Monday, 30 June 2008

Myriad Genetics Reports Results of U.S. Phase 3 Trial of Flurizan™ in Alzheimer's Disease

Flurizan Fails to Achieve Significance on Either Co-Primary Endpoint; Company Has Decided to Discontinue Its Development of Flurizan


Myriad Genetics today announced results of the Act-Earli-AD trial, an 18-month Phase 3 study of Flurizan (tarenflurbil) in patients with mild Alzheimer's disease. The study did not achieve statistical significance on either of its primary endpoints -- cognition and activities of daily living.

"We are disappointed that Flurizan failed to achieve significance in this study, and we will now discontinue development of this compound," said Peter Meldrum, President and Chief Executive Officer of Myriad Genetics, Inc. "The discontinuation of Flurizan will reduce our pharmaceutical development spend substantially and should enable Myriad to achieve profitability next year, ending June 30, 2009."

During fiscal 2008, Myriad spent approximately $60 million on development of Flurizan. The remaining expenses to wrap up its Flurizan program are projected to be approximately $8 million in total, spread primarily over the next two fiscal quarters.

Myriad to End Development of Flurizan

clipped from www.thestreet.com

Myriad Genetics MYGN said Monday that it will stop development of its experimental Alzheimer's disease drug Flurizan due to the failure of a pivotal phase III study.

The Flurizan study, which enrolled patients with mild to moderate Alzheimer's, did not achieve statistical significance on either of its two primary endpoints -- cognition or activities of daily living, the company said.

While disappointing, the negative outcome from the Flurizan study was not unexpected, given the relatively poor results coming out of the drug's phase II study.
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Friday, 27 June 2008

Myriad Genetics' Alzheimer's Disease Drug Mechanism of Action Detailed in Nature Article

"The article in Nature adds to the understanding of the mechanism of action of Flurizan, providing a molecular basis for its ability to slow the progression of Alzheimer's disease, as was demonstrated in previous human clinical studies"



Myriad Genetics' Alzheimer's Disease Drug Mechanism of Action Detailed in Nature Article

Myriad Genetics, Inc. (NASDAQ: MYGN) announced today that the mechanism of action of Flurizan(R) (tarenflurbil) -- its drug candidate for the treatment of Alzheimer's disease, is elucidated in the scientific journal Nature. The article, "Substrate-targeting Gamma-secretase Modulators," will be published in the June 12, 2008 issue of Nature.

Previous studies, in vitro, in animal models and in humans, have demonstrated that Flurizan selectively lowers toxic amyloid beta 42, and is the first member of a new class of drugs known as selective amyloid lowering agents (SALAs). Further, Flurizan has been shown to modify the processing of the amyloid precursor protein (APP) by the gamma secretase enzyme. The specific way in which Flurizan accomplishes this reduction in the toxic amyloid beta 42 had remained a mystery until now.

The Nature paper confirms the SALA properties of Flurizan and establishes the mechanism by which Flurizan modulates the APP-gamma secretase interaction. The authors demonstrate that the molecular target of Flurizan is the amyloid precursor protein itself -- the substrate of gamma secretase. Flurizan modifies the conformation of the APP molecule as it is bound to the gamma secretase complex. This change in the shape and/or position of APP in the complex results in cleavage by gamma secretase that produces shorter length, non-toxic amyloid beta fragments, such as amyloid beta 38 and amyloid beta 40. This exciting finding is novel in that most drugs target enzymes, blocking their function directly, but the substrate of an enzyme has not generally been seen as a drug target. These new findings are consistent with previous studies that show that Flurizan selectively lowers amyloid beta 42 by shifting the conformation of the APP/gamma secretase complex through allosteric binding.

"The article in Nature adds to the understanding of the mechanism of action of Flurizan, providing a molecular basis for its ability to slow the progression of Alzheimer's disease, as was demonstrated in previous human clinical studies," said Adrian Hobden, Ph.D., President of Myriad Pharmaceuticals, Inc. "The findings help explain why compounds like Flurizan can have a dramatic effect on lowering amyloid beta 42, the initiator of plaque formation in the human brain, and offer hope for the treatment of patients who suffer from Alzheimer's disease."

Flurizan U.S. Phase 3 Clinical Trial

Flurizan has recently completed a Phase 3 clinical trial in the U.S. of 1684 patients from 131 investigator sites. Topline data from the trial is scheduled for reporting in June 2008, and a full analysis of the data will be presented at the Alzheimer's Association's International Conference on Alzheimer's Disease in Chicago on July 29, 2008.

Flurizan is a registered trademark of Myriad Genetics, Inc. in the United States and other countries.

Myriad Genetics, Inc. is a biopharmaceutical company focused on the development of novel healthcare products. The Company develops and markets predictive medicine products, and is developing and intends to market therapeutic products. Myriad's news and other information are available on the Company's Web site at www.myriad.com.


