Saturday, March 31, 2012

Role of amyloid beta as sensors and protectors in Alzheimer's and other diseases explored

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sciencecodex


Amsterdam, NL -- Alzheimer's disease is the sixth leading cause of death in the United States and the only cause of death among the top 10 in America without a way to prevent, cure or even slow its progression, according to the Alzheimer's Association. Today, 5.4 million Americans are living with the disease, and another American develops it every 69 seconds.

Unfortunately, many Alzheimer's disease drugs targeting the misfolding of the amyloid beta protein have failed clinical trials, leading some to question the validity of the amyloid hypothesis.

In upcoming issues of the Journal of Alzheimer's Disease, Dr. Ian Murray of the Texas A&M Health Science Center College of Medicine provides a new way of looking at amyloid – not only in Alzheimer's, but also in other amyloid diseases – with a hypotheses paper and separate supporting data paper.

Murray, Ph.D., assistant professor in the Department of Neuroscience and Experimental Therapeutics in the college, is one of four authors on a hypotheses paper supporting Amyloids as Sensors and Protectors (ASAP). This hypothesis incorporates both the emerging idea that amyloid is protective and the pathological amyloid hypothesis.

Amyloid senses cellular environmental stress, such as elevation of reactive metabolites and oxidative products or metals, and then misfolds. This misfolding initiates a protective cellular response in the short term. Long-term or chronic stress such as metabolic dysfunction (diabetes) would lead to the pathological consequences of amyloid misfolding (as diabetes is a risk factor for Alzheimer's).

This interesting ASAP hypothesis is supported by existing publications in the Alzheimer's disease field, as well as from several other amyloid diseases. It also explains several disparate findings in the field and suggests further experiments to test the hypothesis.

In the supporting data paper, Dr. Murray and four other authors mechanistically linked diabetes and Alzheimer's. They demonstrated the first part of the ASAP hypothesis – amyloid can detect metabolic dysfunction. Reactive metabolites, elevated during metabolic dysfunction such as diabetes, chemically modify and misfold the amyloid protein in the test tube. These metabolites play a role in chemical glycation reactions to eventually form advanced glycation end products.

Dr. Murray demonstrates, similar to previous reports, that such modifications localize to the misfolded amyloid in Alzheimer's disease.

Source: IOS Press

Thursday, March 29, 2012

Best ever Easter gifts for those with dementia

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Choosing the right present for someone with Alzheimer’s disease or a related dementia is certain to give him/her joyful times independently or with a loved one. Here are some tips on how to pick a perfect gift.

Over 5.4 million Americans are living with dementia. Is one of them someone you know or work with? Get him/her or anyone with Alzheimer's disease an Easter gift that will keep on giving long after the holiday is gone.

Of course, person appropriate offerings are the best. This means matching a gift to a person’s interests and abilities, However, there are some presents that will make them smile no matter what.

One such gift is a book by Susan Berg called Adorable Photographs of Our Baby -- Meaningful, Mind-Stimulating Activities and More for the Memory Challenged, Their Loved Ones and Involved Professionals, This book features baby photographs that seniors with dementia love. This book shares a plethora of ideas and resources for you.
There is an activity related to hats that is most appropriate around Easter time.

If the person is a hat lover, buying him/her a new bonnet for Easter is an extraordinary idea. It will bring back fond memories of past Easters. Perhaps you can dig out some old Easter bonnets to try on as well as talk about, together, as Susan Berg suggests in her book. You could also have fun going through an old chest of clothes,


Sharing happy times and moments of joy will make both of you feel terrific. Inviting children to partake in this experience will make the time spent together even better. Berg says that dementia folks love children. This is another reason why her book is so popular with people who have Alzheimer’s disease or a related dementia.

While you have the children around, why not go through an old chest of clothes. Children love to play dress up. Dementia folks love children and reminiscing. Surely a lively discussion will ensue putting a smile on everyone’s face. Isn’t that a priceless gift?

Another gift dementia persons will fancy is a classic musical video or DVD especially for Easter. A classic movie of this type is Rogers and Hammerstein’s movie, Easter Parade. Any Roger’s and Hammerstein movie is a good choice, However matching their interests and favorite actors and actresses should simplify the gift giving process. You can even discuss some of the movies to get a better feel for the one they might like the best.

A video sing along is great for persons who has Alzheimer’s disease or another dementia. Even if they were not music lovers in the past, music is extremely therapeutic for them. Often non-verbal folks with dementia will sing along to a song that is familiar to them. Russ Carlton has a series of videos that will enchant a person with dementia.

An audio cassette or CD is another good choice. Just as with the movies, talking about songs often brings to light a good musical selection. There are some by Mitch Miller that are favorites of many. Also Broadway tunes are a preference of those with Alzheimer’s disease or a related dementia.

Especially for a lower functioning person with dementia is the gift of hand or body lotion. Any kind will do. Just be aware of any allergies or pain issues he/she might have. If he/she can tolerate it, those with a pleasant scent work well. Give him/her a relaxing hand massage talking about how good the hand massage feels, how much you love this person, and an Easter experience you both share from the past.

If you cannot afford or do not have time to get these gifts before Easter, give the gift of yourself. No matter how hard it is for you to visit a dementia person, he/she will appreciate your company even though he/she may not be able to express it. Take him/her for a walk, sing some of your favorite songs together, or share some messages of love. Just spend some quality time with a dementia person. Both of you will feel better. Do remember to be upbeat animated and excited about visiting.

