Saturday, February 28, 2009

New clue to Alzheimer's Astrocyte Cells


Using a cutting-edge imaging technique, scientists were able to get a real-time view of the activity of brain cells in living mice. The study investigators labeled astrocytes with a dye that lights up when a cell is active and shuts off when it is not. They were surprised to see astrocytes flicker on and off at much higher rates in transgenic mice with an abundance of plaques than in plaque-free animals.


Our work suggests that amyloid plaques might have a more complex role in altering brain function than we had thought.

This new research featured in the latest issue of Science raises the possibility of a new target for drugs to treat Alzheimer's disease. Astrocytes are abundant throughout the brain, making up about half of its total volume. The impact of amyloid plaques in the brains of people with Alzheimer's disease has already been well documented.

Yale Researchers Find New Piece in Alzheimer's Puzzle


Yale researchers have filled in a missing gap on the molecular road map of Alzheimer's disease.
By Bob DeMarco
Alzheimer's Reading Room


"We have known that amyloid-beta is bad for the brain, but we have not known exactly how amyloid-beta does bad things to neurons," said Stephen M. Strittmatter, senior author of the study

Friday, February 27, 2009

Snippet: Alzheimer's Costs to Soar in California, Researchers Say


By Bob DeMarco
Alzheimer's Reading Room
The cost of caring for Californians with Alzheimer's disease will almost double over the next 20 years, from $50 billion to $98.8 billion, a report released by the Alzheimer's Association says. According to figures from the University of California, San Francisco Institute for Health and Aging, the number of California residents with the disease will nearly double to 1.1 million as the baby boom generation ages and people live longer, the San Francisco Chronicle reports.

Costs of Alzheimer’s Disease


Alzheimer's nose spray: New Alzheimer's treatment?


Answer

Insulin — a hormone that helps regulate your blood sugar — appears to play a role in normal memory processes. Insulin irregularities may contribute to cognitive and brain changes associated with Alzheimer's disease.

Research in the past few years has been investigating the use of insulin to treat Alzheimer's disease. One of the challenges is how to provide insulin in such a way that it improves brain function without disrupting your blood sugar levels. If you blood sugar drops too low, for example, it can create complications such as confusion, heart palpitations, anxiety and visual disturbances.

Preliminary research suggests that when taken as a nose spray, insulin reaches the brain within a few minutes, improving memory without affecting blood sugar or insulin levels. This research involved only 26 participants who had either early Alzheimer's disease or mild cognitive impairment. Although this research is promising, more research on the safety and effectiveness of intranasal insulin therapy for Alzheimer's disease is necessary. A phase II clinical trial on the use of inhaled insulin to treat Alzheimer's disease is currently under way. It will involve about 90 participants who have Alzheimer's disease or mild cognitive impairment and is due to be completed in August of 2009.

Here is the link to the clinical trial--Study of Nasal Insulin to Fight Forgetfulness

ASK AN ALZHEIMER'S SPECIALIST--The Mayo Clinic

Thursday, February 26, 2009

Link found between Alzheimer's, mad cow protein


This article is getting some buzz on the Internet and on Twitter due to the headline. Fans of the show Boston Legal and Denny Crane will get the connection between Alzheimer's and mad cow.
In the search for a possible therapy for Alzheimer's, Bredesen is focusing on a molecule that seems to block the destruction switch. The nerve growth factor netrin-1 appears to curb the release of the amyloid peptide from APP, he said. Work is under way on methods to deliver netrin-1 to people with early signs of Alzheimer's, but it could take five years to produce an approved drug, he said.

Mucke said the Gladstone Institute is working on an array of strategies, which include preventing the amyloid peptide from finding molecules that pass along its destructive signals.

Scientists are starting to see Alzheimer's as a complex disease like cancer or hypertension, which can arise from various root causes. That means patients may need a cocktail of several drugs, and maybe a custom-made mix for each individual.

"I'm absolutely convinced that different people get Alzheimer's for different reasons, and drug development will have to take that into account," Mucke said.

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Seventy percent of newly diagnosed Alzheimer's disease patients do not receive treatment within a year of diagnosis


I moved to Delray Beach, Florida five years ago to take care of my mother who now suffers from Alzheimer's disease. I didn't know it back then, but my mother was clearly suffering from mild cognitive impairment (MCI) when I arrived on the scene. MCI is often a precursor to Alzheimer's disease and dementia. It is my belief that the early detection of the disease in my mother is the reason why we had a good outcome using Aricept, other medications, and introducing exercise and healthy living into her life.

Wednesday, February 25, 2009

Does Music Unlock Memory in Alzheimer's Sufferers


So let me ask you, don't you have certain songs that you associate with certain persons or situations that occurred in the distant past?

This is very interesting to me and should be to you.

According to a new study, listening to favorite songs could slow the progression of Alzheimer's. The study also found that listening to tunes from the past seems to evoke powerful memories that are not chocked off by Alzheimer's disease.

I saw this in my mother when she was in the mild stage of Alzheimer's. However, as the disease has progressed she is remembering less and less of the past. She is at the point where her short term memory is gone.

Tuesday, February 24, 2009

DNA Test Tells a Fat Man He can't Hide Behind Mom's Genes


I read the article below by Jim Kling on the Washington Post website. I believe many of us can identify with him. The article is interesting and has some very funny perspective.

I wrote previously about how baby boomers need to be wary of their predisposition to Alzheimer's disease. In my article Five Ways to Keep Alzheimer's Away, I noted that a big belly triples the chances that you could suffer from Alzheimer's (Jim you need to pay attention to this). I even wrote about a genetics test that tests predisposition to Alzheimer's disease.

Jim Kling ended his article with this,
Nevertheless, I printed out a copy of my report and brought it to my physician. Like the other experts I had consulted, he at first expressed doubt about the reliability of genetic tests. Then he pointed to my increased risk of diabetes and said, "I'd be most concerned about this one -- especially given that you're carrying some extra weight."