Wednesday, 25 June 2008

Overuse Of Antipsychotics Among Nursing Home Residents With Dementia

This excellent article really got my blood flowing. It reminded me about a similar situation that occurred with my mother's personal physician. The doctor wanted to put my mother on an anti-depression drug. I was far enough in and had read enough information about dementia and Alzheimer's to understand this was a bad idea. At that point we did change physicians (three times in fact).

It turned out that my mother was likely suffering from Alzheimer's and she needed Aricept. It also turned out she was suffering from unrecognized hypothyroidism, although this diagnosis came later.

I learned two very important lessons. First, once dementia is diagnosed you need to find a personal physician that understands the disease and is well educated about the appropriate actions that need to be taken. Second, I learned that every person suffering from dementia should have their thyroid checked. After almost two years of never smiling and laughing, my mother began to smile and laugh after she received the proper medication for her thyroid.

My mother actually sang the other day for the first time in several years. I believe the introduction of the thyroid medication is partly responsible for this very positive change.
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The clip below is a snippet of the article that appeared in the New York Times. Click the link in the clip to read the entire article. It is important. Please share this information with others.
clipped from www.nytimes.com

Ramona Lamascola thought she was losing her 88-year-old mother to dementia. Instead, she was losing her to overmedication.

Last fall her mother, Theresa Lamascola, of the Bronx, suffering from anxiety and confusion, was put on the antipsychotic drug Risperdal. When she had trouble walking, her daughter took her to another doctor — the younger Ms. Lamascola’s own physician — who found that she had unrecognized hypothyroidism, a disorder that can contribute to dementia.

Theresa Lamascola was moved to a nursing home to get these problems under control. But things only got worse. “My mother was screaming and out of it, drooling on herself and twitching,” said Ms. Lamascola, a pediatric nurse. The psychiatrist in the nursing home stopped the Risperdal, which can cause twitching and vocal tics, and prescribed a sedative and two other antipsychotics.

“I knew the drugs were doing this to her,” her daughter said. “I told him to stop the medications and stay away from Mom.”


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Also See;

Abnormal Thyroid Levels Can Increase Risk For Alzheimer’s Disease in Women

Early Alzheimer's patients speak up for others

"It's labeled incurable and you end up being a vegetable. People think as soon as you're labeled that way, you are. A lot of us aren't," says Hayen, 74, a retired San Diego physician who joined about 30 other early-stage Alzheimer's patients last month for a lobbying blitz at the nation's capital.

Follow the link in the clip below to read this interesting story.
clipped from www.msnbc.msn.com
Don Hayen has a handy way of deflecting the instant pity that comes when he reveals his Alzheimer's disease: "But I haven't lost my keys all day," he quickly jokes.

Hayen is part of a growing new movement in Alzheimer's: Patients diagnosed early enough to still be articulate and demand better care and better research. They are giving a voice to a disease whose victims until now have remained largely silent, and powerless.

It is a shift with big ramifications.


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Scientists identify possible Alzheimer's gene

As some of you know, I am always looking for information about genes that predispose individuals to Alzheimer's. If you are genetically predisposed to Alzheimer's by birth you might consider taking calcium or increasing your calcium intake.
Gene hampers cell's ability to absorb calcium, raises risk by 45 percent
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Scientists identify possible Alzheimer's gene

Scientists have identified a gene that may raise the risk of getting the most common kind of Alzheimer's disease by about 45 percent in people who inherit a certain form of it.

That form of the gene appears to hamper a brain cell's ability to take in calcium, researchers said. If drugs can be found that reverse its effect, they may be useful in fighting Alzheimer's, researchers said.

Most cases of Alzheimer's appear after age 65. So far, only one gene has been firmly established as affecting the risk of this late-onset version. The gene proposed in the new study, called CALHM1, appears to have a much smaller impact on the disease risk.

Dozens of other genes are also under study as possibly affecting risk of the disease.

The new work appears Friday's issue of the journal Cell. The work is reported by Philippe Marambaud of the Feinstein Institute for Medical Research in Manhasset, N.Y., and others in the United States and elsewhere.

They studied the gene with data from more than 2,000 people with Alzheimer's and about 1,400 people without the disease.

Bob DeMarco is a citizen journalist, blogger, and Caregiver. In addition to being an experienced writer he taught at the University of Georgia , was an Associate Director and Limited Partner at Bear Stearns, the CEO of IP Group, and a mentor. Bob currently resides in Delray Beach, FL where he cares for his mother, Dorothy, who suffers from Alzheimer's disease. He has written more than 500 articles with more than 11,000 links to his work on the Internet. His content has been syndicated on Reuters, the Wall Street Journal, Fox News, Pluck, Blog Critics, and a growing list of newspaper websites. Bob is actively seeking syndication and writing assignments.