A phone call or an Easter card will do if there is no way you can visit in person. At least they will know you are thinking of them. Then visit on another day.

So no matter what you do, do not forget the person with dementia this Easter because it will make you and him/her feel good. What could be better than that?

Order most of the products mentioned in the article at Amazon.com or from the artists directly

Tuesday, March 27, 2012

Alzheimer’s drug sharply criticized

McClatchy News Service |


WASHINGTON — Watching Alzheimer’s disease steal away the memory, talents and very selves of its victims is hard enough for the people who love them. But a new pill formulated by a respected pharmaceutical company and approved by the Food and Drug Administration will do little to help most patients and bring misery to some, say two medical investigators.


The drug, Aricept 23 mg, is no more effective on the whole than the disappointing ones already on the market — but is more likely to cause gastrointestinal problems, wrote Drs. Steven Woloshin and Lisa Schwartz of Dartmouth Medical College in an article published Thursday in the medical journal BMW


The new formulation was devised to serve commercial objectives, they say, and was approved despite a poor showing in company-sponsored tests.


Woloshin and Schwartz described Aricept 23’s march to market in 2010 as “perplexing” and “depressing” and wrote “there is no excuse for manipulating vulnerable patients, desperate family members and their doctors to use a product that is most likely to cause net harm.”


Dr. Marcia Angell, former editor of the New England Journal of Medicine and author of “The Truth About the Drug Companies,” said the critique was important. “It illustrates very well how drug companies exaggerate the benefits of their drugs, minimize the side effects, and through misleading marketing to both doctors and the public convince them that a new version of a drug, with a new patent, is better than the old one, whose patent has expired,” Angell told the Los Angeles Times.


Not really a new solution


In 2010, the FDA and the pharmaceutical giant Eisai handed caregivers of those with Alzheimer’s a new option for treating their loved ones — a 23-milligram dose of the long-available Alzheimer’s drug donepezil, better known by its commercial name, Aricept.
Aricept 23 was aggressively marketed (Eisai’s marketing partner in the United States is Pfizer Inc.) in magazine advertisements in a campaign touting clinical benefits and plucking at caregivers’ heartstrings.


But Schwartz and Woloshin say the new option was a commercial plan to extend a brand-name medication’s profit-making life by t
three years.


Renewing profitability


The practice, a common response to a drug company’s imminent loss of patent rights on a product, is known as “evergreening.” Aricept’s patent rights were due to expire in November 2010, and generic drug manufacturers in short order were sure to market donepezil much more cheaply.


Pharmaceutical companies routinely look for ways — all perfectly legal — to extend the profit-making life of their product: They make a slight change to a drug’s formula or dosage, or they combine it with another drug. With FDA approval, the new product is granted three years of legal protection from generic competition.
In the case of Aricept, developing a 23-milligram tablet created a dose that couldn’t be reproduced by any combination of Aricept’s existing 5- and 10-milligram pills, making the product new enough to win a three-year reprieve from low-cost competitors.
But Woloshin and Schwartz noted Eisai’s research showed that the pill offered a greater risk of side effects such as nausea and vomiting with no proof of benefit that a caregiver would be likely to notice.


FDA officials should not have allowed it, the authors said, because the clinical studies Eisai offered in support of its application did not meet standards the agency itself had laid out.


© 2012 Herald and News. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.

Sunday, March 25, 2012

Alzheimer’s breakthroughs revealed

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Sydney conference hears of significant research results which could lead to new diagnostic and therapeutic approach to the disease

Australian researchers have outlined new approaches for the diagnosis and treatment of Alzheimer's disease, which could result in accurate identification of the disease before more debilitating symptoms arise.

The diagnosis of Alzheimer’s is currently only possible through post-mortem examination of the brain, yet early diagnosis is paramount to preventing the disease from causing widespread damage to the brain.

Speaking at The Royal College of Pathologists of Australasia (RCPA) 11th annual Pathology Update conference in Sydney, two teams of scientists announced the results of extensive research which found a range of possible “biomarkers” which could result in a new diagnostic and therapeutic approach to tackling the disease.

Dr Simon Laws, from Edith Cowan University and the Australian Imaging Biomarker and Lifestyle (AIBL) research group, announced two major findings from his studies.

In the first, Laws identified a panel of eight potential plasma biomarkers for the disease.

The second study found that sex hormone levels, especially testosterone and luteinizing hormone, correlated with the presence of Alzheimer’s causing plasma and cerebral amyloid-beta in the brain, which could lead to new methods of diagnosis and treatment.

Laws said the identification and validation of a short panel of biomarkers has significant implications for the future diagnosis, prediction and monitoring of Alzheimer’s disease.

"The close association of hormones with Alzheimer’s pathology has significant implications on future treatments of the disease, with a clinical trial being the next stage in assessing the efficacy of this approach," Laws said in a statement.

The second team, led by Dr Ashley Bush of the Department of Pathology and Mental Health Research Institute at the University of Melbourne, was examining how impairments to the brain's ability to export concentrations of transition metals, like zinc, copper and iron, correlate with the presence and formation of plaques. This could provide pathologists with new methods of diagnosis and treatment of Alzheimer’s.