I nodded, and considered asking him for suggestions. But I knew what he would say: "Eat right and exercise. You'll lose weight and you'll feel better.
Eating right and exercise are two good ways to ward off Alzheimer's disease. However, if Jim's doctor had been better schooled in the causes of Alzheimer's he would have warned him of the possible consequences of a big belly. Get rid of that big belly Jim, you won't miss it.

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Monday, February 23, 2009

Advances for Alzheimer's, Outside the Lab


Wow. This article is fantastic--I give it five stars. As I read this, an array of positive emotions ran through my body. This is not a tear-jerker, its is uplifting. Much of what I read is about mice. This article is all about people. It is full of activities that would be wonderful for Alzheimer's sufferers and Alzheimer's caregivers.
Medicine has long fought two fronts in the battle against disease — in the research lab and at the bedside. The race toward a treatment for Alzheimer's has focused almost exclusively on research in psychopharmacology, immunology and gene therapy...Meanwhile, low-tech memory-enhancing devices like diaries, Post-It notes and portable cameras are used increasingly by Alzheimer's caregivers, leading some researchers to contemplate whether the consistent and comprehensive use of bedside solutions may actually slow the progression of the disease. If rudimentary tools have any chance of inhibiting the disease, health-care workers are interested. When it comes to Alzheimer's, even incremental improvements can have a profound effect..
In this article you will read about interesting activities that seem to enhance the lives of people suffering from memory loss or memory disease. No rocket science, no mice, just ordinary folks focusing on improving the daily life of Alzheimer's sufferers.

As you can see, I get very excited when I read about things that improve the life of patients and caregivers. I am always searching for new ideas to help my mother live a better life. Amazing.

This article is a bit long. But, I believe it is worth reading, thinking about, and commenting on.

Sunday, February 22, 2009

Buck Scientist Propose New Model for Alzheimer's Disease


A study from the Buck Institute for Age Research offers a revolutionary new model for Alzheimer’s disease.
In their study, scientists from the Buck Institute and the CNRS (Centre Nationale de la Recherche Scientifique) show that amyloid precursor protein (APP) binds to netrin-1, a protein that helps to guide nerves and their connections in the brain, as well as helping nerve cells to survive. When netrin-1 was given to mice that have a gene for Alzheimer’s disease their symptoms were reversed, and the sticky amyloid was reduced.
We believe that Alzheimer’s disease is somewhat analogous to cancer, which results from an imbalance between the normal processes that support cell survival and those that cause cell turnover.

Saturday, February 21, 2009

Exercise Your Brain To Prevent Memory Loss


I write often about how to keep Alzheimer's away and about mild cognitive impairment (MCI) as a precursor to Alzheimer's disease.

A new study from the Mayo Clinic Study of Aging indicates that participating in mental activities like reading books, playing games, participating in computer activities and crafting may delay or prevent memory loss. The study reported that these kinds of activities lead to a 30 to 50 percent decrease in the risk of developing mild cognitive impairment (MCI).

Neuropsychiatrist Yonas Geda led this study on exercise and mild cognitive impairment.
"Exercise conducted between ages 50 and 65 at a frequency of about two to five times a week in moderate intensity seems to be protective against mild cognitive impairment," he says.
A new Mayo Clinic study found that engaging in cognitive activities like reading books, playing games or crafting in middle age or later life are associated with a decreased risk of mild cognitive impairment. Mild cognitive impairment (MCI) is a transitional state between normal aging and the earliest features of Alzheimer’s disease.

“This study is exciting because it demonstrates that aging does not need to be a passive process,” says Yonas Geda, M.D., a Mayo Clinic neuropsychiatrist and author of this study. “By simply engaging in cognitive exercise, you can protect against future memory loss.”

As part of the Mayo Clinic Study of Aging, Dr. Geda and his colleagues identified more than 1,300 people between the ages of 70 and 89. Of those, 197 individuals had mild cognitive impairment and 1,124 were cognitively normal. Both groups answered questions about their activities within the past year and when they were between 50 and 65 years old.

The study found that reading books, playing games, participating in computer activities and crafting led to a 30 to 50 percent decrease in the risk of developing mild cognitive impairment. People who watched television for less than seven hours a day in later years were 50 percent less likely to develop mild cognitive impairment than those who watched more than seven hours of television per day. Additionally, individuals who participated in social activities and read magazines during middle age were about 40 percent less likely to develop mild cognitive impairment than those who did not participate in those activities.

This study will be presented at the American Academy of Neurology’s Annual Meeting in Seattle, April 25-May 2, 2009.

Related Articles
___________________________________
+Bob DeMarco  is the Founder of the Alzheimer's Reading Room (ARR). Bob is a recognized expert, writer, speaker, and influencer in the Alzheimer's and Dementia Community worldwide. The ARR Knowledge Base contains more than 4,000 articles. Bob lives in Delray Beach, FL.
To learn more about Alzheimer's and dementia visit the Alzheimer's Reading Room

New insights into the structure and interaction of a protein relevant to Alzheimer’s disease


Coordination becomes difficult, items disappear, keeping new information in the mind is impossible. Worldwide almost 30 million people suffer from Alzheimer’s disease, a neurodegenerative, irreversible ailment which starts with memory gaps and ends in helplessness and the loss of personality. The most critical factor in developing Alzheimer’s disease is age. Most cases occur after the age of 65.


Max Planck scientists obtained important new insights into the structure and interaction of a protein relevant to Alzheimer’s disease

Which modules of the tau protein, in neurons of Alzheimer disease patients, may act in a destructive manner were investigated by researchers from the Max Planck Institute for Biophysical Chemistry (Göttingen) and the Max Planck Unit for Structural Molecular Biology (Hamburg) with the help of Nuclear Magnetic Resonance Spectroscopy (PLoS Biology, February 17, 2009).

Coordination becomes difficult, items disappear, keeping new information in the mind is impossible. Worldwide almost 30 million people suffer from Alzheimer’s disease, a neurodegenerative, irreversible ailment which starts with memory gaps and ends in helplessness and the loss of personality. The most critical factor in developing Alzheimer’s disease is age. Most cases occur after the age of 65.

