on cognitive function in older, non-demented adults. Half of the study participants had abnormal levels of beta amyloid and half vascular brain injury, or infarcts. It was really very clear that the amyloid had very little effect, but the vascular brain injury had distinctly negative effects.” 

“The more vascular brain injury the participants had, the worse their memory and the worse their executive function – their ability to organize and problem solve,” Reed said.

The research was conducted in 61 male and female study participants who ranged in age from 65 to 90 years old, with an average age of 78. Thirty of the participants were clinically “normal,” 24 were cognitively impaired and seven were diagnosed with dementia, based on cognitive testing. The participants had been recruited from Northern California between 2007 to 2012.

The study participants underwent magnetic resonance imaging (MRI) - to measure vascular brain injury - and positron emission tomography (PET) scans to measure beta amyloid deposition: markers of the two most common pathologies that affect the aging brain. Vascular brain injury appears as brain infarcts and “white matter hyperintensities” in MRI scans, areas of the brain that appear bright white.

The study found that both memory and executive function correlated negatively with brain infarcts, especially infarcts in cortical and sub-cortical gray matter. Although infarcts were common in this group, the infarcts varied greatly in size and location, and many had been clinically silent. The level of amyloid in the brain did not correlate with either changes in memory or executive function, and there was no evidence that amyloid interacted with infarcts to impair thinking.

Bruce Reed said the study is important because there’s an enormous amount of interest in detecting Alzheimer’s disease at its earliest point, before an individual exhibits clinical symptoms. It’s possible to conduct a brain scan and detect beta amyloid in the brain, and that is a very new development, he said.

“The use of this diagnostic tool will become reasonably widely available within the next couple of years, so doctors will be able to detect whether an older person has abnormal levels of beta amyloid in the brain. So it’s very important to understand the meaning of a finding of beta amyloid deposition,” Reed said.

“What this study says is that doctors should think about this in a little more complicated way. They should not forget about cerebrovascular disease, which is also very common in this age group and could also cause cognitive problems. Even if a person has amyloid plaques, those plaques may not be the cause of their mild cognitive symptoms.”

(Source:  Alzheimer's Weekly & Dementia Weekly, posted 17 February 2013)

Amyvid® Now Available To Diagnose Alzheimer’s

Beta-almyloid plaque is a marker for Alzheimer's Disease and for a number of years, the only way to find it was through a brain biopsy or an autopsy. Now a new test has been approved to help doctors diagnose the disease.

It's been an emotional day for 73-year-old Hilda McIntosh. Her son- a psychiatrist- started noticing mental changes in his mom about a year ago and wanted to have her checked for Alzheimer's Disease.

"Her memory isn't quite the same, she is repeating stories and becoming more forgetful," said Hilda's son.

Along with other exams, she also got a PET scan with a recently FDA-approved radioactive dye called Amyvid.

Dr. Rajan Agarwal of Abington PET/CT of Willow Grove says the dye travels through the bloodstream to the brain. If there are amyloid plaques, the dye will bind to them.

"This is the first scan of all the scans out there that actually looks for Beta-almyloid deposits in the brain," said Dr. Agarwal.

Simply because amyloid plaques are detected, doesn't necessarily mean the patient has Alzheimer's. This is just one piece of the puzzle but it does give doctors more confidence in diagnosing the disease.

"This would just help us determine if their cognitive impairment could be related to amyloid deposits in the brain, which might be related to Alzheimer's," said Dr. Agarwal.

Dr. Agarwal says if other tests also point to Alzheimer's, then medication can be started early to slow its progression.
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The scans can also help advance research to find better treatments. This is something Hilda would like to see for the millions of people and their families affected with the disease.

"It's so painful. I would like to be a part of helping in any small way to find answers and bring this to some better level than it is today," she said.

There was other good news for Hilda - her scans were negative which means it's highly unlikely she has Alzheimer's Disease.

Regarding the new testing, the dye was just approved in April and it could start being used at more centers soon.

It's important to note that it is not a screening tool. It won't predict Alzheimer's but it can help lead to a more accurate diagnosis.

(Source : Alzheimer's & Dementia Weekly, 3 June 12 -10 June 2012)

Is Coconut Oil Effective For Alzheimer Disease?

(Source : Medscape, 30 May 2012)

Response from Gayle Nicholas Scott, PharmD, Assistant Professor, Eastern Virginia Medical School, Norfolk, Virginia; Clinical Pharmacist, Chesapeake Regional Medical Center, Chesapeake, Virginia.

