Souvenaid – A Nutritional Drink for Alzheimer's Disease?

(Soruce:  Alzheimer's Society, March 2016 Research Update)

       

On 10th March 2016, news outlets reported on a nutritional drink that claimed to "stop the brain from shrinking" and "slow the progression of Alzheimer's disease". We examine the science behind these headlines.

The story is based on clinical trial results that were presented at the Advances in Alzheimer's Therapy congress in Athens. This research team provided evidence that this drink may help to improve some aspects of memory in people who have mild cognitive impairment due to the very early stages of Alzheimer's disease. However, it is recommended that you speak to your GP before starting to take this drink or any other nutritional supplements or medication.

What is the drink?

Souvenaid is a nutritional drink containing an active ingredient called Fortasyn Connect. This is a combination of fatty acids, vitamins and other nutrients. It was developed with the aim of preventing the loss of important connections between brain cells that occurs in Alzheimer's disease. Whilst this effect on brain cells has been shown in animal studies, it has not yet been confirmed that the drink has the same effect in people.

Previous trials of the drink were not able to show any effect on its ability to slow or prevent cognitive decline but there was evidence that it may improve some kinds of memory in people in the early stages of Alzheimer's disease. Therefore, it is approved as a food for medical purposes for people in the earlier stages of the condition and is available over the counter at £3.50 for a daily dose.

What was this trial and what were the results?

The study involved 311 people who had mild cognitive impairment, which is a condition where someone has mild memory problems that are not severe enough for them to be diagnosed with dementia. The study participants had also had tests like brain scans or spinal taps to show that their memory problems were most likely due to the very early stages of Alzheimer's disease.

Half of the people on the trial took the drink containing Fortasyn Connect once a day for two years; the other half took a drink with the same calorie content but without the active ingredient. When the researchers analysed the results at the end of the trial, there was no difference in overall cognitive performance between the two groups.

However, when the researchers used more sensitive tests they found that the people who had taken the drink containing Fortasyn Connect had improvements in their episodic memory (memories of specific events and the time and place that they happened). Brain scans from the trial also showed that the people who took Souvenaid had less shrinkage in certain areas of their brain, including in the hippocampus, which is involved in memory.

There was no evidence presented that those who took Souvenaid were less likely to experience cognitive decline or to progress to full Alzheimer's disease. The research team are still analysing this data from the LipiDiDiet trial.

What do these results mean?

These trial results have not yet been published which means they have not yet been rigorously scrutinised by the scientific community. We need to wait for the trial results to be published to be able to get a detailed understanding of what they mean for people with early Alzheimer's disease.

Based on the results presented at the conference, we cannot say that the drink is able to prevent cognitive decline in those mild cognitive impairment due to the very early stages of Alzheimer's disease. The drink has no overall effect on cognition when it is taken for two years.

There is evidence that it can bring improvements in some aspects of memory after two years. This means it might be able to help people in the very early stages of Alzheimer's disease to manage some of the memory problems they commonly experience.

I'm worried about my memory - should I buy this drink?

If you are worried about your memory, or have a diagnosis of mild cognitive impairment, you should see your GP to discuss the options that are suitable for you.

This trial only looked at people with mild cognitive impairment due to the very early stages of Alzheimer's disease, but there are many other causes of mild cognitive impairment. There is no evidence that this drink would improve memory in everyone who has this condition so it is best to consult with your GP before beginning any nutritional supplement.

There is evidence that regular physical activity, avoiding smoking, eating a healthy, balanced diet and keeping your blood pressure in check are all ways to reduce your risk of developing dementia. This nutritional drink might improve memory in some people with mild memory problems but there is currently no evidence that it will slow cognitive decline or prevent dementia.

DOES POOR SLEEP AFFECT DEMENTIA RISK?

Several people find that having a bad night’s sleep can affect their memory and thinking abilities the next day. But does poor sleep have an effect on your memory in the longer term? This article explores the research into whether there is a link between sleep and dementia risk.

Sleep

People affected by dementia often have several issues with getting a good night's sleep, and sometimes people report that their memory seems worse after a bad night. However, the evidence is unclear on whether poor sleep is a risk factor for dementia.

Sleep and dementia is a complicated topic. Different types of dementia are associated with different sleep problems. Researchers are also not yet sure which way the interaction goes - whether poor sleep causes or exacerbates dementia or if dementia leads to poor sleep. Some researchers believe that both of these theories could be true, and the relationship could be circular. On top of this, it is unclear what the mechanisms are that underlie these interactions.