Two hallmarks are typical for Alzheimer affected brains. One of them, located between nerve cells, is amyloid plaques - extracellular protein aggregates mainly composed of a protein named beta-amyloid. The other clue is intracellular tau fibrils. In the interplay with genetic factors, the latter contribute to a disordered communication within the cell. This triggers cell death.

But the tau protein is not only harmful. Quite the contrary is the case. In its normal non-pathogenic form tau binds to microtubules, long tubular cytoskeletal building blocks, which serve as "tracks" for intracellular transport. In patients afflicted by Alzheimer’s disease or similar dementia, tau is abnormally altered. In its pathogenic form tau possesses more phosphorylated amino acids than in its normal healthy counterpart. "Our interest was focussed on how certain phosphorylated residues alter the structure of tau in a way that it can not bind to microtubules anymore" explains Markus Zweckstetter at the Max Planck Institute for Biophysical Chemistry.

Exotic among proteins

Tau is special and with most biophysical methods, such as X-ray crystallography, not analyzable. Neither heat nor acid can harm the protein. Whereas most proteins fold to adopt the structure necessary for their function, tau can do it in the absence of folded structure, is very flexible and changes its form very rapidly.

With Nuclear Magnetic Resonance Spectroscopy the scientists where able to shed light on the structural properties of tau and followed its fast motions. For the first time detailed investigations of structural changes from a large almost unfolded protein where conducted. "The financial support was granted by the DFG Research Center "Molecular Physiology of the Brain" (CMPB) in Göttingen, the Volkswagen foundation and an institute overlapping Max Planck Society project, ‘Toxic protein conformation’ ", says Christian Griesinger, head of the department of NMR-based structural biology at the Max Planck Institute.

"We can directly observe which modules of the tau protein bind to microtubules. If the protein is equipped with more phosphates than usual we can see that in this case the binding becomes significantly weaker. Tau and microtubule proteins can no longer interact" summarizes Zweckstetter. As a direct consequence the transport along the microtubule "tracks" is disturbed and nerve cell endings do not grow.

The interplay with binding partners is also possibly broken down. "We now hold the tau protein in our hands and are able to look at the interaction with its binding partners in the cell in a very detailed way".

Tau as a drug target

Eckhard and Eva Mandelkow at the Max Planck Unit of Structural Molecular Biology in Hamburg are optimistic about using tau as a pharmaceutical target. On genetically altered mice, Eva Mandelkow and co-workers were able to show reversibility of the fatal consequences of tau aggregation. The next step for the Max Planck scientists would be the investigation of possible inhibitors which interact with the tau protein to prevent fibril formation.

Original work:

Marco D. Mukrasch, Stefan Bibow, Jegannath Korukottu, Sadasivam Jeganathan, Jacek Biernat, Christian Griesinger, Eckhard Mandelkow, Markus Zweckstetter
Structural Polymorphism of 441-residue tau at single residue resolution.
PLoS Biology, February 17, 2009.

Dr. Christina Beck | Source: Max Planck Society

EATING less may help older people improve their memory and prevent


clipped from www.thestar.com.my

EATING less may help older people improve their memory and prevent or delay the onset of Alzheimer’s and other forms of dementia, according to a German study published recently.

“This is the first study that has shown that caloric restriction might be beneficial for memory function in elderly humans,” Floel said.

But the men and women in the group told to eat less showed a 10% to 20% improvement in a memory test given three months after they began their diet, the researchers said.

Socially active people who were not easily stressed had a 50% lower risk of developing dementia compared with men and women who were isolated and prone to distress, they reported in the journal Neurology.



EATING less may help older people improve their memory and prevent or delay the onset of Alzheimer’s and other forms of dementia, according to a German study published recently.

The findings suggest that simple lifestyle changes could help treat dementia and confirm benefits previously shown in animals, said Agnes Floel, a neurologist at the University of Munster in Germany, who led the study.

“This is the first study that has shown that caloric restriction might be beneficial for memory function in elderly humans,” Floel said.

An estimated 24 million people worldwide have memory loss, problems with orientation and other symptoms that signal Alzheimer’s disease and other forms of dementia.

Researchers believe the number of people with dementia may quadruple by 2040, straining national health services and raising the need for new treatments.
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Floel and her team divided 50 people with an average age of 60 into three groups. One group worked with a dietitian to cut their daily calories by about 30% while another had no eating restrictions.

The third group ate more food containing unsaturated fatty acids found in olive oil and fish, but this appeared to make no difference in boosting memory, Floel said.

But the men and women in the group told to eat less showed a 10% to 20% improvement in a memory test given three months after they began their diet, the researchers said.

“Our study may help to generate novel prevention strategies to maintain cognitive functions into old age,” the researchers wrote in the Proceedings of the National Academy of Sciences.

The team is now conducting a larger trial using brain imaging scans to better understand the mechanisms by which eating less may improve mental function, Floel said.

One possibility is that decreased levels of insulin and inflammation may boost brain cells and improve memory, she added in a telephone interview.

“We think that, similar to what has been found in animal studies, the changes of insulin levels and inflammation are good for neurons and bring about the improvement,” Floel said. – Reuters

Stay busy

KEEPING a full social calendar may help protect you from dementia, researchers said.

Socially active people who were not easily stressed had a 50% lower risk of developing dementia compared with men and women who were isolated and prone to distress, they reported in the journal Neurology.

“In the past, studies have shown that chronic distress can affect parts of the brain, such as the hippocampus, possibly leading to dementia,” said Hui-Xin Wang of the Karolinska Institute in Sweden, who led the study.

“But our findings suggest that having a calm and outgoing personality in combination with a socially active lifestyle may decrease the risk of developing dementia even further.”

The Swedish study involved 506 elderly people who did not have dementia when first examined. The volunteers were given questionnaires about their personality traits and lifestyles and then tracked for six years.

Over that time, 144 people developed dementia with more socially active and less stressed men and women 50% less likely to be diagnosed with the condition.