The levels of these ions in the brain rise with ageing and rise even more as the symptoms of Alzheimer’s set in. The abnormal regulation of metals in the brain is key to the formation of Alzheimer’s causing plaques and tau.

"These recent discoveries concerning the metal-centred neuropathology of Alzheimer’s are the target for a new class of drugs which have shown considerable promise in clinical trials. These abnormalities are also reflected in the periphery in Alzheimer’s disease and may be the basis for predictive biomarkers," said Bush.

Friday, March 23, 2012

Lifelong learning may be the best defense against Alzheimer’s disease

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By TIMI GUSTAFSON
Covington Reporter Columnist

Exercising the brain as much as exercising the body to keep both fit and healthy has become the new mantra for the aging baby boomer generation. Scientists seem to agree. Studies show that people who were cognitively active throughout their lives are less likely to experience mental decline as they grow older.

Age-related dementia such as Alzheimer’s disease is the most feared health condition among older Americans today, second only to cancer. It is also one of the most significant health threats of the 21st century, according to a report by the Alzheimer’s Association and the Harvard School of Public Health that was first published at an international conference on the subject in Paris, France, last year.

The causes for Alzheimer’s are not yet fully understood and there are currently no effective treatments that can halt or reverse the progressively debilitating disease. Researchers have suggested that diet and exercise as well as mental stimulation may serve as preventive measures, but there is not enough scientific evidence that these have a significant impact.

There are a number of health conditions, however, believed to promote the development of dementia. One is inflammation of the brain caused by stress hormones such as cortisol, which is toxic to nerve cells in the brain and especially to those responsible for memory. Another contributing factor is cardiovascular disease because it can prevent the brain from receiving sufficient blood supply, thereby damaging it.

A more controversial suggestion is that education, or lack thereof, can make a difference in the likelihood of someone becoming demented later in life. Obviously, the notion that the well-educated have a better shot at staying mentally healthy while the unschooled run the risk of losing their minds is hard to accept because it sounds elitist and snobbish. That makes it difficult to raise the issue without provoking strong reactions. Still, we have to look at the evidence.

Neuroscientists say that the reason why education can help prevent or at least slow down an aging person’s cognitive decline is that during learning processes structural changes in the brain’s neural network take place as neurons connect with one another. This is only possible because the central nervous system is in constant dynamic flux, which enables it to respond and adapt to changing requirements.

The more learning experiences we undergo over the years, the more neural connections we develop in the brain. This does not only happen when we learn something brand new – like a foreign language or a computer program – but even when we do routine work or play our favorite games. The already established neural connections just multiply as we repeat similar mental processes. That is why most tasks become easier to master over time, which is what learning is. This process is called “neural redundancy,” meaning that many neural connections become redundant through repetition – but not obsolete because when some connections get damaged or degenerate, others take over and continue to function in their place. In other words, the more “redundant” connections we develop over a lifetime through constant learning, the less likely we will lose our skills and abilities as we age.

So the question arises whether we can avoid the decline of our mental capacities by, let’s say, learning Mandarin, reading philosophical books or mastering programming software? Not if you start late, scientists say. Being mentally active from early on and throughout life, not just when you reach old age, is what makes the difference, according to Dr. William Jagust, a professor of public health and neuroscience at the University of California at Berkeley. What you do at 40 or 50 is more important than what you take on at 75.

“Older people seem to have less efficient brains [than younger people] and have to work their brains harder,” said Dr. Jagust in an interview on the subject with the New York Times. “People who stay cognitively active may be able to use their brains more efficiently,” he added.

Does it then still make sense to strive for mental fitness when you are already approaching retirement age or even later? Within limits, yes, Dr. Jagust agrees. Memory usually diminishes with age, even with people who do not have dementia, he said. It’s more about preserving the abilities you have than acquiring new ones, although both go hand in hand.

For those looking for learning opportunities in their later years, there is no shortage of programs offered by universities and colleges throughout the country. And these are not the only options. Educational travel programs are becoming extremely popular among retirees and the travel industry is more than happy to accommodate them.

Thursday, March 22, 2012

WOMENS BOXING

Guest post of the week by Brittany Booker

I recently upgraded our television package by logging onto http://www.giveadish.com/. I added a television in our bedroom. I was surprised when I was watching the news getting ready the other day and I saw a news special on one of my students that I teach. It was a story highlighting her and a sport that she participates in that is a traditional male sport. She is involved in female boxing, which is making its debut at the summer Olympics this year in 2012. It was an ad that said they were going to air the full story in the evening. I made sure that I watched it and was really impressed with my student. She had been into boxing for the last five years. She was also involved in rallying to have women’s boxing become an Olympic sport. Of course, she wasn’t trying to make it to the Olympics, but loves the sport and encourages other young women to participate in it. What I didn’t know is that women who are female boxers still wear skirts in the ring!

Wednesday, March 21, 2012

Can Vitamin D3 in Combination with This Spice Reverse Alzheimer’s Disease Progression?

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Health News

Patients with Alzheimer's disease tend to suffer from brain amyloidosis, a condition related to defective clearance of amyloid-beta in their brains by their innate immune system.

In order to improve the innate immune system of Alzheimer’s patients, researchers looked at the immune stimulation effects of vitamin D3 in combination with curcumin, an active compound found in the spice turmeric.

