Dimebon Dimebolin Information Availability » Alzheimer Disease

What Is Alzheimer’s Disease? What Causes Alzheimer’s Disease?

admin — Wed, 16 May 2012 12:52:33 +0000

Alzheimer’s disease is a progressive neurologic disease of the brain leading to the irreversible loss of neurons and the loss of intellectual abilities, including memory and reasoning, which become severe enough to impede social or occupational functioning. Alzheimer’s disease is also known as simplyAlzheimer’s, and Senile Dementia of the Alzheimer Type (SDAT) .

During the course of the disease plaquesand tangles develop within the structure of the brain. This causes brain cells to die. Patients with Alzheimer’s also have a deficiency in the levels of some vital brain chemicals which are involved with the transmission of messages in the brain – neurotransmitters.

Alzheimer’s disease is the most common form of dementia. The disease gets worse as it develops – it is a progressive disease. There is no current cure for Alzheimer’s, although there are ways of slowing down its advance and helping patients with some of the symptoms. Alzheimer’s is also a terminal disease – it is incurable and causes death.

According the National Institute on Aging, there are estimated to be between 2.4 million and 4.5 million Americans who have Alzheimer’s. There are approximately 417,000 people in the UK with Alzheimer’s, according to the Alzheimer’s Society.

http://www.medicalnewstoday.com/articles/159442.php

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Alzheimer’s Risk Falls With Activity

admin — Sat, 12 May 2012 12:49:43 +0000

Intensity matters, but it isn’t just about exercise.

Cleaning house and doing yard-work are taking on new importance. A higher level of physical activity – not just exercising – is linked to a reduced risk of developing Alzheimer’s disease even in people over 80, suggests research published Wednesday in the journal Neurology.

Protective activities washing dishes, cooking, cleaning, gardening – even playing cards. People who scored in the bottom 10% of physical activity were more than twice as likely to develop Alzheimer’s. Study participants did not have dementia at the start of the four-year study, which is part of the ongoing Memory and Aging Project at Rush University Medical Center in Chicago.

“The implication of this study is really outstanding,” says physician Aron Buchman, the lead author. “Exercise is good, without a doubt, but this study is about more than exercise. Older people who might not be able to exercise can tailor activities that are right for them.”

There is no cure or drug to delay onset of Alzheimer’s, which affects about 5 million in the USA; numbers are expected to triple as Baby Boomers get older. Aging is the main risk factor.

During the study, 71 of the 716 study participants developed Alzheimer’s. Study author’s say this is the first study to use an objective measurement of all physical activity in addition to self-reports. Participants wore and actigraph on their wrists to assess levels of activity.

Their mean score was 3.3 hours a week. Exercise intensity also mattered; those in the bottom 10% for intensity of physical activity were almost three times as likely to develop Alzheimer’s.

The study is the latest evidence that physical activity, even in later years, aids in delaying Alzheimer’s. The study did not attempt to measure which activities were most helpful.

“We’ve known that muscle activity generates neurons in the brain, but this study gives us additional motivation,” says physician Gary Kennedy, director of geriatric psychiatry at Montefiore Medical Center in New York City, who was not associated with the study. “It shows you don’t have to go to the gym. Older people very often don’t want to do that.”

Results did not vary by age, sex or education. The authors also looked at chronic health and genetic factors. Among the findings:

Body mass index, depressive symptoms or vascular risk factors did not change the association between activities and risk.
Having the gene APOE4, which puts people at higher risk for developing Alzheimer’s, did not affect the results.

Alzheimer’s develops for years prior to symptoms occurring, Kennedy notes. The authors tried to control for that possibility by administering baseline cognitive tests.

“This is an important message for society, as the largest growing segment of our population is old people,” Buchman says. “We need to be encouraging physical activities even in very old individuals, even if their health doesn’t allow them to take part in fitness programs.”

In an accompanying editorial, the authors cite physical activity as a promising, low-cost, accessible and safe means to prevent Alzheimer’s.