“The good news is, lifestyle factors can be modified as opposed to genetic factors which cannot be controlled,” Wang said. “But these are early results, so how exactly mental attitude influences risk for dementia is not clear.” – Reuters

More from the Alzheimer's Reading Room
  • A Simple Three Minute Test Can Detect the Earliest Stage of Alzheimer's Disease
  • Five Ways to Keep Alzheimer's Away
  • Ten Million Baby Boomers likely to suffer from Alzheimer’s during their lifetime
  • Living Alzheimer's From the Front Row
  • High cholesterol levels in your 40s raises Alzheimer's risk
  • Is Alzheimer's a type of diabetes of the brain?
  • Alzheimer's Disease Facts and Figures 2008
  • Is Mild Cognitive Impairment (MCI) an Early Stage of Alzheimer's
  • Is Etanercept the Cure for Alzheimer's
  • A Wonderful Moment in Time--Mom at the Banana Boat




  • Friday, February 20, 2009

    Study of Parental Alzheimer's should be Worrisome to Children


    I have written repeatedly about the need for baby boomers to be aware of the devastating effects of Alzheimer's.

    By Bob DeMarco
    Alzheimer's Reading Room

    A new study, to be presented at the annual meeting of the American Academy of Neurology, indicates that children of Alzheimer's sufferers performed less well on formal memory testing when compared to people of the same age whose parents never developed Alzheimer's disease. This is worrisome and should be a wake up call to those of us who have parents with Alzheimer's. The following statement caught my attention:
    Researchers from the Framingham Heart Study (FHS) are following three generations of participants to study the risk factors and earliest biomarkers of Alzheimer's disease, stroke and other cardiac and neurological diseases. The first generation has been followed since 1948. Since both the parental and offspring generation are enrolled as study participants, researchers could accurately identify which parents did or did not develop Alzheimer's disease or other dementia in their lifetime.

    Thursday, February 19, 2009

    OT: Inside the Meltdown--How the Economy went so Bad so Fast


    I understand this if off track (OT) for the Alzheimer's Reading Room. However, my quantcast statistics indicated that many of the subscribers to this blog are interested in investments. This should come as no surprise because so many Americans own IRAs and 401Ks.

    PBS is now airing FRONTLINE INVESTIGATES HOW THE ECONOMY WENT SO BAD SO FAST. This show has an easy to understand, in-depth explanation, of the financial crisis. I worked on Wall Street for over twenty years and I found the show fascinating and informative. The show is still scheduled for additional airings on PBS, and it is also available for viewing on the Internet. To find out when the show is airing in your market go here and enter your zip code.
    FRONTLINE investigates the causes of the worst economic crisis in 70 years and how the government responded. The film chronicles the inside stories of the Bear Stearns deal, Lehman Brothers’ collapse, the propping up of insurance giant AIG, and the $700 billion bailout. Inside the Meltdown examines what Treasury Secretary Henry Paulson and Federal Reserve Chairman Ben Bernanke saw and tried to fix.
    The trailers are a bit eerie. However, they should help you determine if you are interested in watching.

    You can watch the Internet broadcast here.


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    FRONTLINE INVESTIGATES HOW THE ECONOMY WENT SO BAD SO FAST



    FRONTLINE Presents Inside the Meltdown

    www.pbs.org/frontline/meltdown

    On Thursday, Sept. 18, 2008, the astonished leadership of the U.S. Congress was told in a private session by the chairman of the Federal Reserve that the American economy was in grave danger of a complete meltdown within a matter of days. “There was literally a pause in that room where the oxygen left,” says Sen. Christopher Dodd (D-Conn.).

    FRONTLINE producer Michael Kirk goes behind closed doors in Washington and on Wall Street to investigate how the economy went so bad so fast and why emergency actions by Federal Reserve Chairman Ben Bernanke and Secretary of the Treasury Henry Paulson failed to prevent the worst economic crisis in a generation on Inside the Meltdown, airing Tuesday, Feb. 17, 2009, at 9 P.M. ET on PBS (check local listings).

    As the housing bubble burst and trillions of dollars’ worth of toxic mortgages began to go bad in 2007, fear spread through the massive firms that form the heart of Wall Street. By the spring of 2008, burdened by billions of dollars of bad mortgages, the investment bank Bear Stearns was the subject of rumors that it would soon fail.

    “Rumors are such that they can just plain put you out of business,” Bear Stearns’ former CEO Alan “Ace” Greenberg tells FRONTLINE.

    The company’s stock had dropped from $171 to $57 a share, and it was hours from declaring bankruptcy. Ben Bernanke acted. “It was clear that this had to be contained. There was no doubt in his mind,” says Bernanke’s colleague economist Mark Gertler.

    Bernanke, a former economics professor from Princeton, specialized in studying the Great Depression. “He more than anybody else appreciated what would happen if it got out of control,” Gertler explains.

    To stabilize the markets, Bernanke engineered a shotgun marriage between Bear Sterns and the commercial bank JPMorgan, with a promise that the federal government would use $30 billion to cover Bear Stearns’ questionable assets tied to toxic mortgages. It was an unprecedented effort to stop the contagion of fear that seemed to be threatening the rest of Wall Street.

    While publicly supportive of the deal, Secretary Paulson, a former Wall Street executive with Goldman Sachs, was uncomfortable with government interference in the markets. That summer, he issued a warning to his former colleagues not to expect future government bailouts, saying he was concerned about a legal concept known as moral hazard.

    Within months, however, Paulson would witness the virtual collapse of the giant mortgage companies Fannie Mae and Freddie Mac and preside over their takeover by the federal government.

    The episode sent shockwaves through the economy as confidence in Wall Street began to evaporate. Within days, in September 2008, another investment bank, Lehman Brothers, was on the brink of collapse. Once again, there were calls for Bernanke and Paulson to bail out the Wall Street giant. But Paulson was under intense political pressure from conservative Republicans in Washington to invoke moral hazard and let the company fail.

    “You had a conservative secretary of the Treasury and conservative administration. There was right-wing criticism over Bear Stearns,” says Congressman Barney Frank (D-Mass.), chairman of the House Financial Services Committee.

    Paulson pushed Lehman’s CEO Dick Fuld to find a buyer for his ailing company. But no company would buy Lehman unless the government offered a deal similar to the one Bear Stearns had received. Paulson refused, and Lehman Brothers declared bankruptcy.