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Alzheimer Disease Behavioral Symptoms Protocols


I found this very informative and valuable handout for caregivers on the Indiana University Center for Aging Research website. The opening webpage is titled Alzheimer Disease Behavioral Symptoms Protocols. On the right hand side of the page you will see a link entitled View Behavioral Symptoms Protocols and this will take you to the handout. If you prefer you can get to the PDF by clicking on this link, Behavioral Symptoms Protocols.

Please pass this information and link on to others. 

Alzheimer’s Disease as a Case of Brake Failure?

If you are like me you will find this research promising. When I read many of these research articles I experience feelings of hope and then frustration. It is clear this won't help my mother who suffers from Alzheimer's. At the same time, I am hopeful that it will help future sufferers of this sinister disease.

“It changes the logic from a search for a trigger that kicks off the dementia to the failure of a safety that has suppressed it”


Rutgers researcher Karl Herrup and colleagues at Case Western Reserve University have discovered that a protein that suppresses cell division in brain cells effectively “puts the brakes” on the dementia that comes with Alzheimer’s disease (AD). When the brakes fail, dementia results.

This discovery could open the door to new ways of treating Alzheimer’s disease, which affects up to half the population over the age of 85.

Determining the protein’s previously unsuspected role in AD is an important piece of the puzzle and it brings a new perspective to the basis of AD. “It changes the logic from a search for a trigger that kicks off the dementia to the failure of a safety that has suppressed it,” said Herrup, chair of the Department of Cell Biology and Neuroscience at Rutgers, The State University of New Jersey.

The researchers reported their findings in the in the June 24 Proceedings of the National Academy of Sciences (PNAS). The paper was previously available online in the PNAS Early Edition.

Herrup has spent a good part of his career seeking to unravel the mystery behind unrestrained cell cycling. Looking at AD through the lens of cancer, Herrup sees the rampant cell division associated with cancer mirrored in AD-related dementia.

In cancer, the seemingly uncontrollable cell division enables the disease to overwhelm normal body cells. Adult neurons, or nerve cells, don’t normally divide. (Cancerous brain tumors do not grow from neurons but from glial cells.) Instead of producing new neurons in the brain, the cycling leads to cell death, which causes progressive dementia.

“Every cell wants to divide, and that basic urge never leaves the cell,” Herrup said.

“Homeostasis in the brain has worked out a way to successfully suppress cell cycling, but with age even that highly successful program sometimes fails, resulting in a catastrophic loss of neurons.”

Herrup’s team experimented with a protein family known as cyclin-dependent kinases (Cdk). These enzymes power the cell cycle, driving it forward through its various phases. The scientists focused on one particular kinase – Cdk5 – termed “an atypical kinase” because they could find no involvement in propelling the cell cycle. They found that while it appears to be inert as a cell cycle promoter, Cdk5 in the nervous system actually functions to hold the cell cycle in check.

“Its mere presence helps protect the brain,” Herrup said. “What we discovered is that Cdk5 acts as a brake, not a driver.”

Their latest laboratory research examined the workings of Cdk5 in human AD tissues and in a mouse model. Normally, the protein resides in the nerve cell nucleus, but in the presence of AD – both in the mouse model and in the human tissue – the disease process drives the protein out into the cell’s cytoplasm. This disrupts the status quo, overrides the brake and unleashes a chain of events that ultimately leads to the death of the cells and the resulting dementia.

“The ejection of Cdk5 out of the nucleus is probably related to the changed chemistry of the Alzheimer’s brain and chronic inflammation that accompanies AD,” Herrup said.


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Alzheimer's Disease -- Advice and Insight

Bob DeMarco is the Founder of the Alzheimer's Reading Room and an Alzheimer's caregiver. The blog contains more than 2,255 articles with more than 272,100 links on the Internet. Bob resides in Delray Beach, FL.

The Alzheimer's Action Plan

 

The Art of Dementia Care


Original content Bob DeMarco, the Alzheimer's Reading Room

Tuesday, 24 June 2008

Pfizer and the International Conference on Alzheimer’s Disease

Pfizer Invites Public to View and Listen to Webcast of July 28 Pfizer Analyst and Investor Meeting at ICAD
clipped from www.pfizer.com

NEW YORK--(BUSINESS WIRE)--Pfizer Inc invites investors, media, and the general public to view and
listen to a webcast of a presentation by Pfizers
neuroscience leadership team at an analyst and investor meeting on
Monday, July 28, at 6:00 p.m. Central Daylight Saving Time, in
connection with the annual meeting of the International Conference on
Alzheimers Disease (ICAD).


To view and listen to the webcast, visit our web site homepage at www.pfizer.com
and click on the Pfizer Analyst and Investor
Meeting at ICAD link in the Investor
Presentations tab. Information on accessing and pre-registering for the
webcast will be available at www.pfizer.com
beginning today.


Visitors will be able to view and listen to an archived copy of the
webcast at www.pfizer.com.