According to the study, as reported by Green Med Info:

“[Vitamin D3] is a promising hormone for [Alheimer’s] immunoprophylaxis because in Type I macrophages combined treatment with ... D3 and curcuminoids has additive effects, and in Type II macrophages ... D3 treatment is effective alone.”

Monday, March 19, 2012

Study Reveals How Anesthetic Isoflurane Induces Alzheimer's-like Changes in Mammalian Brains

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Sciencenewsline medicine

Massachusetts General Hospital

The association of the inhaled anesthetic isoflurane with Alzheimer's-disease-like changes in mammalian brains may by caused by the drug's effects on mitochondria, the structures in which most cellular energy is produced. In a study that will appear in Annals of Neurology and has received early online release, Massachusetts General Hospital (MGH) researchers report that administration of isoflurane impaired the performance of mice on a standard test of learning and memory – a result not seen when another anesthetic, desflurane, was administered. They also found evidence that the two drugs have significantly different effects on mitochondrial function.

"These are the first results indicating that isoflurane, but not desflurane, may induce neuronal cell death and impair learning and memory by damaging mitochondria," says Yiying (Laura) Zhang, MD, a research fellow in the MGH Department of Anesthesia, Critical Care and Pain Medicine and the study's lead author. "This work needs to be confirmed in human studies, but it's looking like desflurane may be a better anesthetic to use for patients susceptible to cognitive dysfunction, such as Alzheimer's patients."

Previous studies have suggested that undergoing surgery and general anesthesia may increase the risk of Alzheimer's, and it is well known that a small but significant number of surgical patients experience a transient form of cognitive dysfunction in the postoperative period. In 2008, members of the same MGH research team showed that isoflurane induced Alzheimer's-like changes – increasing activation of enzymes involved with cell death and generation of the A-beta plaques characteristic of the disease – in the brains of mice. The current study was designed to explore the underlying mechanism and behavioral consequences of isoflurane-induced brain cell death and to compare isoflurane's effects with those of desflurane, another common anesthetic that has not been associated with neuronal damage.

In a series of experiments, the investigators found that the application of isoflurane to cultured cells and mouse neurons increased the permeability of mitochondrial membranes; interfered with the balance of ions on either side of the mitochondrial membrane; reduced levels of ATP, the enzyme produced by mitochondria that powers most cellular processes; and increased levels of the cell-death enzyme caspase. The results also suggested that the first step toward isoflurane-induced cell death was increased generation of reactive oxygen species – unstable oxygen-containing molecules that can damage cellular components. The performance of mice on a standard behavioral test of learning and memory declined significantly two to seven days after administration of isoflurane, compared with the results of a control group. None of the cellular or behavioral effects of isoflurane were seen when the administered agent was desflurane.

In another study by members of the same research team – appearing in the February issue of Anesthesia and Analgesia and published online in November – about a quarter of surgical patients receiving isoflurane showed some level of cognitive dysfunction a week after surgery, while patients receiving desflurane or spinal anesthesia had no decline in cognitive performance. That study, conducted in collaboration with investigators from Beijing Friendship Hospital in China, enrolled only 45 patients – 15 in each treatment group – so its results need to be confirmed in significantly larger groups.

"Approximately 8.5 million Alzheimer's disease patients worldwide will need anesthesia and surgical care every year," notes Zhongcong Xie, MD, PhD, corresponding author of both studies and director of the Geriatric Anesthesia Research Unit in the MGH Department of Anesthesia, Critical Care and Pain Medicine. "Developing guidelines for safer anesthesia care for these patients will require collaboration between specialists in anesthesia, neurology, geriatric medicine and other specialties. As the first step, we need to identify anesthetics that are less likely to contribute to Alzheimer's disease neuropathogenesis and cognitive dysfunction." Xie is an associate professor of Anesthesia at Harvard Medical School (HMS)

Saturday, March 17, 2012

Adding Second Drug No Help in Alzheimer's

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Medpage Today

Action Points
In moderate-to-severe Alzheimer's disease, continuing treatment with donepezil, a cholinesterase inhibitor, had some benefits, but adding memantine (Namenda) did not.
Note that memantine yielded similar benefits compared with placebo but the combination of memantine and donepezil was no better than donepezil alone.

For patients with moderate-to-severe Alzheimer's disease, continuing treatment with donepezil -- a cholinesterase inhibitor -- has some benefits, but adding memantine (Namenda) does not, a randomized trial showed.

Compared with stopping donepezil, continuing treatment for a year resulted in significant improvements in cognition and performance of the activities of daily living (P<0.001 for both), according to Robert Howard, MD, of King's College London, and colleagues.

Memantine yielded similar benefits compared with placebo but the combination of memantine and donepezil was no better than donepezil alone, the researchers reported in the March 8 issue of the New England Journal of Medicine.

In an accompanying editorial, Lon Schneider, MD, of the University of Southern California in Los Angeles, said the results with donepezil in the trial may not apply to other cholinesterase inhibitors because of differences in pharmacokinetics and mechanisms of action.

"Nor should the ... results be interpreted as evidence of the efficacy of indefinite treatment with donepezil," he noted. "More research is needed to assess the long-term benefits, the potential for harm and physiological tolerance, and the safe discontinuation of cholinesterase inhibitors as Alzheimer's disease progresses."