    FRONTLINE then chronicles the disaster that followed. Within 24 hours, the stock market crashed, and credit markets around the world froze. “We’re no longer talking about mortgages,” says economist Gertler. “We’re talking about car loans, loans to small businesses, commercial paper borrowing by large banks. This is like a disease spreading.”

    “I think that the secretary of the Treasury could not fully comprehend what that linkage was and the extent to which this would materialize into problems,” says former Lehman board member Henry Kaufman.

    Paulson was thunderstruck. “This is the utter nightmare of an economic policy-maker,” Nobel Prize-winning economist Paul Krugman tells FRONTLINE. “You may have just made the decision that destroyed the world. Absolutely terrifying moment.”

    In response, Paulson and Bernanke would propose—and Congress would eventually pass—a $700 billion bailout plan. FRONTLINE goes inside the deliberations surrounding the passage of the legislation and examines its unsuccessful implementation.

    “Many Americans still don’t understand what has happened to the economy,” FRONTLINE producer/director Michael Kirk says. “How did it all go so bad so quickly? Who is responsible? How effective has the response from Washington and Wall Street been? Those are the questions at the heart of Inside the Meltdown.”

    Inside the Meltdown is a FRONTLINE co-production with Kirk Documentary Group, Ltd. The writer, producer and director is Michael Kirk. The producer and reporter is Jim Gilmore. FRONTLINE is produced by WGBH Boston and is broadcast nationwide on PBS. Funding for FRONTLINE is provided through the support of PBS viewers. Major funding for FRONTLINE is provided by The John D. and Catherine T. MacArthur Foundation. Additional funding is provided by the Park Foundation. FRONTLINE is closed-captioned for deaf and hard-of-hearing viewers and described for people who are blind or visually impaired by the Media Access Group at WGBH. FRONTLINE is a registered trademark of WGBH Educational Foundation. The executive producer of FRONTLINE is David Fanning.

    pbs.org/pressroom
    Promotional photography can be downloaded from the PBS pressroom.

    Press contacts
    Diane Buxton
    (617) 300-5375
    diane_buxton@wgbh.org

    Alissa Rooney
    (617) 300-5314
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    Wednesday, February 18, 2009

    Fantasy Author Terry Pratchett received Knighthood.


    First, congratulations Terry Pratchett. Mr. Pratchett has done much to spread the word about Alzheimer's disease. He should also be congratulated for these good works.

    Terry is a good example that Alzheimer's disease knows no boundaries. It can strike anyone at anytime.

    Terry is to be admired. He decided to fight and to me this is a good thing. Terry is a good role model to all of us. His wonderful attitude is uplifting to millions of families that know and understand the devastation called Alzheimer's disease.
    clipped from www.express.co.uk
    BRITISH author Sir Terry Pratchett was today knighted for his services to literature.
    The 60-year-old, who has sold more than 60 million books worldwide, received the honour from the Queen at Buckingham Palace this morning.
    The writer is best known for the phenomenal success of his prolific Discworld series, which started in 1983 with The Colour of Magic and now stretches to 36 novels.
    In December 2007 Sir Terry announced he was suffering from early-onset dementia and has since been campaigning for research funding to help sufferers - even making a £500,000 donation to the Alzheimer's Research Trust.


    HONOUR: The Queen knights Sir Terry

    Monday, February 16, 2009

    ICARA, Bapineuzumab Clinical Trial for Alzheimer's


    By Bob DeMarco
    Alzheimer's Reading Room
    I first reported on this phase three clinical trial back in July, Bapineuzumab in Patients With Mild to Moderate Alzheimer's Disease.
    Funded by Elan Pharmaceuticals, the study, named Investigational Clinical Amyloid Research in Alzheimer’s (ICARA), will last about 18 months and will include up to 1,500 patients enrolled at research sites in North America.
    Researchers want to see if the drug can slow the progression of Alzheimer’s disease by blocking the amyloid precursor protein, which causes the brain cells to stop working. Amyloid beta peptide is the primary protein found in amyloid plaques in the brains of patients with Alzheimer’s disease. It is expected that by blocking the formation of this peptide, the rate of disease progression can be slowed.
    “Our goal is to explore if this investigational drug can help control the progression of Alzheimer’s,” said Franklin Watkins, M.D., the principal investigator for the study and medical director for the Acute Care for the Elderly Unit at the Medical Center. “Most current therapies for Alzheimer’s treat the symptoms associated with it and not the disease itself. It is important for patients and families affected by Alzheimer’s to consider participating in clinical studies. They are the best chance we have for fighting this disease.”
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    This clinical trial has a separate website that makes it very easy to apply. To view the ICARA study site go here. I really like this web site because it has a separate page where you can apply and determine if you are eligible to be interviewed for the clinical trial.
    • If you want to read all about the Phase III clinical trial for Bapineuzumab go here first.
    • If you want to determine if there is a study location near you go here and enter your zip code. There are 193 locations in North American alone so this is a widely available clinical trial.
    • If you would like to see if you or a loved one is eligible go here and fill out the form on the Internet. This is a first necessary step if you want to participate in the clinical trial. If you are unable to use the Internet you can call this number--877-797-8839--and talk to a study representative.


    More from the Alzheimer's Reading Room

    Original content Bob DeMarco, the Alzheimer's Reading Room

    Higher Blood Sugar Levels Linked to Lower Brain Function in Diabetics, Study Shows


    Diabetes is a risk factor for mild cognitive impairment, vascular dementia and Alzheimer’s disease. Previous studies have shown that people with diabetes are 1.5 times more likely to experience cognitive decline and develop dementia than people without diabetes. The ACCORD-MIND study supports the idea that the brain’s chronic exposure to elevated blood glucose levels may be part of the explanation for this phenomenon.
    "One of the little known complications of type 2 diabetes is memory decline leading to dementia, particularly Alzheimer's dementia," said Williamson, a professor of internal medicine, director of gerontology and geriatrics research, and director of the Roena Kulynych Center for Memory and Cognition Research at Wake Forest Baptist. "This study adds to the growing evidence that poorer blood glucose control is strongly associated with poorer memory function and that these associations can be detected well before a person develops severe memory loss."
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    Higher Blood Sugar Levels Linked to Lower Brain Function in Diabetics, Study Shows

    Results of a recent study conducted by researchers at Wake Forest University Baptist Medical Center and colleagues show that cognitive functioning abilities drop as average blood sugar levels rise in people with type 2 diabetes.
    The study appears in this month’s issue of Diabetes Care.