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New drug may mitigate Alzheimer's disease

CNI-14493

The researchers discovered the medicine, CNI-14493, can transform amyloid into a form that doesn't aggregate to form plaques in the brain and also neutralizes the toxicity of the amyloid.

In his latest work, al-Abed was looking for a way to target the amyloid plaques that clump together between neurons in the brains of people with Alzheimer's disease.

Al-Abed, along with Michael Bacher and Richard Dodel of Marburg University in Germany, found the amyloid burden in the brain was reduced by 70 percent to 85 percent in areas hard hit in Alzheimer's patients -- the cortex and the hippocampus.

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Thursday, 19 June 2008

The Doctor Will See You on the Webcam Now

Depending on cost this might work very well for people without health insurance. Many illnesses require a simple prescription for an antibiotic.

Many people I know can't get into a doctor on the first day when they start feeling ill. As a result, the lack of immediate treatment and a prescription drug causes the illness to linger and lengthens the recovery time.

This is an interesting counterpoint to retail clinics and behind the counter generic antibiotics.
clipped from blogs.wsj.com
To the Health Blog, American Well sounds like a company that’s selling doctor visits via webcam. But Roy Schoenberg, the CEO, tells us we don’t get it.
“The fact that you can engage in a Web video chat with a provider is a nice exercise, but it’s not the fundamental offering of the system,” is how he put it in a recent conversation.

The company’s business model is to partner with insurers, who agree to reimburse in-network doctors for patient e-visits. Docs who choose to work with American Well can sign on whenever they want and see patients who are looking for an online visit.

Today, the company announced its first big customer: HMSA, Hawaii’s Blue Cross Blue Shield provider, which has just under a million members and is the state’s biggest insurer.

The visits are reimbursed through relatively new standardized billing codes that allow docs to get paid for electronic visits. The insurer pays the doc, and American Well takes a cut. The company also charges an up-front licensing fee.

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Molecular Imaging Sheds New Light On Progression Of Alzheimer's Disease

The groundbreaking discovery by University of Pittsburgh researchers Chester Mathis, PhD, and William Klunk, MD, PhD, is being watched with great interest.

Pittsburgh Compound B (PIB) binds to the abnormal amyloid plaque in the brain. When imaged with a PET scan, PIB shows researchers actual pathological changes in the brain that could turn out to be the best and earliest signs of the disease.




Pittsburgh at the forefront of Alzheimer's research


Researchers at the University of Pittsburgh Medical Center (UPMC) are revolutionizing the fight against Alzheimer’s disease (AD). Scientists and researchers at the University of Pittsburgh recently discovered a new agent, dubbed “Pittsburgh Compound B,” which allows researchers to visualize for the first time in living people the brain plaque suspected of causing the memory-stealing disease. Previously, the presence of plaque could be confirmed only during autopsy.

Pittsburgh Compound B (PIB) binds to the abnormal amyloid plaque in the brain. When imaged with a PET scan, PIB shows researchers actual pathological changes in the brain that could turn out to be the best and earliest signs of the disease. It may be possible that these changes could be detected as many as 10 years before patients experience serious memory loss.

The groundbreaking discovery by University of Pittsburgh researchers Chester Mathis, PhD, and William Klunk, MD, PhD, is being watched with great interest. Along with Drs. Klunk and Mathis, researchers like Steven DeKosky, MD, director of the Alzheimer Disease Research Center at UPMC, are currently collaborating with investigators around the world to further study PIB and other compounds, as well as potential new treatments for Alzheimer’s.

Pittsburgh Compound B was developed after more than a decade of work by University Drs. Klunk and Mathis. Dr. Klunk is an associate professor of psychiatry who studies Alzheimer’s disease, while Dr. Mathis specializes in developing radiopharmaceuticals — compounds that are injected into the body and temporarily emit radioactive particles that can be captured by PET imaging to reveal anatomical clues.

Working with three classes of dyes used to detect plaque in the lab, Drs. Klunk and Mathis worked for years testing hundreds of compounds before developing PIB.

“This is in the early stages of development,” says Dr. DeKosky. “But if our success continues, it’s possible there could be a commercially available product for the early diagnosis of Alzheimer’s within the next decade.”

Using PIB, doctors may someday be able to follow the progression of the disease and identify people who are at increased risk for AD long before any symptoms occur.

“Until the development of Pittsburgh Compound B, there was no way to measure a decrease in AD plaque or possible remission of the disease,” says Dr. DeKosky. “What makes PIB remarkable is that, for the first time, doctors may be able to tell definitively if treatment is working.” Dr. DeKosky says before this discovery by Drs. Mathis and Klunk, no one was able to develop a tracer that binds to the specific abnormal protein in AD. All of the other imaging studies simply show shrinkage in parts of the brain or brain activity changes in different regions.