Coconut oil and a related medical food, Axona® (Accera, Inc; Broomfield, Colorado), are being promoted as treatments for Alzheimer disease (AD). Obtained from the kernel of the coconut palm (Cocos nucifera),[1] coconut oil contains medium-chain fatty acids, predominately lauric acid but also caprylic, myristic, and palmitic acids. Medium-chain triglycerides are the esterified form of medium-chain fatty acids; the terms are often used interchangeably.[2] The active ingredient of Axona is caprylic triglyceride. In the published research available, the product is called AC-1202.[3-5]

Proponents claim that coconut oil and Axona provide ketones as an alternative to glucose for cerebral metabolic processes. Advocates of these treatments describe AD as "diabetes of the brain" and contend that the AD brain is better able to use ketones than glucose.[6] This theory is not widely accepted among AD clinicians and researchers,[7] but some speculate that ketogenesis might improve free radical-mediated pathologies associated with AD.[8]

Normally, metabolic energy comes from glucose. When glucose availability is reduced, the liver produces ketone bodies (primarily acetoacetate and beta-hydroxybutyric acid [beta-OHB]) as energy sources. Unlike the heart and skeletal muscle, the brain cannot use fatty acids as an energy source because it requires glucose or ketone bodies.[8]

Medium-chain triglycerides are more ketogenic than long-chain triglycerides, such as those in animal fat. Ketogenic diets, which are diets high in fat and low in carbohydrates and proteins, have been used since the time of Hippocrates for treatment of epilepsy; the mechanism is still unknown.[8] Ketogenic diets are still used in refractory epilepsy, but poor tolerance of the gastrointestinal side effects and dislike for the diet limit effectiveness.[9] Medium-chain triglyceride diets are better tolerated than classic ketogenic diets, which include more long-chain triglycerides. Because medium-chain triglycerides are highly ketogenic, patients can consume more carbohydrates, making the diet more palatable.[8]

Several theories have been proposed for beneficial effects of ketones in AD, including prevention of amyloid plaques, reduction of proinflammatory mediators associated with neurodegeneration, and a neurotrophic effect of cerebral ketone metabolism.[10] Studies with encouraging results using ketogenic diets in AD have been published.[10-13] In a 6-week clinical study of 23 elderly patients with mild cognitive dysfunction, a diet very low in carbohydrates, which increased ketone levels, improved memory function better than a high-carbohydrate diet.[10] In another preliminary clinical study of 20 persons with AD or mild cognitive impairment, administration of a medium-chain triglyceride beverage was associated with improvement on some cognitive measurements in response to acute elevation of beta-OHB levels 90 minutes after treatment in 2 single-dose study visits, but only in patients without the apolipoprotein E gene (n = 9).[14]

A literature search for coconut oil and AD revealed no clinical studies. A search for the medical food Axona yielded 1 manufacturer-sponsored study and 2 substudies.[3-5] In a 90-day, randomized, double-blind phase 2 study, 152 persons diagnosed with mild to moderate AD received Axona10-20 g/daily or placebo. The primary endpoint was improvement on the AD Assessment Scale-Cognitive subscale (ADAS-Cog). At 45 days, patients receiving the study drug showed improvement on the ADAS-Cog, as noted in company advertising. However, scores were similar in both groups at day 90 and after a 2-week washout period on day 104. In patients without the apolipoprotein E gene, Axona was superior to placebo at both time points.[3]

According to the Alzheimer's Association, the manufacturer of Axona elected to market the product as a medical food rather than conducting phase 3 studies in a larger population to prove effectiveness. Medical foods do not require phase 3 studies.[15]

Both coconut oil and Axona are high in calories and saturated fat, but some research suggests that coconut oil neither increases weight nor adversely affects lipid levels.[2,16,17] Gastrointestinal adverse effects, particularly diarrhea, were frequent causes of discontinuation in the phase 2 study.[3] Coconut oil costs about $12 for 16 oz. Axona costs about $85 per month.

Currently, neither coconut oil nor Axona can be recommended for AD due to lack of credible effectiveness research. For patients or family members who insist on these products, suggest starting with a low dose and gradually increasing the dose to avoid adverse gastrointestinal effects. Healthcare providers should monitor for adverse effects and effectiveness and possibly increased lipid levels. 

Measuring Blood Pressure, Two Arms Are Better Than One

Odds are that when your doctor takes your blood pressure, he or she measures it in only one arm. Yet, guidelines from the American Heart Association have for some time recommended measuring blood pressure in both arms at a patient's initial visit - and findings from a recent study suggest why clinicians should routinely perform the two-arm measurement. The study, published in the Lancet, found that a substantial difference in blood pressure readings between arms indicates an increased risk of developing vascular disease and of dying from heart disease.