    The ongoing Memory in Diabetes (MIND) study, a sub-study of the Action to Control Cardiovascular Risk in Diabetes Trial (ACCORD), found a statistically significant inverse relationship between A1C levels (average blood glucose levels over a period of two to three months) and subjects’ scores on four cognitive tests. No association, however, was found between daily blood glucose levels (measured by the fasting plasma glucose test) and test scores.

    For the study, researchers at 52 of the 77 ACCORD sites throughout the United States and Canada administered a 30-minute battery of cognitive tests to nearly 3,000 individuals ages 55 years and older.

    “The tests used in the study measured several aspects of memory function,” said Jeff Williamson, M.D., M.H.S., principal investigator for the study at the Wake Forest clinical site. “For example, we tested one's ability to switch back and forth between memory tasks or to ‘multitask,’ an important skill for people needing to manage their diabetes.”

    The results showed that a 1 percent increase in A1C corresponded to slightly lower scores on tests of psychomotor speed, global cognitive function, memory and multiple task management.

    “One of the little known complications of type 2 diabetes is memory decline leading to dementia, particularly Alzheimer's dementia,” said Williamson, a professor of internal medicine, director of gerontology and geriatrics research, and director of the Roena Kulynych Center for Memory and Cognition Research at Wake Forest Baptist. “This study adds to the growing evidence that poorer blood glucose control is strongly associated with poorer memory function and that these associations can be detected well before a person develops severe memory loss.”

    Diabetes is a risk factor for mild cognitive impairment, vascular dementia and Alzheimer’s disease. Previous studies have shown that people with diabetes are 1.5 times more likely to experience cognitive decline and develop dementia than people without diabetes. The ACCORD-MIND study supports the idea that the brain’s chronic exposure to elevated blood glucose levels may be part of the explanation for this phenomenon.

    Alternatively, people with impaired cognitive ability have higher A1Cs because they are less compliant in taking medications and controlling their diabetes. The ongoing ACCORD-MIND study, which is overseen by Williamson and a team of Wake Forest Baptist researchers, will test the hypothesis that lowering A1C could result in improved cognitive function.

    Meanwhile, “people with type 2 diabetes and their health care providers need to be careful in situations where there is education and teaching about diabetes care, as patients may need a little more time to absorb and process information,” Williamson said. “Patients also need to be open to having a family member periodically making sure they are keeping track of managing their diabetes through monitoring, diet, exercise and medication.”

    The ACCORD-MIND study was funded by the National Institute on Aging in collaboration with the ACCORD trial funded by NHLBI with additional support from the National Institute of Diabetes and Digestive and Kidney Diseases, the National Eye Institute, the National Institute on Aging and the Centers for Disease Control and Prevention.

    Media Relations Contacts: Jessica Guenzel, jguenzel@wfubmc.edu, (336) 716-3487 or Bonnie Davis, bdavis@wfubmc.edu, (336) 716-4977.

    Wake Forest University Baptist Medical Center (www.wfubmc.edu) is an academic health system comprised of North Carolina Baptist Hospital, Brenner Children’s Hospital, Wake Forest University Physicians, and Wake Forest University Health Sciences, which operates the university’s School of Medicine and Piedmont Triad Research Park. The system comprises 1,154 acute care, rehabilitation and long-term care beds and has been ranked as one of “America’s Best Hospitals” by U.S. News & World Report since 1993. Wake Forest Baptist is ranked 32nd in the nation by America’s Top Doctors for the number of its doctors considered best by their peers. The institution ranks in the top third in funding by the National Institutes of Health and fourth in the Southeast in revenues from its licensed intellectual property.


    Sunday, February 15, 2009

    Clinical Trial: Efficacy and Safety Study of ST101 Plus Aricept in Alzheimer's Disease


    This study is not yet open for participant recruitment; however, it is expected to start soon and the locations are already up and listed. If you are interested you might want to check the locations and make contact now.

    Detailed Description:
    Alzheimer's disease (AD) is a progressive and fatal neurological illness. It produces changes in the brain that include loss of cells and accumulation of abnormal protein deposits. Initial symptoms are cognitive, with deficiencies in short-term memory the most common symptom. As the disease progresses so does the severity of cognitive deficiency. Loss of speech and immobility occur in the terminal stages There is no cure for AD and no marketed treatment that modifies the underlying disease process. Available therapies improve some symptoms of AD by increasing brain concentrations of molecules involved in cognition. ST101 differs from marketed therapies in that it has demonstrated two actions in animal research testing. It improves cognition and it also reduces the accumulation of abnormal protein deposits in the brain. These two properties suggest that ST101 may be a promising agent for the treatment of AD. This study is designed as a preliminary dose exploration/proof-of¬concept investigation of the ability of ST101 to improve cognition during 12 weeks of administration.

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    Eligibility

    Ages Eligible for Study: 50 Years and older
    Genders Eligible for Study: Both
    Accepts Healthy Volunteers: No

    Inclusion Criteria:

    Diagnostic evidence of mild to moderate Alzheimer's disease.
    CT or MRI results within the past 12 months that rule out dementia due to non-Alzheimer's etiology.
    A reliable and capable caregiver.

    Exclusion Criteria:

    Subjects who reside in a skilled nursing facility.
    Subjects with B12 or folate deficiency.
    Subjects with chronic hepatic disease.
    Subjects with a recent history of hematologic/oncologic disorders.
    Subjects who have experienced a myocardial infarction with the past year.
    Dementia caused or complicated by other organic disease

    Locations
    Go here to check the list of participating locations.