Cholinesterase inhibitors -- including donepezil -- have shown some benefits in patients with mild-to-moderate Alzheimer's disease, although no treatments have been able to halt disease progression.

When the disease worsens, clinicians must make a decision about continuing treatment, which is complicated by a greater risk of adverse outcomes, the need for permanent pacemakers, and hip fractures when treatment is not stopped.

In the DOMINO study, Howard and colleagues evaluated the effects of continuing donepezil with or without the addition of memantine in 295 patients with moderate-to-severe Alzheimer's disease who had been treated with donepezil for at least three months.

The patients were living in the community and either had a live-in caregiver or someone who visited them at least once a day.

The researchers assigned the patients to one of four groups for one year:

Continue donepezil at a dose of 10 mg daily and start placebo memantine
Continue donepezil and start memantine at a dose increasing to 20 mg daily
Gradually discontinue donepezil and receive placebo donepezil and placebo memantine
Gradually discontinue donepezil, receive placebo donepezil, and start memantine
The coprimary outcomes of the trial were changes on the Standardized Mini-Mental State Examination (SMMSE) and on the caregiver-rated Bristol Activities of Daily Living Scale (BADLS). The minimum clinically important differences were defined as 1.4 points and 3.5 points, respectively.

Compared with patients who stopped donepezil, those who continued treatment scored 1.9 points better on the SMMSE and 3 points better on the BADLS. Only the difference on the SMMSE exceeded the minimum clinically important threshold.

In his editorial, Schneider said the 1.9-point difference "is potentially important because many of the patients were severely impaired, on the cusp for needing nursing home care, and slightly worse cognitive function could affect their ability to remain at home."

Compared with patients who received placebo memantine, those who started the drug scored 1.2 points better on the SMMSE and 1.5 points better on the BADLS (P≤0.02 for both), although both figures fell short of being clinically important.

Combining donepezil and memantine was not superior to donepezil alone.

"Although memantine appears to be helpful for the treatment of moderate-to-severe Alzheimer's disease when used alone or when replacing donepezil, the results of the DOMINO trial do not support the typical use in the U.S., and an FDA-approved use, as add-on therapy to established donepezil treatment," according to Schneider, who noted that the finding conflicts with a previous, shorter trial.

Howard and colleagues pointed out that neither donepezil nor memantine halted the overall loss of cognitive function and functional abilities.

Compared with the changes in patients who received placebo for both drugs, the gains seen in the SMMSE score with donepezil and memantine represented just 32% and 20%, respectively, of the total decline during the study. The figures for the BADLS scores were 23% and 11%, respectively.

There were 188 serious adverse events, but only six were considered possibly related to the study drugs. Rates did not differ between groups.

Thursday, March 15, 2012

Assessment of Challenging and Management Problems Initiating Options for New Solutions

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careforumwales.co.uk

Responsible care providers are committed to finding sensitive creative and individualized
appropriate care interventions to safely manage behaviour that challenges, exhibited by
service users with dementia, and thereby avoiding administration of antipsychotic
medications as far as is practicable and safe to do so.
The elimination of or successful management of catalysts and identification of common
denominators will inform care intervention strategies and promote problem resolution.
Please tick the appropriate boxes, as relevant and complete the document which is
designed to take no more than 5 minutes.
This document is suitable for use in all care delivery settings and can be completed by
careworkers, carers, nurses or others providing care in hospitals, clinics, day centres, care
homes, domiciliary care or care at home tby family members or others.

DEMENTIA CARE: ‘A CHAMPIONS’ DOCUMENT

Tuesday, March 13, 2012

Donepezil For Treatment Of Moderate To Severe Alzheimer's

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Medical News Today

A new study, published in New England Journal of Medicine, conducted by Professor Robert Howard at the King's College London Institute of Psychiatry, and funded by the Alzheimer's Society and the Medical Research Council, reveals that the drug donepezil, used for the treatment of dementia and mild to moderate Alzheimer's Disease, which targets 750,000 people around the world, may be effective in treating patients with moderate to severe cases, as well.

The authors state that this new breakthrough may result in helping twice as many people around the world who suffer from dementia. Although donepezil has previously been used for treating early stages of dementia, the authors say that it is actually more helpful for the treatment of patients suffering from the later stages of dementia.

During the trial, the researchers analyzed two drugs: memantine and donepezil. Donepezil has previously been recommended by doctors for people who are experiencing the early symptoms of Alzheimer's, and is currently the most prevalent drug for the treatment of dementia.

As of now, doctors are told not to prescribe donepezil after the early stages of dementia because of lack of evidence proving it is effectiveness in treating the later stages of the disease.

Professor Robert Howard, from the Institute of Psychiatry at King's, and lead researcher of the study commented:


"As patients progress to more sever forms of Alzheimer's disease, clinicians are faced with a difficult decision as to whether to continue or not with demtia drugs and, until now, there has been little evidence to guide that decision. For the first time, we have robust and compelling evident that treatment with these drugs can continue to help patients at the later, more severe stages of the disease."


During this study, the people who took donepezil after their symptoms worsened to the stages of moderate to severe, were seen to have much less of a rapid decline in cognitive memory, and were able to live their lives more normally than they would have without the drug. The patients who had been given memantine had better memory function as well, but less than the patients who had been given donepezil. The patients who took the placebo did not show improvement in cognitive ability.