A gap between arms in readings of systolic pressure - the top number in the reading, which measures pressure in the arteries when the heart muscle contracts, or beats - can reveal impaired blood flow stemming from vascular diseases, specifically peripheral arterial disease (PAD) and cerebrovascular disease.

When researchers analyzed data from 20 studies involving 16,428 people, they found that a difference of 15 millimeters of mercury (mm Hg) or greater between arms was associated with more than twice the risk of developing PAD when compared with people who had smaller systolic variations. PAD occurs when plaque builds up in the arteries (atherosclerosis), mostly affecting the legs. The blockages, similar to coronary artery disease, increase the risk of a heart attack or stroke.

The study analysis also showed that a difference of 15 mm Hg or more was associated with underlying cerebrovascular disease caused by atherosclerosis in the arteries that deliver blood to the brain, which can lead to stroke or dementia. People in the study with at least a 15 mm Hg difference had a 60 percent increased risk of suffering from the disease.

The difference of 15 mm Hg or more was also associated with a heightened likelihood of premature death from heart disease or another medical condition. And the number of people showing such a gap wasn't insignificant. In one study the researchers analyzed for the Lancet study, up to 7 percent of participants had a difference of 15 mm Hg or higher.

Take away. But another compelling reason to check for a pressure difference between arms is to accurately identify the presence of hypertension, or high blood pressure. If a clinician measures blood pressure in only one arm, and the blood pressure is lower in that arm than in the other, he or she may miss hypertension. For that reason, as well as for potentially identifying a sign of vascular disease, having your blood pressure measured in both arms is certainly worth discussing with your doctor at your next visit

(Source:  John Hopkins Health Alert, 1 June 2012)

Research Update : In Mice, Cancer Drug Reduces Beta-Amyloid and Helps Memory

(Source: Alzheimer's Association Research Update, 10 February 2012)

A report published online by Science Express on Feb. 9, 2012, describes a research study in mouse models of Alzheimer's disease of an FDA-approved cancer therapy called bexarotene. The researchers believe that drug will enhance clearance of an abnormal protein associated with Alzheimer's (beta amyloid protein) from the brain by increasing levels of another protein, known as ApoE. The scientists found that the orally-administered drug rapidly lowered levels of soluble beta amyloid and amyloid plaques in both young and older test animals, and also improved some cognitive and behavioral deficits. This study is exciting because it investigates a possible new approach to treating Alzheimer's disease.

Bexarotene is used to treat cutaneous T-cell lymphoma (CTCL, a type of skin cancer) in people whose disease could not be treated successfully with at least one other medication.

This study, while very interesting, is also very preliminary. Mouse models of Alzheimer's are limited in how closely they represent human Alzheimer's. We are still far away from knowing if this has potential as a therapy for people with Alzheimer's. However, it is intriguing preliminary research that deserves further study.

People with Alzheimer's and their caregivers should not ask their doctor for this drug to treat Alzheimer's disease. That said, investigating an already FDA-reviewed and -approved therapy may mean that the drug development process takes a somewhat shorter time because the drug has already been tested in people. There is still a great deal to learn. For example, without trials in people with Alzheimer's, we know nothing yet about dose levels or how this compound may interact with approved Alzheimer's drugs.

To learn more, following is a report from the Washington Post on 10 February 2012

Cancer Drug Shows Promise In Mouse Alzheimer’s Study

Mice in the early stage of Alzheimer’s disease had some of their brain abnormalities reversed and their declining mental function restored when they were given low doses of a rarely used cancer drug.

The drug, bexarotene, stimulated the removal of ­beta-amyloid, a substance whose accumulation in the brain appears to be the main cause of Alzheimer’s dementia. After treatment, the animals fared better in tests of memory and social behavior, according to a study published online Thursday by the journal Science.

The findings were dramatic, but their relevance to people with Alzheimer’s disease is unknown. But because the drug is already approved for human use, finding out may be easier than if the drug were an entirely new chemical compound.

“It has to work in humans like it works in mice or we can pick up and go home,” said Gary E. Landreth, a neuroscientist at Case Western Reserve University School of Medicine, who headed the experiment.

A study of bexarotene’s effects in normal brains will start in a few months. Clinical trials in people with early Alzheimer’s — or at high risk for the disease for genetic reasons — will take years. If the drug’s effect in human brains turns out to be different, it may never move on to be tested in Alzheimer’s patients.

Nevertheless, the researchers think speed is important, as they fear that people might start using the drug before it is fully evaluated. A few days ago, Landreth got a call from a physician in another city. A person who had heard of the drug through the grapevine had asked for a prescription for bexarotene.