“For the last 20 years, we’ve talked about finding a noninvasive way to make a definite and specific diagnosis and being able to quantify the amount of plaque in the brains of people who have AD,” says Dr. DeKosky. “If we can make a specific diagnosis through imaging, then we can track the effectiveness of new drugs and other treatments. There is nothing out there right now anywhere near as direct, that can tell us definitively whether or not a drug reaction and response helps the disease.”

Furthermore, use of the compound may also tell researchers whether the hypotheses upon which therapies are being developed are correct. “That’s important, as is identifying early-stage patients before it’s too late,” says Dr. DeKosky.

“The future is very exciting, and it’s satisfying to know that we were at the forefront of advancing the science,” says Dr. Mathis. “Right now we’re setting the stage to use Pittsburgh Compound B in collaboration with a number of companies that are trying to target therapies for AD. If these therapies do what we hope they will do, then it will become more important to determine if a person has AD at an earlier stage.”

Dr. Mathis says another very important goal will be to nail down amyloid plaque’s exact role in Alzheimer’s disease. While most doctors suspect that it causes Alzheimer’s, there isn’t yet 100 percent agreement on the theory. If amyloid plaque turns out not to be a central cause, Dr. Mathis says, such a finding could completely redirect research.

Finally, PIB and improved radiotracers now under development at the University of Pittsburgh will allow researchers to follow amyloid deposits in Alzheimer’s patients and older people without the disease, helping to better define the normal aging process in the brain.

Alzheimer’s is a very complex disease, one that is just beginning to be understood. It steals the mind and memory. It devastates families and makes strangers out of life-long partners. Approximately 4 million Americans have Alzheimer’s, and if left unchecked, it will strike as many as 14 million during the next 50 years. UPMC’s new research may stem the advance of this debilitating disease.



Wednesday, 18 June 2008

GRAPE SEED EXTRACT MAY REDUCE COGNITIVE DECLINE ASSOCIATED WITH ALZHEIMER’S DISEASE

This inforamtion about grape seed extract and MegaNatural-AZ. is new to me and I thought I would pass it along.

Since I am genetically predisposed to Alzheimer's via birth I am always searching for information and alternatives that might be beneficial in the long run.
clipped from www.sfn.org
A compound found in grape seed extract reduces plaque formation and resulting cognitive impairment in an animal model of Alzheimer’s disease, new research shows. The study appears in the June 18 issue of The Journal of Neuroscience.

The researchers tested a grape seed polyphenolic extract product sold as MegaNatural-AZ, made by Polyphenolics, which in part supported the study. Polyphenolic compounds are antioxidants naturally found in wine, tea, chocolate, and some fruits and vegetables. To determine whether the extract could mitigate the effects of Alzheimer’s disease, the researchers used mice genetically modified to develop a condition similar to Alzheimer’s disease. They exposed pre-symptomatic “Alzheimer’s mice” to the extract or placebo daily for five months. The daily dose of the polyphenolic extract was equivalent to the average amount of polyphenolics consumed by a person on a daily basis.

Fish Oil Pinch Spurs Search for Alternative Omega 3

I guess we can expect prices for Omega-3 to start rising fast soon. My mother and I take three capsules each every day so cost could become an issue at some point.

As for genetically modified Omega-3, I guess we will make the decision when the new products become available.
clipped from blogs.wsj.com
The global commodities boom extends even to the ocean depths: The price of crude fish oil has nearly tripled in the past five years.
This matters to you, Health Blog reader, because fish oil is a primary source of omega-3 fatty acids, the nutritional supplements that may reduce the risk of heart disease and a host of other ailments.

The price has been rising as Baby Boomers (and others) have been swallowing ever more fish oil. Global fisheries, alas, are already under pressure and can’t keep up with the habit.

Responding to this growing imbalance, some big corporate players are using biotech gene-splicing techniques to create land-based supplies of omega-3s, Dow Jones Newswires reports.

DuPont hopes to use genetically modified yeast to crank out omega-3s. Monsanto is trying soy beans. And Dow AgroSciences and Martek Biosciences are splicing algae genes into canola seeds. The products could come to market within the next few years.


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Insight and Advice

Bob DeMarco is the Founder of the Alzheimer's Reading Room and an Alzheimer's caregiver. Bob has written more than 2,011 articles with more than 200,000 links on the Internet. Bob resides in Delray Beach, FL.

The Alzheimer's Action Plan   300 Tips for Making Life Easier


Original content Bob DeMarco, the Alzheimer's Reading Room

A Doctor’s Lessons From a Dying Patient

Sometimes patients know they’re about to die. Doctors, accustomed to saving lives rather than passively awaiting death, don’t always handle those situations all that well.

clipped from blogs.wsj.com
“Even though death is an inevitable part of the human condition, it’s not something that most doctors, including me, ever get too comfortable with,” family doc Ben Brewer writes this week in his WSJ column. “We get used to pushing it off until another day.”
Brewer writes, the final few days of a patients life can be illuminating for doctors who make the time. He describes the last days of a 95-year-old patient who came down with pneumonia.
The patient took to telling stories of his youth. He described visiting Germany with his family as a young man, during the 1930s. At one point, as he was walking down a deserted street, he encountered a soldier who stopped, raised his hand and said, “Heil Hitler.”
My patient, who wasn’t Jewish but wasn’t saying “Heil Hitler” to anybody, affected a broad smile, and replied, “Good morning,” as pleasantly as he could. He kept walking without looking back and wondered if he would still have his head as he passed by. He survived unharmed.