It is clear that more research is needed to understand this relationship; in particular research that observes large groups of affected people for very long periods of time.

Light Sleep Disorders

Light sleep disorders are often called rapid eye movement sleep behaviour disorder (RBD), and cause people to act out their dreams through moving or talking in their sleep. Dementia with Lewy bodies and Parkinson's disease seem to be particularly associated with light sleep disorders and some studies have suggested that light sleep disorders are a very early indicator of these conditions, particularly in older men.

Some researchers believe that the part of the brain that is damaged with dementia with Lewy bodies or Parkinson's disease also plays a role in light sleep, explaining why people with these conditions are particularly affected by light sleep disorders.

Sleep-Wake Cycle Disorders

The sleep-wake cycle is the 24 hour cycle that the body goes through each day, normally ensuring that we are active during the day and sleepy at night. When this cycle is altered is causes many unusual and disruptive sleep patterns. These include wakefulness at night and problems falling asleep and staying asleep, as well as drowsiness and napping during the day.

These sorts of sleep disturbances are associated with many kinds of dementia, most notably Alzheimer's disease. They also affect people with Parkinson's disease.

It is thought by some researchers that the Alzheimer's hallmark protein amyloid may be behind the link between Alzheimer's disease and sleep-wake cycles. Increased amyloid in the brain is commonly seen in people with Alzheimer's and studies have shown that raised amyloid levels may be associated with poor sleep quality.  The amyloid protein has also been linked to problems with storing memories whilst we sleep and other research indicates that poor sleep may affect the body's ability to clear the toxic amyloid protein from the brain.

This has led to the suggestion that improving sleep quality may have the potential to delay progression of Alzheimer's disease. However, it is also possible that the changes to the sleep-wake cycle are caused by other changes in the brain, and do not have an impact on risk of the condition. More research is needed to understand what the mechanisms linking sleep-wake cycles and Alzheimer's are.

Sleep Disordered Breathing

Sleep disordered breathing is when someone has difficulty breathing when they are asleep. This may be because of obstructions to the airway, making breathing harder work. Sleep disordered breathing is sometimes called sleep apnoea.

People of all ages can be affected by sleep disordered breathing, but it is most common in older people and people with obesity. Some research has suggested that people who are affected by sleep disordered breathing may be at higher risk of cognitive decline or impairment. This is because sleep disordered breathing may cause damage to the brain due to changes of levels of oxygen and carbon dioxide in the blood. It may also change flow of blood to the brain.

Treatments for Poor Sleep

Good quality sleep is linked to good health, including cognitive health. Researchers have also investigated whether there are effective treatments for poor sleep and whether these treatments can affect dementia risk. Some drug treatments for poor sleep, such as benzodiazepines, have been linked to an increased risk of dementia although the evidence behind this link is conflicting. Alzheimer's Society is funding a study into the effects these drugs could have on dementia risk.

Many treatments that have been suggested to improve quality of sleep involve lifestyle changes. Regular sleep regimes, eating schedules and diets, exercise, and ensuring exposure to bright light in the morning are all ways that you can improve your sleep quality. However more research is needed to indicate whether these activities have an effect on risk of dementia or disease progression. There is more information in treatment of sleep disorders on the NHS Choices website or you can speak to your GP.

A machine called continuous positive airway pressure (CPAP) has been shown to reduce the consequences of sleep apnoea by several studies. Before this treatment can be used, research is needed to indicate with more detail how to use it, for example how long the treatment should last and what lifestyle changes can be made to help.

There are also several drugs that have been trialled to improve sleep. Some doctors may prescribe melatonin, a hormone believed to be important in maintaining regular sleep-wake cycles. There is some evidence that this treatment does improve sleep quality in people with Alzheimer's disease and Parkinson's disease but so far evidence suggests melatonin does not affect risk of dementia or cognitive function.

Please consult your GP before making any decisions about taking sleep medication.

(Source:  Alzheimer's Society, March 2016 Research Update)

A DICE-Y APPROACH TO TAMING DEMENTIA SYMPTOMS

Treatment for managing dementia depends on its type and severity, but drug therapy often plays a role. Drugs can't cure dementia, but psychotropic medications, which include antipsychotics, antidepressants and anticonvulsants, are used with extreme caution in certain cases to help improve behavioural symptoms such as aggression, agitation, lack of inhibition and depression -- symptoms that caregivers tend to feel are more stressful or difficult to handle than the trademark memory loss associated with dementia.