Howard says:


"'We observed that patients who continued taking donepezil were better able to remember, understand, communicate and perform daily tasks for at least a year longer than those who stopped taking the drugs. These improvements were noticeable to patients, their caregivers and doctors. Both donepezil and memantine will soon be off patent and available in very cheap generic preparations. These findings will greatly increase the numbers of patients in the developed and developing world that we are able to treat."


Professor Clive Ballard, Director of Research at Alzheimer's Society said:


"Thanks to the Alzheimer's drug donepezil, tens of thousands of people in the early to moderate stages of the condition are able to recognise their family for longer, play with their grandchildren and make vital plans for the future. This major new trial now shows that there could also be significant benefits on continuing the treatment into the later stages too. There are 750,000 people with dementia in the UK yet currently prescription levels of Alzheimer's drugs are still low. If this is to change we have to improve the shocking diagnosis rates and ensure everyone is given the opportunity to try treatments."


Written By Christine Kearney
Copyright: Medical News Today

Sunday, March 11, 2012

Mitochondria in the brain are dysfunctional early on in Alzheimer's disease,

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Ivanhoe Newswire

With the help of mice, researchers have now found that mitochondria in the brain are dysfunctional early on in Alzheimer's disease, even before memory loss.

The team examined mitochondria in three mouse models, each using a different gene shown to cause familial, or early-onset, Alzheimer's disease. The specific mitochondria changes corresponded with the mutation type and included altered mitochondrial movement, structure, and energy dynamics. The changes occurred in the brain even before the mice showed any symptoms such as memory loss. The group also found that the mitochondrial changes contributed to the later loss of mitochondrial function and the onset and progression of Alzheimer's disease.

"One of the most significant findings of this study is our discovery of the impact of mitochondrial dysfunction in Alzheimer's disease," Eugenia Trushina, Ph.D., Mayo Clinic pharmacologist and senior investigator on the study, was quoted saying. "We are asking: Can we connect the degree of mitochondrial dysfunction with the progression of symptoms in Alzheimer's disease?"

With the help of a Mayo researcher Petras Dzeja, Ph.D., the team applied a fairly new method called metabolomics, which measures the chemical fingerprints of metabolic pathways in the cell — sugars, lipids, nucleotides, amino acids and fatty acids.

The researchers hope that the panel of metabolomic biomarkers they discovered can eventually be used for early diagnosis, treatment, and monitoring of Alzheimer's progression.

"We expect to validate metabolomic changes in humans with Alzheimer's disease and to use these biomarkers to diagnose the disease before symptoms appear -- which is the ideal time to start treatment," Dr. Trushina was quoted saying.

The researchers examined neurons of three various genetic animal models of Alzheimer's disease. Researchers applied a mitochondria-specific dye and observed their motion along axons, a process called axonal trafficking. Demonstrating that even in embryonic neurons afflicted with Alzheimer's disease, well before the mice show any memory loss, mitochondrial axonal trafficking is inhibited. Using a panel of techniques that included electron and light microscopy, they determined that in the brains of mice with Alzheimer's disease, mitochondria tended to lose their integrity, ultimately leading to the loss of function. Importantly, dysfunctional mitochondria were detected at the synapses of neurons involved in maintaining memory.

"We are not looking at the consequences of Alzheimer's disease, but at very early events and molecular mechanisms that lead to the disease," Dr. Trushina was quoted as saying. The next step is looking at the same mitochondrial biomarkers in humans, she says. As the researchers begin to understand more about the mitochondrial dynamics that are altered in Alzheimer's disease, they hope to move on to designing drugs that can restore the abnormal bioenergetics and mitochondrial dynamics to treat the disease.

Friday, March 9, 2012

New report reveals care costs for people with Alzheimer'​s and other dementias reach $200 billion

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Alzheimer's Association

Medicare costs for individuals with Alzheimer’s and other dementias are three times higher than for older people without these conditions. Medicaid costs are 19 times higher. These are just a few of the sobering statistics featured in the Alzheimer’s Association® 2012 Alzheimer’s Disease Facts and Figures report, which captures the rapidly escalating impact of the Alzheimer’s epidemic.

While care costs for individuals with Alzheimer’s and other dementias are significant to the nation, the newly released report also illustrates the burden of the disease on caregivers. More than 15 million friends and family members provide 17.4 billion hours of unpaid care valued at $210 billion. Other key statistics include:

5.4 million Americans are living with Alzheimer’s disease, including 5.2 million people age 65 or older and 200,000 people under the age of 65.

By 2025, as many as 6.7 million people will be living with Alzheimer’s, and by midcentury up to 16 million could have the disease. As the baby boomers age, the prevalence of Alzheimer’s disease will continue to soar and so will the costs to the nation. This includes a 500% increase in combined Medicare and Medicaid spending and a 400% increase in out-of-pocket costs for families.

1 out of 7 people with Alzheimer’s lives alone and up to half of these individuals do not have an identifiable caregiver.

Wednesday, March 7, 2012

New Alzheimer's Marker Strongly Predicts Mental Decline

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Science Daily

A new marker of Alzheimer’s disease can predict how rapidly a patient’s memory and other mental abilities will decline after the disorder is diagnosed, researchers at Washington University School of Medicine in St. Louis have found.