    Responsible Party: Sonexa Therapeutics, Inc. ( Barbara Finn/Sr. VP Regulatory Affairs and QA )
    Study ID Numbers: ST101-A001-202
    Study First Received: February 10, 2009
    Last Updated: February 11, 2009
    ClinicalTrials.gov Identifier: NCT00842816 history of changes since first registered
    Health Authority: United States: Food and Drug Administration

    Study placed in the following topic categories:

    Delirium, Dementia, Amnestic, Cognitive Disorders
    Mental Disorders
    Alzheimer Disease
    Alzheimer disease
    Central Nervous System Diseases
    Neurodegenerative Diseases
    Brain Diseases
    Dementia
    Cognition Disorders
    Delirium

    Information provided by Sonexa Therapeutics, Inc.

    Previously on the Alzheimer's Reading Room



    Author Terry Pratchett blames his Alzheimers on mercury fillings


    clipped from www.guardian.co.uk

    Terry Pratchett has reopened the controversy about the safety of mercury-based tooth fillings by blaming them for his Alzheimer's disease.

    The author of the Discworld series describes the fillings - which millions of Britons have - as "toxic waste".

    "Having something like mercury in your mouth seemed to me to be a really bad idea and I got rid of the stuff," said Pratchett.

    blog it

    Friday, February 13, 2009

    Alzheimer's Disease Genetics Study--Clinical Trial


    By Bob DeMarco
    Alzheimer's Reading Room
    Editor


    This is an important genetics study that has been going on for seven years. They are still recruiting new participants. Please share this information with others that you think might be interested in participating. We can all benefit from the findings of this important.

    Wednesday, February 11, 2009

    Terry Pratchett: Living with Alzheimer’s


    Judging by the number of "tweets" on Twitter the documentary Terry Pratchett: Living with Alzheimer's is creating a stir across the pond. People seem to be genuinely moved. There can be little doubt that this documentary is raising awareness of Alzheimer's disease in Great Britain. This is a good thing.

    Terry Pratchett: Living with Alzheimer’s

    Subscriber Alert--Important Notice of Change


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    Bob

    Eat a Mediterranean Style Diet to Ward Off Alzheimer's


    More American's--especially the baby boom generation--are learning the importance of eating healthy.

    By Bob DeMarco
    Alzheimer's Reading Room

    A new research study indicates that eating Mediterranean-style seems to reduces the risk of mild cognitive impairment, dementia, and Alzheimer's.

    There are numerous studies that indicate this style of eating helps reduce cardiovascular risk factors like high cholesterol, hypertension and diabetes.

    All of these are linked to Alzheimer's and I have written about them previously on this blog (use the search box for more information).

    Tuesday, February 10, 2009

    Can a person suffering from Alzheimer's or Dementia Drive a car?


    I know the answer to this question is Yes. My mother drove her car over a concrete abutement, through a hedge, tore the entire side of her car off, and fortunately came to a stop about six inches from her building. The car was totaled. My mother spent the night in the hospital. She was released the next day and the doctor's told me there was nothing wrong with her. This is when I started to worry.

    Even after my mother was diagnosed with likely Alzheimer's she still had a drivers license. It is now clear--at the minimum-- she was mildly cognitively impaired and still driving for years.

    I cannot tell you how many people I have met that are clearly suffering from some form of dementia and are still driving down here in south Florida.

    See - Driving with Alzheimer's Can Mean Death

    Sunday, February 8, 2009

    Facts about Huperzine A


    Huperzine A, is a naturally occurring sesquiterpene alkaloid found in the plant extracts of the firmoss Huperzia serrata. Huperzine A may have cognition-enhancing activity in some Alzheimer's patients. 

    This substance is really more of a drug than an herb and is sold over the counter as a dietary supplement for memory loss and mental impairment.

    The google keyword search for huperzine A sends many people to this website. I am not surprised. You can read more about huperzine A below. One word of caution: do not mix huperzine A with Aricept befor consulting with your doctor or memory specialist.
    Use of huperzine A along with the acetylcholinesterase inhibitors donepezil or tacrine may produce additive effects, including additive adverse effects. Other acetylcholinesterase inhibitors include neostigmine, physostigmine and pyridostigmine, and use of these agents along with huperzine A may produce additive effects, including additive adverse effects.
    Before using huperzine A tell your doctor. It you are considering using huperzine as an alternative treatment for Alzheimer's I suggest you read up on the drug on the Internet and then discuss the drug with a memory specialist before moving forward.
    I have no opinion on the drug/herb huprezine a and this article is strictly informational. I am not recommending or endorsing the use of huperzine A.

    Huperzine A is available from numerous manufacturers generically. Branded products include Brain Elevate, Huperzine Rx-Brain and Huperzine A.

    Thursday, February 5, 2009

    Safety Of PF 04494700 In Mild To Moderate Alzheimer's Disease


    This is a Phase II clinical trial that is currently recruiting participants. The good news is this study is open to anyone 50 years or older. There are 54 available locations all across the country.

    Please note the inclusion criteria:
    • Mini Mental State Exam (MMSE) score between 14-26 (inclusive) at screening.
    • Participants must be receiving acetylcholinesterase inhibitors on a stable dose for at least 4 months prior to randomization

    Please note the exclusion criteria:
    • Current evidence or history of neurological, psychiatric and any other illness that could contribute to non-Alzheimer's dementia.
    • Known history of familial AD or any evidence for early onset AD known or possibly associated with genetic mutations.
    • Evidence or history of diabetes mellitus Type 1 or Type 2.
    • History or symptoms of autoimmune disorders.

    Sponsors and Collaborators: Alzheimer's Disease Cooperative Study (ADCS)
    The drug being tested in this study seeks to stop the protein amyloid beta from binding to a receptor in the brain called RAGE (receptor for advanced glycation endproducts). In earlier studies, inhibiting the RAGE protein in animal models led to a reduction of plaque formation.
    The researchers hope that by blocking plaque-caused nerve damage and inflammation, this drug will slow the progressive decline associated with Alzheimer’s disease in humans. But regardless of how the drug performs in the study, Ashford said the research is crucial to scientists’ understanding of the disorder.
    Currently testing in 54 locations
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    Alzheimer's patients needed for Stanford study

    STANFORD, Calif. — A national team of scientists is trying to determine if an experimental drug, called a RAGE inhibitor, can help Alzheimer’s disease patients with memory loss and other symptoms. Researchers at the Stanford University School of Medicine are among those looking for people with mild to moderate Alzheimer’s disease to participate in this phase-2 clinical trial.