For many people with dementia, the potential risks of psychotropics outweigh their potential benefits. All antipsychotics, including haloperidol (Haldol), olanzapine (Zyprexa), quetiapine (Seroquel) and risperidone (Risperdal), significantly increase the risk of death, perhaps because they also increase the risk of stroke, heart attack and falls.

The DICE approach. In exploring ways to improve symptoms without depending on potent psychotropic drugs, experts from the University of Michigan and Johns Hopkins Medicine developed DICE, a strategy designed to minimize problems by changing a patient's behaviour. The acronym DICE stands for describe, investigate, create and evaluate. The DICE approach is a collaboration among a caregiver, a clinician and, if feasible, the individual with dementia. DICE consists of the following four steps:

Describe: The caregiver describes to the clinician specific behavioural problems the patient is exhibiting and the circumstances and environment under which they occur. The person with dementia describes the situation if he or she has the ability to do so. Both the caregiver and patient convey the degree of distress this behaviour causes them.

Investigate: The clinician examines, excludes and identifies possible underlying medical and mental health causes for the patient's actions as well as drugs the patient may be taking that contribute to the behaviour. The clinician reviews the caregiver's handling of the behaviour and advises the caregiver on issues such as appropriate reaction and expectations. Finally, the clinician will examine the environment for possible improvements, such as reducing clutter or noise and improving lighting.

Create: The clinician and the caregiver create a plan to prevent or respond to either a specific action or general behaviour to enhance the environment and improve caregiver skills and well-being.

Evaluate: The clinician evaluates and assesses the patient's and caregiver's compliance with the suggested plan and makes any needed changes if the desired effects aren't achieved.

The Centers for Medicare and Medicaid Services recommend the DICE approach in an effort to reduce the need for psychotropic drugs. The authors caution that doctors should prescribe psychotropics only after they've made other attempts to change behaviour - unless patients have severe depression, psychosis or aggression that poses a risk to themselves or those around them. The study outlining the DICE approach appeared in the Journal of the American Geriatrics Society.

(Source:  Scientific American Health After 50, 30 March 2015)

Has Stanford University Found A Cure for Alzheimer's Disease?

Scientists at Stanford University believe Alzheimer's disease could be prevented and even cured by boosting the brain's own immune response.

Researchers discovered that nerve cells die because cells which are supposed to clear the brain of bacteria, viruses and dangerous deposits, stop working.

These cells, called 'microglia' functioned well when people are young, but when they age, a single protein called EP2 stops them operating efficiently.

Now scientists have shown that blocking the protein allows the microglia to function normally again so they can hoover up the dangerous sticky amyloid-beta plaques which damage nerve cells in Alzheimer's disease.

The researchers found that, in mice, blocking EP2 with a drug reversed memory loss and myriad other Alzheimer’s-like features in the animals.

“Microglia are the brain’s beat cops,” said Dr Katrin Andreasson, Professor of Neurology and Neurological Sciences at Stanford University School of Medicine.

“Our experiments show that keeping them on the right track counters memory loss and preserves healthy brain physiology.”

By 2015 there will be 850,000 people with dementia in the UK, with Alzheimer's disease being the most common type. The disease kills at least 60,000 people each year.

Microglial cells make up around 10 to 15 per cent of cells in the brain. They act as a frontline defence, looking for suspicious activities and materials. When they spot trouble, they release substances that recruit other microglia to the scene which then destroy and get rid of any foreign invaders.

They also work as garbage collectors, chewing up dead cells and molecular debris strewn among living cells including clusters of amyloid-beta which aggregate as gummy deposits and break the connections between neurons, causing loss of memory and spatial awareness. These clusters are believed to play a substantial role in causing Alzheimer’s.

“The microglia are supposed to be, from the get-go, constantly clearing amyloid-beta, as well as keeping a lid on inflammation,” added Dr Andreasson. “If they lose their ability to function, things get out of control. A-beta builds up in the brain, inducing toxic inflammation.”

The scientists discovered that in young mice, the microglia kept the sticky plaques under control. But when experiments were done on older mice, the protein EP2 swung into action and stopped the microglia producing enzymes which digested the plaques.

Similarly mice which were genetically engineered not to have EP2 did not develop Alzheimer's disease, even when injected with a solution of amyloid-beta, suggesting that their cells were getting rid of the protein naturally.