“We’ve got to work fast, and we have got to be right. We can’t screw this up,” Landreth said.

About 5.4 million Americans have Alzheimer’s disease, which is the leading cause of dementia. About 5 percent of people in their late 60s suffer from it, and possibly half of people in their late 80s. By 2050, 1 in 85 people worldwide will have the disease, according to one estimate.

Bexarotene is in the retinoid family of compounds, which are all chemically related to Vitamin A. Retinoids affect cell division and growth, immunity and other essential biological functions.

Sold under the trade name Targretin, bexarotene is approved by the Food and Drug Administration as a treatment for cutaneous T-cell lymphoma, a disease diagnosed in about 3,000 Americans a year. It is an “orphan drug,” a designation that gives drug companies an incentive to develop medicines for rare diseases. Orphan drugs stay under patent protection longer than regular drugs. It has been tried against other forms of cancer, without impressive results.

Numerous “candidate” Alz­heimer’s drugs, which looked promising in lab studies, have washed out in recent years.

Last month, Pfizer and a smaller partner announced that they were abandoning a drug called Dimebon as a possible Alzheimer’s drug after it failed to show benefit in a clinical trial. In 2010, Lilly halted development of a different compound, sem­agacestat. At the Alzheimer’s Association, an advocacy organization, the new study’s results were greeted with that history noted.

“This is an early study and it was in mice,” said Maria C. Carrillo, the organization’s director of scientific relations. “We need to be cautiously optimistic and pursue this lead as we would any other.” She added that what makes “this an exciting study is that it involves a repurposed drug.”

The Case Western experiments were conducted by Paige E. Cramer, a graduate student in Landreth’s lab. The mice used had genetic defects that allowed beta-amyloid to accumulate in their brains, which in turn changed their behavior. The animals, however, are an imperfect model for the human disease. They don’t lose brain cells after beta-amyloid accumulates as people with Alzheimer’s do. (In people, dementia can begin even before cells die, as beta-amyloid disrupts the normal firing of nerve cells.)

Bexarotene spurred the production of “apoE,” a protein that breaks down beta-amyloid molecules floating in the watery fluid between brain cells. Beta-amyloid levels fell by 25 percent within a few days of a single dose. The drug also stimulated housekeeping cells called microglia to consume plaques of solidified beta-amyloid.

While the density of plaques fell by 75 percent over a few weeks, eventually they reaccumulated. Curiously, however, the animals’ behavior didn’t regress to its former state.

“It appears that the measurable activity of the brain is not affected by the presence of the plaques. I think that is a really interesting finding that will stimulate a lot of new science,” Landreth said.

The behavioral tests involved an animal’s ability to remember a cage in which it had gotten a shock, to find a submerged platform in a pool of water, to identify a smell and to build a nest. After treatment with the drug, all those activities returned to normal.

Several physicians with patients taking bexarotene say they’ve never noticed mental improvement from the drug, although they have few, if any, demented patients under their care.

“I have treated over 500 patients with cutaneous T-cell lymphoma in studies and in practice with bexarotene and have not heard any beneficial effect on the brain or cognitive function,” Madeleine Duvic of M.D. Anderson Cancer Center in Houston wrote in an e-mail.

“We really didn’t see anything like this,” said Heather Wakelee, a cancer researcher at Stanford University. She noted, however, that demented people were excluded from studies of bexarotene in advanced cancer.

ALZHEIMER'S ASSOCIATION INVOLVEMENT

Six months before this research was published, the Alzheimer's Association awarded the senior scientist on this article, Gary Landreth of Case Western Reserve University, Cleveland, our prestigious Zenith Award in 2011 for research that will follow on from this study to investigate this drug and how and why it works in this way, perhaps setting the stage for trials in people.

We need to create more treatment targets for Alzheimer's disease and the only way to do that is with more research, especially basic research into the causes and progression of the disease. The Alzheimer's Association commendsthe Obama Administration for dedicating new resources in the fight against Alzheimer's in a uniquely challenging fiscal year in advance of the first ever National Alzheimer's Plan. The Alzheimer's Association will continue to support the process underway to develop the first National Alzheimer's Plan led by Health and Human Services Secretary Kathleen Sebelius. This will help ensure the nation is equipped to overcome Alzheimer's the public health crisis of this century and meet the goal set forth by the Administration to prevent and effectively treat Alzheimer's disease by 2025.

New Research Focuses on Lowering Levels of Beta Amyloid

Mounting evidence suggests that beta amyloid accumulation in the brain is an early biomarker and a critical event in the early progression of Alzheimer's. Researchers are targeting amyloid-based therapies to be given in earlier stages of the disease, perhaps even before symptoms emerge. While more research is needed, some scientists believe these therapies could reduce the risk of, and possibly prevent, cognitive impairment and dementia.