Tuesday, 17 June 2008

Ben Bernanke: ‘Disturbing Gap’ in American Health Care

clipped from blogs.wsj.com

The question for economists isn’t whether the country is spending too much on health care, Ben Bernanke said today. “Rather, the question, whatever we spend, is whether we are getting our money’s worth.”

While Bernanke said there’s much to praise about American health care, he also said we could get more for our money. “The evidence … suggests that the cost of health care in the United States is greater than necessary to allow us to achieve the levels of health and longevity we now enjoy,” he said. “Although some patients do not receive the care they need, others receive more (and more expensive) care than necessary.”
He was speaking at a Senate committee hearing on health reform; the text of his speech is online here.
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Study Shows Alzheimer's Drug Bapineuzumab effective in some patients

clipped from online.wsj.com
Pharmaceutical partners Wyeth and Elan Corp. said Tuesday results from a highly anticipated midstage study of their experimental Alzheimer's disease drug bapineuzumab show the treatment appears to be effective in some patients.

Bapineuzumab didn't show a statistically significant difference compared with placebo in all patients, but the companies said it suggested a trend toward improving cognitive function.

Bapineuzumab is designed to work by attacking a substance in the brain called beta-amyloid. There is a growing scientific consensus that a buildup of beta-amyloid is responsible for Alzheimer's.

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Change in Depressive Symptoms During the Prodromal Phase of Alzheimer Disease

Those who developed AD (n = 190) showed no increase in depressive symptoms before the diagnosis was made, and this finding was not modified by age, sex, education, memory complaints, vascular burden, or personality. There was no systematic change in depressive symptoms after the AD diagnosis, although symptoms tended to decrease in women relative to men and in those with a higher premorbid level of openness and a lower premorbid level of agreeableness. Among those without cognitive impairment at baseline, depressive symptoms did not increase in those who subsequently developed mild cognitive impairment.
Conclusion  We found no evidence of an increase in depressive symptoms during the prodromal phase of AD.
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Alzheimer's Disease -- Advice and Insight


Bob DeMarco is the Founder of the Alzheimer's Reading Room and an Alzheimer's caregiver. The blog contains more than 2,255 articles with more than 272,100 links on the Internet. Bob resides in Delray Beach, FL.

The Alzheimer's Action Plan

 

The Art of Dementia Care


Original content Bob DeMarco, the Alzheimer's Reading Room

Ginkgo biloba does not help people with dementia, study finds

Ginkgo biloba has no benefit for people with dementia, according to new Alzheimer's Society research.

One of the longest and most rigorous studies yet on Ginkgo biloba found it does not slow progression of dementia and does not significantly effect cognitive function or quality of life.

The study was the first to test the effects of Gingko biloba on people with dementia in a community setting in the UK and showed no significant benefit over a  six month period. 176 people with mild-moderate dementia took part in the placebo-controlled trial. Ahead of print publication, the study is now available for 'early viewing' on the International Journal of Geriatric Psychiatry online.

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Sunday, 15 June 2008

I broke down on live TV over my dad's Alzheimer's

The article on the following page is important and uplifting. I remember during those first few months of caring for my mother how sad and frustrated I was feeling. Then, I met a young couple in the gym that had gone through the entire experience from beginning to end with their mother who suffered and died from Alzheimer's disease.

I remember as I related my own experience to them how they shook their heads up and down indicating they knew exactly what I was experiencing. They recounted their similar experiences and always with a smile on their face. I remember feeling immediately "I was not alone". The feelings of frustration, fear and sadness dissipated and I now find myself thinking, "I can do it".

'Alzheimer's is such a cruel disease because that vibrant person is taken away from you. They are still there in body but it's like the shell. The person you remember has gone.'



I broke down on live TV over my dad's Alzheimer's.

Driving across Dartmoor with her parents one sunny afternoon in 1995, Ruth Langsford's father Dennis observed a beautiful barn conversion and said he had admired it earlier in the day.

When Ruth irritably pointed out that she had taken a different road on the outward journey, he insisted she was wrong. 'He got quite cross and we had a discussion that almost turned into a row, while Mum kept quiet in the back of the car. He was adamant that he was right,' Ruth recalls.



'Then we saw a man leaning over a five-bar gate and Dad said, "I remember that man. He waved at us." At that moment I thought, oh my God, he's gone mad. What's the matter with him?

'When I got home I even got a map out to show him the way we had gone. But he still wouldn't have it. That evening I said to my Mum I thought something wasn't right.'