And for those mice who developed Alzheimer's, blocking EP2 reversed memory decline.

Now Stanford is hoping to produce a compound which only blocks EP2 to prevent unnecessary side effects.

The study was published in the Journal of Clinical Investigation.

 (Source:  The Telegraph, 27 December 2014)

ADI NEWS RELEASE - SMOKING INCREASES RISK OF DEMENTIA

The World Health Organization (WHO) and Alzheimer’s Disease International (ADI) in its latest report highlighted the serious risk that tobacco use creates for dementia. 

The Key Message is:

▪     Smoking is a risk factor for dementia, and quitting could reduce the dementia  burden.

▪     Second-hand smoke exposure may also increase the risk of dementia.

▪     14% of Alzheimer’s disease cases worldwide are potentially attributed to   smoking.

▪     As no treatments are currently available to cure or alter the progressive course of dementia, it is essential to identify modifiable risk factors for reducing the occurrence of the disease, delaying its onset or reducing its burden.

▪     Governments should actively implement and enforce the measures of the WHO Framework Convention on Tobacco Control, especially smoke-free environment laws and systematic access to tobacco cessation services.

Geneva, 09 July 2014:

Smokers have a 45% higher risk of developing dementia than non-smokers, according to information published today by the World Health Organization (WHO) in collaboration with Alzheimer’s Disease International (ADI).

Evidence reviewed by WHO reveals a strong link between smoking and the risk of dementia, and the more a person smokes, the higher the risk. It is estimated that 14% of Alzheimer’s disease cases worldwide are potentially attributable to smoking.

WHO warns that exposure to second-hand smoke (passive smoking) may also increase the risk of dementia.

"Since there is currently no cure for dementia, public health interventions need to focus on prevention by changing modifiable risk factors like smoking,” says Dr Shekhar Saxena, Director of the Department for Mental Health and Substance Abuse at WHO. “This research shows that a decrease in smoking now is likely to result in a substantial decrease in the burden of dementia in the years to come."

Tobacco use is already recognized as the one risk factor common to four main groups of non-communicable diseases (NCDs): cancers, cardiovascular disease, chronic lung disease and diabetes.

“Tobacco is one of the biggest public health threats the world has ever faced, killing nearly six million people a year,” says Dr Douglas Bettcher, Director of the Department for Prevention of Non-communicable Diseases at WHO. “WHO urges governments to actively implement and enforce the measures of the WHO Framework Convention on Tobacco Control, especially smoke-free environment laws and access to tobacco cessation services”.

Laurent Huber, Director of the Framework Convention Alliance (FCA) for Tobacco Control, comments: “It is no surprise to see these findings confirm that tobacco smoking is a major risk factor for dementia. This adds yet another item to the long list of the devastating consequences of tobacco and gives even more reason for personal and public health action to help people to quit smoking.”  

“The research also shows that quitting smoking later in life might be beneficial so encouraging and supporting current tobacco users to quit should be a priority,” says Serge Gauthier, chair of the ADI’s Medical Scientific Advisory Panel.

Dementia affects more than 44 million people worldwide, with almost two thirds of them living in low- and middle-income countries. 

“Every year, there are 7.7 million new cases of dementia. In 2010, the global cost was calculated at US$ 604 billion, which represents 1% of global GDP (gross domestic product),” says Marc Wortmann, ADI Executive Director. “No government can ignore the opportunity to link this new information into its planning and health system activities to reduce smoking and control NCDs.”

ADI believes that this information brief can form the basis for countries to add messages about brain health and dementia risk into public health anti-smoking programs and interventions. 

For further information:
Click on -> Tobacco Use and Dementia   
Visit : http://www.who.int/tobacco/publications/en/ 

ALZHEIMER'S DISEASE COULD BE PREVENTED AFTER NEW BLOOD TEST BREAKTHROUGH

Scientists at Oxford University and Kings College London develop blood test which can predict the onset of Alzheimer's so that drugs could target the disease before symptoms appear

A blood test has been developed to predict if someone will develop Alzheimer’s within a year, raising hopes that the disease could become preventable.

After a decade of research, scientists at Oxford University and King’s College London are confident they have found 10 proteins which show the disease is imminent.

Clinical trials will start on people who have not yet developed Alzheimer’s to find out which drugs halt its onset.

The blood test, which could be available in as little as two years, was described as a “major step forward” by Jeremy Hunt, the Health Secretary, and by charities which said it could revolutionize research into a cure.