    “The number of Alzheimer’s patients is expected to triple or even quadruple by the year 2050,” said J. Wesson Ashford, MD, PhD, who is leading the Stanford portion of the multicenter study. “We don’t want people to be completely infirm and unable to take care of themselves, so it’s important that we find some drugs that can prevent the problem.”

    More than 5 million Americans suffer from Alzheimer’s, which is characterized by an excessive amount of proteins that build up in plaque deposits and cause damage to nerve cells and inflammation in the brain. The disease was recently ranked by the Centers for Disease Control and Prevention as the sixth-leading cause of death in the country, and societal costs of Alzheimer’s amount to nearly $150 billion each year.

    The drug being tested in this study seeks to stop the protein amyloid beta from binding to a receptor in the brain called RAGE (receptor for advanced glycation endproducts). In earlier studies, inhibiting the RAGE protein in animal models led to a reduction of plaque formation.

    The researchers hope that by blocking plaque-caused nerve damage and inflammation, this drug will slow the progressive decline associated with Alzheimer’s disease in humans. But regardless of how the drug performs in the study, Ashford said the research is crucial to scientists’ understanding of the disorder.

    “This type of research helps us learn more about the disease and study it more effectively,” said Ashford, a senior research scientist with the Stanford/VA Aging Clinical Research Center, a joint project of Stanford University and the Veteran Affairs Palo Alto Health Care System.

    During the 18-month, double-blind study, which will involve 400 volunteers at 40 sites nationwide, participants will receive either the drug or a placebo pill. Researchers will monitor the participants during regular visits and measure disease progression using standard cognitive tests. They will also examine various biological markers of the disease, using magnetic resonance imaging to measure the degree of shrinkage in the brain and positron emission topography to assess the extent of amyloid buildup in the brain.

    Researchers are looking for people age 50 or older who have been diagnosed as having probable Alzheimer’s disease or dementia. They must be currently taking medication for their disease and have a caregiver or family member who can accompany them to each study visit.

    Those who are interested in learning more about participating should contact Ellen Kim at (650) 496-2578 or the national Alzheimer’s Disease Education and Referral Center at (800) 438-4380.

    The study is being conducted by the Alzheimer’s Disease Cooperative Study, a consortium of leading researchers supported by the National Institute on Aging, and is led by researchers at the University of California-San Diego. Funding for the study comes from Pfizer, which manufacturers the drug being tested.

    # # #
    Stanford University Medical Center integrates research, medical education and patient care at its three institutions - Stanford University School of Medicine, Stanford Hospital & Clinics and Lucile Packard Children's Hospital. For more information, please visit the Office of Communication & Public Affairs site at http://mednews.stanford.edu/.


    Wednesday, February 4, 2009

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    Bob DeMarco Alzheimer's Reading Room Related Content
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    Bob DeMarco
    Bob DeMarco  is the Founder of the Alzheimer's Reading Room (ARR). Bob is a recognized expert, writer, speaker, and influencer in the Alzheimer's and Dementia Community worldwide. The ARR Knowledge Base contains more than 4,600 articles. Bob lives in Delray Beach, FL.
    Original content the Alzheimer's Reading Room

    Tuesday, February 3, 2009

    The Memory Loss Tapes


    The Memory Loss Tapes takes an intimate look at seven individuals living with Alzheimer’s, seeking to introduce a new understanding by sharing the devastating experience of memory loss from the point of view of the person with the disease.

    Grandpa, Do You Know Who I Am? With Maria Shriver is a is geared toward children and young teens coping with a grandparent’s illness, and presents vignettes that can help a child understand and deal with a relative’s gradual decline into Alzheimer’s.

    Momentum in Science is a two-part, state-of-science odyssey that takes viewers inside the laboratories and clinics of 25 leading physicians, revealing some of the most cutting-edge Alzheimer research advances.

    Caregivers is a collection of five family portraits that illustrate caring for the different stages of Alzheimer’s disease.

    Follow the Alzheimer's Reading Room on Twitter

    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.



    Can Apple Juice Delay the Onset of Alzheimer's Disease


    A big story going around the Internet is about apple juice and Alzheimer's disease.

    Thomas B. Shea, PhD, of the Center for Cellular Neurobiology; Neurodegeneration Research University of Massachusetts, Lowell and his research team have carried out a number of laboratory studies demonstrating that drinking apple juice helped mice perform better than normal in maze trials, and prevented the decline in performance that was otherwise observed as these mice aged.
    This reminded me of a broader study that had been done with humans, Drinking juice could delay onset of Alzheimer's disease.
    Researchers at the Group Health Center for Health Studies in Seattle, Washington following nearly 2,000 adults for 10 years found drinking fruit or vegetable juice more than three times a week cuts the risk of developing Alzheimer's by 76 percent compared to drinking it less than once a week. They found having juice once or twice a week reduced risk by 16 percent.

    Monday, February 2, 2009

    Is Alzheimer's a type of diabetes of the brain?


    William Klein of Northwestern University is publishing a study that shows that insulin appears to shield the brain from toxic proteins associated with disease.

    The study found that the GlaxoSmithKline's diabetes drug Avandia, which increases sensitivity to insulin, appears to enhance this protective effect.
    "In Type 1 diabetes, your pancreas isn't making insulin. In Type 2 diabetes, your tissues are insensitive to insulin because of problems in the insulin receptor. Type 3 is where that insulin receptor problem is localized in the brain," Klein said in a telephone interview.

    "As you get older, some individuals start to have less effective insulin signaling, including in the brain," he said, making the brain more vulnerable to toxins that cause Alzheimer's disease.