In 60 patients with early Alzheimer’s disease, higher levels of the marker, visinin-like protein 1 (VILIP-1), in the spinal fluid were linked to a more rapid mental decline in the years that followed.
Scientists need to confirm the results in larger studies, but the new data suggest that VILIP-1 potentially may be a better predictor of Alzheimer’s progression than other markers.
“VILIP-1 appears to be a strong indicator of ongoing injury to brain cells as a result of Alzheimer’s disease,” says lead author Rawan Tarawneh, MD, now an assistant professor of neurology at the University of Jordan. “That could be very useful in predicting the course of the disease and in evaluating new treatments in clinical trials."
The study appears March 6 in Neurology.
VILIP-1 was originally identified as a potential indicator of brain cell damage in the laboratory of Jack Ladenson, PhD, the Oree M. Carroll and Lillian B. Ladenson Professor of Clinical Chemistry in Pathology and Immunology at Washington University. Scientists think VILIP-1 serves as a calcium sensor in brain cells. It is released into the cerebrospinal fluid when the cells are injured.
Tarawneh is a former postdoctoral research associate in the laboratory of David Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of Washington University’s Department of Neurology. In an earlier study, she and her colleagues showed that healthy subjects with high levels of VILIP-1 were more likely to develop cognitive impairment and Alzheimer’s disease over a two- to three-year follow-up period.
For the new study, scientists identified patients with very mild or mild Alzheimer’s disease enrolled in studies at the Charles F. and Joanne Knight Alzheimer’s Disease Research Center at Washington University School of Medicine. At the outset, researchers measured levels of VILIP-1 in patients’ spinal fluid and assessed their mental abilities using an extensive battery of tests. The cognitive function testing was repeated annually.

“Memory and other mental abilities declined faster in patients with the highest levels of VILIP-1,” Tarawneh says. “In patients with early symptoms of Alzheimer’s disease, VILIP-1 seems to be at least as good as — and potentially even better than — the other prognostic indicators we used in the study.”
The two additional indicators studied were the proteins amyloid beta and tau. Changes in the spinal fluid levels of those proteins mainly reflect the fact that amyloid beta and tau are starting to form abnormal deposits in the brain. In contrast, VILIP-1 appears to reveal how much damage to brain cells has occurred as a result of brain changes caused by Alzheimer’s.
“These results are intriguing, but we need a larger study to fully understand how the insights provided by VILIP-1 compare to those we can gain from other markers,” Tarawneh says.
She is working with Washington University scientists to standardize the tests that measure VILIP-1 for expanded use in research.
Funding from the National Institutes of Health (NIH), Siemens Health Care Diagnostics and the Charles and Joanne Kn

Monday, March 5, 2012

Alzheimer’s-Like Memory Loss Reversed in Mice

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Businessnews.com
By Amir Khan:


Alzheimer's patients have a molecular blockade that could be potentially broken to reverse the disease after researchers showed Wednesday that removing the blockade improved cognition in mice with Alzheimer's-like disease.

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Sponsorship LinkHow to make money from gold investment Researchers injected mice with a molecule that stops overproduction of a protein called HDAC2. High levels of HDAC2 are found in Alzheimer's patients and overexpression of the HDAC2 gene causes Alzheimer's-like symptoms in mice.

The mice regained their cognitive abilities when researchers reduced the buildup of the protein, suggestive that neurodegenerative conditions such as Alzheimer's are reversible.

Researchers warned that any drug is at least five to 10 years away from human trials and would only treat the symptoms of Alzheimer's, not the root cause. However, the researchers said simply proving the disease is potentially reversible is a huge step forward.

"If your memory is everything that you know written in a book, then in order to have access, you have to open the book and to turn the pages," Johannes Graff, lead researcher and a postdoctoral researcher at Massachusetts Institute of Technology, told HealthDay. Buildup of the protein makes the pages inaccessible, Graff said.

"We are proposing to reopen the book and allow it to be more easily read," Graff told HealthDay.

Nature published the study online Wednesday.

Alzheimer's is the most common form of dementia in the United States, affecting more than 5 million people, according to the Centers for Disease Control and Prevention. The number of people who suffer from the disease is expected to double every 20 years.

Symptoms of Alzheimer's include memory loss, confusion, difficulty completing familiar tasks, decreased judgment and problems speaking or writing.

Healthcare costs related to Alzheimer's disease totaled almost $8 billion in 2010, according to the Alzheimer's Association, a nonprofit organization that advocates for Alzheimer's patients in the federal and state governments.

There is as yet no cure or successful treatment for Alzheimer's disease. The Obama administration set a goal of 2025 to find an effective treatment and pledged to spend an additional $50 million on dementia research on top of the $450 million the government spends annually until a treatment is found

Saturday, March 3, 2012

Obama's Alzheimer's plan focuses on treatment, care

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By Julie Steenhuysen

(Reuters) - The Obama administration's plan to fight Alzheimer's disease aims to harness the nation's expertise to find real treatments by 2025 and improve the care and treatment of the 5.1 million Americans already afflicted with the brain-wasting disease.

The draft plan, issued by the Department of Health and Human Services on Wednesday, makes treatment a top priority, but it also focuses on the burden the disease places on families and caregivers.

"Alzheimer's disease burdens an increasing number of our nation's elders and their families, and it is essential that we confront the challenge it poses to our public health," President Barack Obama said in a statement marking the plan's unveiling.