“Although we are making drugs they are all failing. But if we could treat people earlier it may be that the drugs are effective,” said Simon Lovestone, Professor of Translational Neuroscience at Oxford. “Alzheimer’s begins to affect the brain many years before patients are diagnosed with the disease. If we could treat the disease in that phase we would in effect have a preventative strategy.”

Clinical trials into so-called “wonder drugs” such as BACE inhibitors and anti-amyloid agents, have shown little improvement for sufferers. Scientists believe that by the time Alzheimer’s is diagnosed, an irreversible “cascade” of symptoms has already occurred.

About 600,000 people in Britain suffer from Alzheimer’s and hundreds of thousands have mild cognitive impairment. Last month, David Cameron pledged to fast-track dementia research.

The new test, which examines 10 proteins in the blood, can predict with 87 per cent accuracy whether someone suffering memory problems will develop Alzheimer’s within a year.

The researchers used data from three international studies. Blood samples were taken from 1,148 people, 476 of whom had Alzheimer’s, 220 with memory problems, and a control group of 452 without any signs of dementia. The scientists found that 16 proteins were associated with brain shrinkage and memory loss and 10 of those could predict whether someone would develop Alzheimer’s.

Mr Hunt said: “This is welcome research on an issue we’re made a national priority. Developing tests and bio markers will be important steps forward in the global fight against dementia as we search for a cure.”

Previous studies have shown that PET brain scans and plasma in lumbar fluid could be used to predict that onset of dementia from mild cognitive impairment. But PET imaging is highly expensive and lumbar punctures are invasive and carry risks.

The first tests are likely to be available in between two and five years. However, the study is likely to throw up ethical dilemmas about whether patients should receive potentially devastating news about their future. Prof Lovestone said it was unlikely that GPs would use the test until a treatment was available.

The breakthrough was welcomed by dementia charities and academics.

Eric Karran, Director of Research at Alzheimer’s Research UK, which helped fund the research, said it brought the prospect of Alzheimer’s becoming a preventable disease “significantly closer”.

Prof Gordon Wilcock, Emeritus Professor of Geratology at Oxford, added that it was “great news”. The study was published in the Journal Alzheimer’s & Dementia.

(Source:  The Telegraph, 8 July 2014)

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)

Memory : Six Key Signs That Memory Loss May Be Serious

At least three-fourths of people over age 50 report that their memory is not as good as it was. The reality is that more than 90 percent of those who do complain about memory impairment do not have Alzheimer's or dementia. Many memory complaints reflect changes in ability over time but appear to be relatively minor and due to normal age-related changes in the function of the brain.

So how do you know if your loved one is part of the minority whose changes in memory are more serious and warrant an evaluation by a health professional?

Red flags - Momentarily forgetting someone's name or a specific word is actually normal and does not necessarily worsen with age. The following behaviors, in contrast, may be signs that something more serious is taking place:

1.   Difficulty with routine tasks. Trouble completing tasks that a person has done many times before, like figuring out a tip at a restaurant, filling out tax forms or managing a checkbook, is a real reason for concern.

2.   Getting lost. Another red flag is when a person becomes lost while walking or driving in a familiar place, even the person says the navigational difficulties were due to inclement weather or having to make a big detour. This too is a potential warning sign of early Alzheimer's or dementia that needs to be investigated further.

3.   Loss of recent memory. Forgetting what you had for dinner the day before or what movie you watched a few hours earlier is not always a sign of normal brain aging. Other warnings include forgetting important dates or events or repeatedly asking the same question.

4.   Forgetting simple words. People with Alzheimer's or dementia may also have difficulty following or joining in a conversation. They may stop in the middle of a sentence and be unable to pick up where they left off. This is different from the occasional difficulty coming up with a name or word.

5.   Poor judgment in financial matters. It's not uncommon for people with Alzheimer's or dementia to buy things they don't need, to give away significant sums of money to telemarketers or unscrupulous salespeople, or to repeatedly make donations in response to mailed or telephoned requests to legitimate organizations.

6.   Mood change. People with Alzheimer's or dementia may exhibit confusion, suspicion, fear, depression or anxiety, traits that they never had before.

Finally, when a person regularly complains about poor memory and mentions that it is worsening from the year before, it should be looked into.

(Source:  John Hopkins Health Alert, 14 May 2012) 

Does Namenda Work? Dr. Rabins Addresses a Difficult Question

In this excerpt from a recent issue of the Memory Disorders Bulletin, Medical Editor Dr. Peter V. Rabins confronts the difficult question: What do you do when a caregiver asks, "Dr. Rabins, do you think that Namenda is really working?"