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Potential Alzheimer’s Drug Dimebon Fails in Clinical Trials

admin — Sat, 14 Apr 2012 08:06:40 +0000

Dimebon, a drug that has been in phase three of clinical trials for treatment of Alzheimer’s disease, has recently been discontinued after studies concluded it was ineffective. Dimebon is a drug that was first used in Russia decades ago as an antihistamine, and in the last few years has undergone testing to treat the symptoms of Alzheimer’s in the United States. Dimebon was never sold or marketed in the United States.

Initially, the drug showed some positive results in patients with Alzheimer’s, so clinical trials were expanded to study its effects when given with the drug denepazil (Aricept), a medication currently used to treat early Alzheimer’s. This past week, Pfizer and Medivation, the two drug companies that were conducting the trials, announced the discontinuation of Dimebon after it failed to show benefits for the recipients. In fact, some of the people receiving it declined more than those who received the placebo.

This is disappointing news, especially in light of ournation’s recent draft document on Alzheimer’s disease and other related dementias. One goal outlined in this draft is to effectively treat and prevent Alzheimer’s by 2025. Evidently, the manner in which we do this won’t include Dimebon.

http://alzheimers.about.com/b/2012/01/22/potential-alzheimers-drug-dimebon-fails-in-clinical-trials.htm

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Cancer drug shows promise in mouse Alzheimer’s study

admin — Sat, 18 Feb 2012 10:49:57 +0000

Mice in the early stage of Alzheimer’s disease had some of their brain abnormalities reversed and their declining mental function restored when they were given low doses of a rarely used cancer drug.The drug, bexarotene, stimulated the removal of beta-amyloid, a substance whose accumulation in the brain appears to be the main cause of Alzheimer’s dementia. After treatment, the animals fared better in tests of memory and social behavior, according to a study published online Thursday by the journal Science.

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

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

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

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

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

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

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

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

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

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

http://www.washingtonpost.com/national/health-science/cancer-drug-shows-promise-in-mouse-alzheimers-study/2012/02/09/gIQAzJct1Q_story.html

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Alzheimer’s drug fails for Pfizer, Medivation

admin — Sun, 29 Jan 2012 08:32:11 +0000

Pfizer and Medivation ended their collaboration on the experimental drug Dimebon for Alzheimer’s disease after the medicine failed in another late-stage clinical trial.

Dimebon was one of two drugs Pfizer had in its late-stage pipeline to treat the neurodegenerative disease. The other is bapineuzumab, which Pfizer is developing with Johnson & Johnson. The treatments have different mechanisms of action.

Dimebon didn’t show statistically significant results in a study that evaluated the compound when added to a standard treatment in patients with mild to moderate forms of the disease, the companies said Tuesday. The companies will end development of the drug for all uses, and will stop a current study.

San Francisco’s Medivation dropped 3.3 percent to $53.90 at the close in New York. Pfizer, the world’s biggest drugmaker, gained less than 1 percent to $21.94.

Dimebon also failed in a late-stage trial in 2010, sending Medivation shares down 67 percent in one day.

The federal Centers for Disease Control and Prevention in Atlanta estimates that at least 5 million Americans have Alzheimer’s. The disease usually begins affecting people around age 60. There is no known cure.

http://www.sfgate.com/cgi-bin/article.cgi?f=/c/a/2012/01/17/BUD01MQG0I.DTL

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Pfizer, Medivation end development of potential Alzheimer’s treatment Dimebon

admin — Sat, 21 Jan 2012 12:26:49 +0000

TRENTON, N.J. — In a major setback for patients and doctors, drugmakers Pfizer Inc. and Medivation Inc. have halted development of a potential Alzheimer’s disease treatment after the drug for a second time yielded disappointing results in a late-stage clinical study.Dimebon was furthest along in testing among the experimental Alzheimer’s drugs being developed to try to stop or even reverse the course of the mind-robbing disease. Dimebon would have been the first such drug and specialists just a couple of years ago had hoped it would be on the market this year.

Pfizer, the world’s largest drugmaker by revenue, and Medivation said on Tuesday that Dimebon failed to significantly improve cognitive ability, as well as self-care and daily functions in patients with mild-to-moderate cases of the disease. The study involved about 1,000 patients who had Dimebon added to their ongoing treatment with Pfizer’s former blockbuster Alzheimer’s drug donepezil, or Aricept.