The White House earlier this month said it would divert an additional $50 million this year from HHS projects to Alzheimer's research, and seek an extra $80 million in new research funding in fiscal 2013.

"These investments will open new opportunities in Alzheimer's disease research and jumpstart efforts to reach the 2025 goal," HHS said in the draft document.

Obama also plans on an additional $26 million in spending on programs to support people who care for Alzheimer's patients.

Current drugs help manage symptoms but so far no therapy can stop the progression of Alzheimer's, which can start with vague memory loss and confusion before progressing to complete disability and death.

Some researchers have criticized the plan and its 2025 target, saying it is too ambitious given that researchers are still just beginning to understand the disease, which develops silently for 15 to 20 years before any memory problems begin to show.

The best hopes for a treatment at this stage lie with two drugs under development: one from Eli Lilly and another from Johnson & Johnson and Pfizer. But some experts worry these drugs are being tested in patients whose disease has already progressed too far for them to benefit from the treatments.

Experts predict that without effective drugs, the number of Americans with Alzheimer's will double by 2050 and related healthcare costs could soar to more than $1 trillion a year.

HHS is planning a scientific summit in May to set research priorities. It seeks to increase participation in Alzheimer's clinical trials, with a special focus on ensuring minority representation, and to shorten the time it takes to develop drugs.

Eric Hall, president and chief executive of the Alzheimer's Foundation of America and a member of the advisory council that has been working with HHS, said it addresses many of the concerns that have been expressed by the panel.

"Given the current economic environment that limits much-needed resources and the scientific unknowns of this disease, we believe that defeating Alzheimer's disease will likely happen in a series of small victories," Hall said in a statement.

He was especially pleased that the plan focuses on educating healthcare providers on how to detect early signs of cognitive impairment and linking newly diagnosed families with appropriate support services.

But George Vradenburg, chairman of USAgainstAlzheimer's and a member of the advisory panel, said the draft plan did not go far enough.

"This first draft fails to present a strategy aggressive enough to achieve the goal of preventing and treating Alzheimer's within 13 years," he said, noting that the plan lacks specific timelines and does not hold any high-level officials accountable for meeting the plan's goals.

The plan is open for public comment through the end of March.

(Reporting by Julie Steenhuysen; Editing by Eric Walsh)

Thursday, March 1, 2012

.How Daylight Savings Time Effects Your Loved One with Dementia

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FirstLight Home Care
How Daylight Savings Time Effects Your Loved One with Alzheimer’s Disease
Posted by Gina Kaurich in Alzheimer's & Dementia Care, Caregiving, Health & Wellness

Daylight Savings Time starts Sundday March 11.Read this for some insight as to how daylight savings time may affect your loved one or client with dementia

It occurred to me as I sat at breakfast with my mother in law, Martha, who suffers with Alzheimer’s disease that she didn’t seem quite herself today. That may sound strange to some of you but even as an individual is progressing through the dementia stages they do retain certain parts of their personality. Now, sometimes the subtle changes can occur before an illness such as a urinary tract infection or even dehydration. So I started this morning with running through the gamut of potential problems. Beginning with the small things such as the lighting being adequate, is she warm enough, does she have her hearing aids in place and are they turned up so she can hear me. I then moved on to what I call the intermediate of potential issues, such as did she take her medications last night and today, did she seem stuffy or congested this morning, had she had a bowel movement yesterday, or did her unusually quiet behavior reflect something else. She seemed tired and when she asked what time it was, it hit me; last night was the shift to Daylight Savings Time.

Now you would not expect this to create any problems for someone who is not cognitively aware of the time of day any longer; but just like a baby or child, the individual with Alzheimer’s has a sense something is different. We did not necessarily get her up an hour earlier or make any changes to her routine but she sensed a change. She asked repeatedly during the day what time it was and finally said she felt tired today. There are times when she is such a “hoot”! Her surprised reaction when we told her the time was, “Oh my, how could I have slept so long.” And when we all laugh, she laughs and enjoys herself right along with the rest of us, it is wonderful. I love to see her have those happy moments.

Meals were the epicenter of her confusion with Day Light Savings time; she just couldn’t believe it was time to eat again. This made us all laugh again since Martha is a very tiny woman who weighs about 98 pounds but eats constantly. Around our house we have candy dishes filled with her favorite “Hershey Kisses” along with bowls of unsalted pecans, almonds and fruit. Needless to say, she does not go hungry. However, today her eating pattern has shifted and instead of eating all of those treats between meals, she is eating them about an hour later. Our grandchildren came over and she helped fix tacos, salad and brownies for dinner and guess who ate her weight in brownies? It is wonderful to watch how animated she becomes when around children. You can see she is back to raising her daughter and five boys; her old behaviors to keep them busy kick in.

Once dinner was over and as the sun went down she began to become restless and uncomfortable; not unusual for most people with dementia. Martha rubs her hands together when she is unsettled which helps by giving us an indicator to her state of mind. Her bright blue eyes begin to fade. She asks my husband to take her home which we finally figured out to mean Tennessee, where she grew up with “Momma and Daddy”. Then she wants to know if the lady of the house cares if she goes to bed. She and I walk together upstairs to begin her bedtime routine and she says to me that she is so tired and the day has gone by so fast. I agree and to some degree am always surprised at how much she continues to teach me every day about those living with dementia.
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