Namenda (memantine) was widely available for about 20 years in Europe before it received approval in 2003 for Alzheimer’s disease therapy from the Food and Drug Administration (FDA). Namenda is approved for people with moderate and severe Alzheimer’s disease, but some doctors, including memory and dementia experts, offer it to all of their patients with Alzheimer's, regardless of the severity of their symptoms.

Many doctors who are specialists in Parkinson's disease and frontotemporal dementia are using Namenda for their patients with dementia symptoms, even though it is not FDA-approved for that. While it is perfectly within their purview to use a medication "off label" for Alzheimer’s disease if they feel it's warranted, I hope studies will be carried out to tell us whether Namenda does have positive benefits.

There is no cure for Alzheimer’s disease, so the goal of drug therapy for Alzheimer’s disease is to help manage the symptoms. Improvement in cognition is an indicator that Namenda might be working. Therefore, when a caregiver asks me if I think that Namenda is working or not for their loved one, I answer "yes" only when I can see an improvement on a scale that measures cognition or thinking.

Should you choose Namenda? The decision to use Namenda depends more on the preferences of the Alzheimer’s disease patient and his or her family than on the science. Many families and caregivers say, "If Namenda might help, even a little bit, I want my loved one to take it."

On the other hand, some families and patients say, "I don't want to take something that will only make a small difference." For these individuals, I work to get them as much information about Alzheimer’s disease as possible to help manage any behavioral or psychiatric symptoms and to address the financial, legal, ethical and social problems they are facing.

There is no "right" or "wrong" when it comes to this issue. It is the patient and family who should make the final decision, not the doctor. I feel the same way about stopping Namenda. It is up to the patient and family to decide once they are given the information in a balanced and fair manner.

However, colleagues whose opinions I value feel that a drug such as Namenda offers false hope and the benefit is so minimal that it should not be used unless family members feel strongly that they want to try it with their loved one.

(Source:  John Hopkins Health Alert, Posted in Memory on 7 November, 2011)

Antipsychotic Medications and Dementia: What Are the Risks?

Most people with dementia or Alzheimer's disease will, at some point in their illness, show signs of aggression, agitation or psychosis. When these symptoms are so severe that individuals present a serious risk to themselves or to others, a class of drugs known as antipsychotics (or neuroleptics) are often used.

However, several recent studies have found that antipsychotics are associated with an increased risk of death when used in older people with dementia and Alzheimer's disease. In fact, the U.S. Food and Drug Administration (FDA) now mandates that drug makers add what is referred to as a "black box" warning to the labels of all antipsychotics, alerting doctors and patients to this increased mortality risk in people with dementia-related psychosis.

Since those warnings were first implemented in 2005, the use of antipsychotics for older people with dementia has declined significantly. Nonetheless, almost 10 percent of antipsychotic use is still attributed to people with dementia. In addition, about one third of nursing home residents with dementia receive antipsychotics.

Typical and Atypical Antipsychotics. Antipsychotic drugs were first developed in the 1950s to treat schizophrenia. 

• The first generation of these drugs is sometimes referred to as "typical" or "conventional" antipsychotics; they include chlorpromazine and haloperidol (Haldol). Typical antipsychotics work by blocking the receptors for the neurotransmitter dopamine and can cause a number of side effects that affect physical movement, such as tremors, rigidity, restlessness and muscle spasms.

•  In the 1990s, a second generation of antipsychotics known as atypical was introduced. These also block dopamine receptors but have fewer of the movement-related side effects that plagued users of the older, typical antipsychotics. Still, atypical antipsychotics have potentially serious side effects, including drowsiness, dizziness, blurred vision, rapid heartbeat, sexual dysfunction and skin rashes. They can also cause significant weight gain, and if left unchecked, people taking them may risk developing diabetes or high cholesterol levels. Examples of atypical antipsychotics include risperidone (Risperdal), olanzapine (Zyprexa) and quetiapine (Seroquel). 

(Source:  John Hopkins Health Alert, 13 February, 2012)

Memory : A New Take on What Causes Alzheimer’s

More than a century after German psychiatrist Alois Alzheimer first lectured about the gooey mass of plaques and tangles he noted in a postmortem brain tissue sample, scientists are still debating what causes Alzheimer's disease.