While the incident may have been minor, it disturbed Ruth, a presenter on ITV1's This Morning and long-term partner of Eamonn Holmes of Sky Breakfast News. She believes now it was the first real indicator that her father was in the early stages of Alzheimer's.

The condition, thought to affect half the 700,000 dementia patients in the UK, begins with short-term memory loss, clumsiness and problems with communication, and gradually robs sufferers of their faculties, leaving them unable to remember close family or perform even the simplest tasks unaided.

Today, Dennis, 81, is in the advanced stages of the illness, and is in full-time residential care in Cornwall.

And as she speaks about her father's illness, Ruth, 48, known for her warmth and humour on the This Morning sofa - regularly co-hosting the Friday edition with Phillip Schofield - often loses her composure.

'I think he still knows my Mum - his eyes always light up when she walks in the room, but sometimes I'm not sure if he knows me anymore,' says Ruth, her eyes filling with tears.

'It is very hard. I adore my Dad. The only way I can describe it is that you are grieving for a loved one while they are still alive. It is the saddest kind of bereavement.'

She adds: 'He was the most clever, funny, vibrant man. He played rugby, scrambled motorbikes and flew gliders. He was handsome, the best storyteller ever and the life and soul of the party.

'He was a fantastic father and, in my opinion, a New Man ahead of his time. He taught my sister Julia and me to fish and sail. We had such good times and love him to bits.

'Alzheimer's is such a cruel disease because that vibrant person is taken away from you. They are still there in body but it's like the shell. The person you remember has gone.'

Her mother Joan admitted that the incident in the car was not the first worrying episode.

When his camera had gone missing, it turned out he had left it in the garden shed. Slippers turned up in the fridge.

She had voiced her concerns to her GP, tentatively suggesting Alzheimer's, only to be told that it was probably forgetfulness and old age.

Despite the alarm bells, Ruth reveals it took several years for her family to get the truth that he was suffering from dementia, and by the time he was formally diagnosed 11 years ago, the disease of the brain was so advanced that doctors could do little to halt its progression with drugs.

'My father was a former Army man - meticulous and tidy,' says Ruth.

'I knew it wasn't right. When I was a child, if I borrowed the Sellotape, it had to go back in the drawer in exactly the right place.'

Her father's vagueness was also a tricky subject to broach as he was 'a fiercely proud, independent man who disliked any fuss'.

In the military for 30 years, rising through the ranks to warrant officer, Dennis moved his family to various Army bases abroad.

Ruth was born in Singapore and her sister Julia, now 50, and a landscape gardener, was born in Germany. Her parents have been married 54 years.

'They met at a dance when Mum was in the Wrens. My dad was a young soldier and she was a gorgeous redhead.

'Apparently, when he saw her on the other side of the room he said to one of his friends, "I'm going to marry that girl."' After he left the Army in 1972 the couple moved to Cornwall where Dennis was born. They set up home in the village of Millbrook on the beautiful Rame Peninsula, where he worked in the education department for Devon County Council.

'I don't think he was ever as happy as he was in the Army. He eventually retired when he was 65. That's another thing that is so sad. My parents had so many plans for their retirement. Dad had lots of hobbies and interests - he loved photography, pottery and music.'

Until this point, Dennis had been fit and healthy. He had a small heart attack in 1996 but had recovered after a pace-maker was fitted.

As his Alzheimer's progressed, Joan's fears intensified.

'Often Mum would discuss the latest bizarre thing he'd done, but because we weren't living with it, we'd say, "I'm sure it's nothing." It was only when I spent time with him that I saw what she meant.'

The turning point was in 1997 when the couple visited London and Ruth took them to Wimbledon Village for afternoon tea. Once again, Dennis swore blind he had been to the café recently.

'But he was clearly talking about when we were children. I felt sick inside. And for the first time I didn't argue with him. Mum and I just said: "Really?" I knew something was seriously wrong.'

When she returned home, Joan, 77, went to the GP alone at Ruth's insistence. The doctor suggested a Mini Mental State Examination (MMSE), a series of simple questions to test mental ability relating to dementia.

The test - carried out at home by an old-age psychiatrist - confirmed the family's fears, but they agreed not to tell him.

'I still question whether that was the right thing to do, but every family has to deal with it their own way,' Ruth says. 'But Dad did get to the stage where he was aware things weren't quite right.'

Some days, Ruth feels angry that the disease has robbed her five-year-old son, Jack, of a loving grandfather. 'I take Jack to the park and see grandparents playing with their grandchildren - it breaks my heart.'

Eamonn, 48, whom she has been with for 12 years, has been a great support. She says: 'He loves my Dad. The two of them would always tease me. Eamonn's a great family man. He lost his own father when he was only in his 60s and was devastated.

'I wish we had been given more information. He's never been put on medication and there are drugs available that can slow Alzheimer's progress. Now I wonder why we didn't ask, but it's too late.'