Researchers Look to Disease-Modifying Therapy to Ward Off, Possibly Prevent Alzheimer’s Disease

Just as statins help lower high cholesterol levels to reduce the risk of heart attacks, researchers are seeking a comparable approach for people with large amounts of beta amyloid, an abnormal protein in the brain commonly found in Alzheimer’s disease patients. Medicines would clear those proteins before any signs of memory loss or other early symptoms of Alzheimer’s appear.

Could amyloid-based drugs given at much earlier stages of Alzheimer’s-even before any clinical symptoms begin-reduce the risk and possibly prevent the emergence of cognitive impairment and dementia?

That is the central question of a provocative commentary in the Nov. 30 issue of Science Translational Medicine, written by a trio of researchers who cite how Alzheimer’s, which affects more than one out of every 10 individuals over the age of 65, is the only leading cause of death for which no disease modifying therapy exists.

Currently, most proposed Alzheimer’s drugs are tested in patients in the later stages of the disease, because no reliable medical test, brain imaging or other method currently exists to accurately detect the disease before initial symptoms appear. Recent clinical trial failures at the dementia stage have raised multiple questions about the current development of disease-modifying therapies, prompting a strategy to begin developing and testing drugs aimed at the initial stages of the disease rather than at the end stage of the illness.

Mounting evidence, the authors note, from natural history studies supports amyloid beta accumulation in the brain as an early biomarker and a critical event in the early progression of Alzheimer’s. Already, some studies have shown that a person’s brain may be damaged at least a decade prior to the first signs of Alzeimer’s symptoms. More than 50% of certain brain cells are already lost by the time a patient shows even the mildest cognitive impairment.

However, it remains unclear whether the buildup of amyloid beta protein (which accumulates in the areas of the brain responsible for learning and creating, retaining and extracting memories) is an early symptom or a cause of the disease. Several small monoclonal antibody studies that reduced the amyloid plaque burden have not shown any clear benefit in the limited number of patients treated at stages of mild to moderate dementia.

Titled “Testing the Right Target and Right Drug at the Right Stage,” the authors suggest specific amyloid-based therapies be directed at much earlier stages of Alzheimer’s-perhaps even before the emergence of clinical symptoms. “Furthermore, we argue that the field has sufficient tools to being secondary prevention trials—those conducted after the disease process has begun in hopes of preventing the emergence of symptoms—in asymptomatic individuals who are at risk for the progression of cognitive impairment and AD dementia.”

Still, one-third of the nation’s aging baby boomers show no signs of Alzheimer’s despite an amyloid burden, prompting the researchers to ask, “How do older individuals spend years with a ‘head full of amyloid’ and remain apparently healthy? Is amyloid ‘necessary but not sufficient’ to result in cognitive impairment?”

Clinical trials to test whether specific drugs can head off the disease at various stages of Alzheimer’s, and thinking about the disease in terms of primary, secondary and tertiary prevention, rather than lumping together all disease modifying treatments, is a first step.

The article’s lead author, Reisa Sperling, M.D., an Alzheimer’s specialist at Brigham and Women’s Hospital in Boston, said she hopes to launch a three-year study of an amyloid clearing medication in 1,000 patients age 70 or older who have no Alzheimer’s symptoms but have amyloid plaque in their brains. The clinical trial also would be a milestone as the first known anti-amyloid drug given to people without Alzheimer’s symptoms.

Dr. Sperling’s plan, which requires major government and industry funding, is among a trio of academic plans to pursue comparable research in populations not diagnosed with dementia, with a goal of launching studies next year, according to Maria Carrillo, M.D., senior director of medical and scientific relations for the Alzheimer’s Association.

"Although nothing is programmed or funded yet, we are having discussions with federal regulators, the National Institutes of Health and various experts, and I think in 2012 we may see the first clinical trials,” said Carrillo, adding that both the FDA and the EMA are involved in the discussions of pre-dementia clinical studies.

She also is optimistic that by next June the FDA could approve a brain imaging product for early amyloid plaque detection that possibly could rule out Alzheimer’s in those with no signs of the amyloid protein in their brain scans.

“The analogy with statins, where you are treating populations with no symptoms early on, is a good one,” said Carrillo, “because we can change the course of Alzheimer’s disease to where it can be delayed, detected early, understanding changes without cognitive impairment—even avoided altogether.”

(Source: By Ronald Rosenberg, 19 December 2011, Alzheimer’s Association)