The majority of scientists have agreed that plaques result from overproduction of beta-amyloid -- a protein found in the cell membrane of neurons. In people with Alzheimer's, this protein accumulates in clumps between brain cells.

But recently, researchers from Washington University in St. Louis arrived at a new theory: that rising brain levels of beta-amyloid do not mean that patients are making more of it but that they can no longer clear it from their brains as effectively.

The study - As reported in the journal Science, the investigators tested 24 people, average age 74, and separated them into a group composed of people with minor Alzheimer's disease and another whose members were cognitively normal. Special testing revealed that both groups produced beta-amyloid at the same average rate within the brain.

The study subjects were then tested to see how the beta-amyloid was cleared from their brains. One of the ways the brain does this is by moving it to the spinal fluid for disposal. The researchers took samples of cerebrospinal fluid by inserting a needle into the subjects' backs and drawing off the fluid that normally surrounds the spinal cord. They found that those with Alzheimer's had decreased clearance of beta-amyloid from the brain to the cerebrospinal fluid -- about 30 percent less than those who were cognitively normal. This suggests that Alzheimer's is associated with disruption of the brain's ability to normally handle the beta-amyloid.

What it means - Early diagnosis of Alzheimer's has been elusive. But because researchers have uncovered a possible mechanism of early disease development, it is possible that this discovery could lead to both a test for early detection and the development of effective therapies to stop or reverse Alzheimer's memory disruption. They calculate that it would take an adult 10 years to build up enough amyloid in his or her brain to reach the amount typically present in someone with Alzheimer's.

This knowledge could offer doctors a window of opportunity to diagnose someone long before dementia symptoms develop. Once they learn they are at risk for dementia, people could make more concerted efforts to reduce their personal risk factors for Alzheimer’s. At the same time, pharmaceutical companies could work on targeted medications to halt brain damage before symptoms become irrevocable.

(Source: John Hopkins Health Alert, 23 April 2012)

Memory : Is Your Loved One Overmedicated?

Behavioral and neuropsychiatric symptoms of dementia can be extremely challenging and distressing for patients and their caregivers. Antipsychotic medications may be the only option if the patient's behavior is potentially harmful to him- or herself or to others.

Antipsychotic medications are often prescribed "off-label" for dementia patients in nursing homes to alleviate the agitation, aggression or psychotic behavior that is either distressing to the patient or else makes them a danger, but the Food and Drug Administration (FDA) has not approved any drugs for the treatment of behavioral symptoms of dementia. What's more, antipsychotics carry an FDA black box warning that older patients with dementia-related psychosis treated with atypical antipsychotic drugs are at an increased risk of death.

Drugs Versus Alternatives

There are ways to deal with difficult dementia patients that don't involve the use of drugs. Once a medical cause has been ruled out, the nursing and medical staff should look for environmental triggers that can be avoided or minimized.

• Changes in the environment might include increasing contact with caregivers, switching roommates, adjusting the temperature in the room or providing stimulating activities.

• Simply paying attention to a patient can often ease disruptive symptoms.

• In some cases, difficult behavior can be safely managed by reducing boredom, providing intellectual and physical stimulation, exercise, calming music and pet therapy.

However, if someone is in psychological agony and nondrug approaches have failed, medication might help. The risks and benefits of prescribing antipsychotics to people with dementia need to be carefully considered. While dementia patients are difficult to care for, even when drugs are administered, the practice of overmedication to make patients "manageable" is certainly not acceptable.

Advocating for your loved one with dementia

When someone with dementia is cared for in a nursing home, the support of family and friends is still critical, since the person can't adequately advocate on his or her own part. Family members must learn about the medications that are being dispensed, the reasons for their use, proper dosages and possible side effects.

If you notice that your loved one seems to be showing greater confusion after starting a drug, say something. Bring this to the attention of the doctor who prescribed the medication and discuss what steps can be taken to improve his or her quality of life. By maintaining this dialogue, you will be doing everything you can to ensure the best care for your loved one.

(Source:  John Hopkins Health Alert, 9 May 2012)

The drugs we take are getting more advanced and more popular ... and yet we're getting sicker. What's the answer?

6 Lifestyle Changes That Work

Statin drugs, diabetic medications and other pharmaceuticals...

The drugs we take are getting more advanced and more popular .. and yet we’re getting sicker. What’s the answer?
Below excerpts from Dr. Loretta Friedman.