Despite the diagnosis, the implications of day-to-day caring for a sufferer didn't sink in. Ruth regularly visited Cornwall from her home in Surrey, but realises her mum protected her from her physical struggle.

Dennis would often close all the curtains in the middle of the day, or Joan would wake to find him fully dressed at four in the morning.

'In a way it's like being a new mother with a baby,' says Ruth.

'Fortunately, he's never been physically aggressive, as some dementia sufferers can be. But he was verbally aggressive a few times and that really upset her. Much as he was quite fiery, he was never cruel before.

'Suddenly he would say quite nasty things to her that really upset her. But that wasn't Dad. He adored Mum.'

A health worker visited Joan regularly, and in recent years Dennis was in a respite home for a week at a time to give her a break.

The final straw was when Ruth bumped into a friend of her mother. 'She said innocently, "We've been worried about your Mum, she looks so tired."

'I felt like the worst daughter in the world. She was trying to protect us and be strong for the man she loved and adored.

'My sister and I are really close but we felt guilty that we didn't have the full picture. We discovered Dad had fallen over a few times. We were worried about her getting ill.'

Eighteen months ago Dennis moved full-time into a local care home, where he seems content, and Joan visits regularly.

'I was distraught but we had to admit defeat. It's hardest for my mum. For her life partner, her lover and friend to be getting to the stage now where he doesn't recognise us, is just devastating,' says Ruth.

Ruth had never spoken publicly about her father's illness until last year, during a studio discussion on This Morning, when she broke down on air talking to a caller about Alzheimer's.

'Thankfully, I was co-presenting with Eamonn.

He squeezed my back to comfort me and he made a joke to break the ice.'

Ruth was deluged by emails and letters from viewers with similar stories. The Alzheimer's Society approached her initially to offer support, then to ask her to be an ambassador for the charity.

'Now we think the disease started five years before we were told Dad had Alzheimer's. Early diagnosis is key - for treatment and to prepare you and your family emotionally.'

By 2025 there will be one million dementia sufferers in the UK according to last year's Dementia UK report prepared by the LSE and King's College, London.

One in three people over 65 will die with dementia, yet up to two thirds will never receive a formal diagnosis. Early diagnosis is crucial, but those with dementia and their families often say that finding out about the problem was the start of getting back in control.

'I do feel guilty that I didn't pursue a diagnosis earlier on,' says Ruth. 'The truth is that I didn't want him to be ill. The thought of it frightened me and I was running away from it. I didn't want my dad to get old and doddery.

'I miss talking to him, I miss going to him for advice. I miss Christmas shopping together and going to the pub together or sneaking off down the garden for a crafty fag. He was my mate as well as my dad.'

Ruth is keen to promote a new Alzheimer's Society initiative, Worried About Your Memory? (WAYM?), encouraging individuals and families to seek help when they notice those vital early signs of forgetfulness.

'GPs are busy and if episodes are sporadic, then it's understandable not to take it too seriously,' says Ruth.

'We all forget things but if you are genuinely worried about your memory, don't think, "It's just me being dotty". Go and see your doctor.'

This weekend, Ruth, who will be appearing on This Morning from July 21 until the end of August, will have made the 500-mile round trip with her sister Julia to Cornwall to visit Dennis on Father's Day, with a kiss, a card and his favourite Mars bars and Maltesers.

'He seems in a good place. My theory is that he is back in the Army, which he loved.

'He says the same thing over and over again: "They're a lovely bunch of lads in here." And that is all he says. Over and over again. He's as happy as Larry.'

• For information on the Worried About Your Memory? campaign, visit www.alzheimers.org.uk or call the Alzheimer's Society Dementia Helpline, 0845 300 0336.


10 things to know about Alzheimer's

• German psychiatrist Alois Alzheimer identified the first case in 1906. It was officially recognised by the medical profession in 1910.

• Alzheimer's is the most frequent type of dementia in the elderly, affecting almost half the 700,000 patients with dementia in the UK.

• About two per cent of those aged 65 show signs of the disease. Every five years after the age of 65, the probability of developing the disease doubles. Some ten per cent of Alzheimer's cases are inherited.

• It is diagnosed by using brain scans, patient history and observing behaviour.

• A shrinking vocabulary, problems talking and short-term memory loss are normally the first signs. Difficulty writing and dressing are also common.

• In the late stages, language is lost and patients cannot perform even simple tasks. Finally deterioration of muscle leads to sufferers becoming bedridden.

• Average life expectancy is about seven years after diagnosis, and less than seven per cent of patients live more than 14 years.

• There is no cure, but a type of drug called cholinesterase inhibitors can slow down progression in those with moderate Alzheimer's.

• Anti-depressants are prescribed to help treat the depression that can be associated with the disease.

• Sufferers have included US President Ronald Reagan, British Prime Minister Harold Wilson and writer Iris Murdoch.