Metabolic syndrome is a constellation of interrelated risk factors that appear to promote the development of heart disease. Metabolic syndrome is characterized by:

- Abdominal Obesity (an abundance of fat around your middle)
- Insulin Resistance (Type II diabetes, coming on later in life)
- Excess Stress Hypertension.

Sounds rare? Not so much. At least one in five people suffer from Metabolic Syndrome. Some studies estimate as much as 25% of the population is suffering from this.

Let's take all this in. Why is this so important?

Because for the last 20 years, the pharmaceutical industry has been coming up with better drugs for diabetes and hypertension and Americans are getting worse, not better.

The medical doctors write the prescriptions and patients are only getting more ill. Why?

People take their insulin and go out and eat every fast food that crosses their path. They take their high blood pressure meds or their heart drugs and the support them by being a couch potato all day, every day.

Here is the bitter pill: The medications don’t work without Life Style Changes. Better yet, you might not even need your medications after Life Style Changes. Get off your butt and help yourself. You might be able to get off your medications.

National Heart, Lung and Blood Institute (NHLBI) Director Elizabeth G. Nabel, M.D., said, “This statement should serve as an alert to physicians that it is vitally important to identify and treat the growing number of people with metabolic syndrome. For individuals with this syndrome, lifestyle treatment…is the primary therapy for lowering their risk factors and reducing the long-term risk for heart disease.”

Helping patients adopt a therapeutic lifestyle is the first and possibly the most important therapy doctors can use to treat many chronic health problems.

As a patient, finding someone who can guide you through this is terribly important.

Consider a few facts:

1. 91% of type II diabetes cases could be prevented by the adoption of healthy habits and lifestyle choices.

2. The National Institutes of Health (NIH) say that lifestyle changes are the most important and cost effective way to lower cholesterol (and not putting the world on statin drugs or other medications.

3. Lifestyle changes are now recommended as the “First Line Therapy” for the major chronic diseases in our society:

Heart Disease
Stroke
Diabetes
Cancer
Arthritis Osteoporosis
Alzheimer’s disease

4. Lifestyle choices are also the key to many symptoms that are not classified as diseases:

Fatigue
Stress-Related Symptoms
Hormonal Imbalances

All these can be helped.

The American Diabetes Association reports that approximately 2200 new cases of diabetes are reported in the US every day. According to estimates from the National Institutes of Health, over 50 million Americans have “Metabolic Syndrome”, a disorder that is directly responsible for America’s unusually large population of Type 2 Diabetics.

What are the key lifestyle changes you should make?
Here are the six steps to a new, therapeutic lifestyle.

6-Step Therapeutic Life Style Program
A regular program of aerobic, strength training and flexibility exercises has been shown to increase vitality and reduce the risk for disease.

1. Knowledge

A healthy lifestyle starts with the knowledge to make an informed decision that impacts your health every day.

2. Balanced Eating
Balanced eating habits have a direct influence on excess insulin production, body composition, and disease prevention.

3. Regular Activity/Exercise

A regular program of aerobic, strength training and flexibility exercises has been shown to reverse insulin resistance, increase vitality and reduce the risk for disease.

4. Appropriate Nutritional Supplementation
Incorporating a foundational nutritional program with targeted nutrients that help to prevent and/or treat specific conditions is an essential part of the therapeutic life style program.

5. Stress Management

For optimal health, regular stress management programs help keep insulin and other hormonal levels balanced, improving vitality.

6. Sleep

Sleep is crucial for the proper functioning of the mind and body. Quality and depth of sleep is of primary importance. Although the amount of sleep individuals need varies, most people should get 7-8 hours per night.

Summing Up:
If you are reaching for that medication to solve your woes, here is my advice:

- Think past the pill.
- Try eating a nutritious diet.
- Get a solid night's sleep.
- Get a little regular exericise.
- Take the right nutritional supplements

You may be AMAZED at what this does to even the most serious maladies you are suffering from.

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Recommended reading are:
1. Walk the Walk


A recent study shows that regular walking protects the aging brain. Even moderate exercise helps ward off Alzheimer's and dementia.

2. Recognize A Stroke - Prevent Dementia


The article details a new, related research breakthrough. The video explains how to quickly identify a stroke and what it is. Watch Video ...

3. Hypertension Usually Goes Undetected


Treatment of hypertension might be a key factor in the prevention of dementias such as Alzheimer's. However, a large proportion of people with hypertension are not even diagnosed or treated.

(Source: Alzheimer's Weekly and Dementia Weekly Newsletter)