Aricept, jointly marketed by Pfizer and Japan’s Esai Co. Ltd. and once heavily advertised, had about $3.7 billion in sales in 2009. It lost U.S. patent protection in November 2010, and sales have since plunged.

Dimebon, known chemically as latrepirdine, would have been an even bigger blockbuster if it had panned out. The experimental drug looked promising after it kept Alzheimer’s symptoms from worsening for a year in an earlier patient study.

But Dimebon didn’t work as hoped in a late-stage trial in which patients took it for six months. After those results, announced in March 2010, the companies said they were continuing three other studies that could prove Dimebon helped patients in combination with other Alzheimer’s drugs or when used for a longer period.

Then last April Pfizer and Medivation said Dimebon also failed in another late-stage clinical trial, when it did not improve symptoms of the neurologic disorder Huntington’s Disease.

After the latest failure, New York-based Pfizer and Medivation, headquartered in San Francisco, said they are ending development of Dimebon, as well as their agreement to market the potential treatment.

Pfizer still has one Alzheimer’s treatment in late-stage testing, bapineuzamab, which it is jointly developing with Johnson & Johnson. It’s a biologic drug, grown in living cells rather than made by mixing chemicals, and works differently than Dimebon.

Alzheimer’s disease is the most common form of dementia, and drugmakers are trying to find a treatment that does more than temporarily ease the symptoms: memory problems, confusion, aggression and a general decline in ability to function, which together can hasten death. Many drugs have flopped in late-stage testing in recent years, including some that seemed to clear harmful plaque from afflicted brains.

The newest drug for Alzheimer’s symptoms, Namenda, was approved back in 2003.

Cases of Alzheimer’s disease are expected to triple by 2050, to around 106 million people worldwide. The disease strikes nearly a half million new patients a year, mainly as people hit their 70s or 80s.

In trading Tuesday, Pfizer shares rose 9 cents to $21.93, while Medivation stock dropped $1.82, or 3.3 percent, to $53.90.

http://www.washingtonpost.com/business/industries/pfizer-medivation-end-development-of-potential-alzheimers-treatment-dimebon/2012/01/17/gIQA91uF5P_story.html

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Sobering Statistics about Alzheimer’s Disease

admin — Thu, 22 Dec 2011 06:10:53 +0000

Each day, 1,232 people are diagnosed with Alzheimer’s disease.

Each week, 8,634 people are diagnosed with Alzheimer’s disease.

Every 70 seconds someone is diagnosed with Alzheimer’s disease….

Editor Note: For more statistics on Alzheimer’s disease see –

Alzheimer’s Disease Statistics

By the time you finish reading this article a few more people will be officially suffering from Alzheimer’s disease.

Here is a startling perspective.

It is not unusual for a person working on Wall Street (New York) to spend a total of three hours a day commuting to and from work. Many of these people live on Long Island, in Connecticut and New Jersey.

There are 180 minutes in three hours. There are 10,800 seconds in three hours.

While these people are commuting to and from work each day, another 154 persons are diagnosed with Alzheimer’s.

_____________________________

Each day, 1,232 people are diagnosed with Alzheimer’s disease.

Each week, 8,634 people are diagnosed with Alzheimer’s disease.

_____________________________A recent Harris Interactive poll showed that more than 100 million Americans have been touched by Alzheimer’s. More than 33 million Americans are worried about Alzheimer’s disease.

Startling numbers.

Alzheimer’s disease is a death sentence. Brain death. A typical person takes from 5-20 years to die. It is not unusual for the disease to take more than a decade to kill someone.

When most people think about Alzheimer’s they think about a person losing their memory. Persons that know someone suffering from Alzheimer’s disease watch them lose their ability to brush their teeth, take a shower, put on their cloths, go to the bathroom, and eat.

They await the worse day of them all — the day the person suffering from Alzheimer’s won’t know them. Or anyone for that matter.

Alzheimer’s disease is sinister and ugly.

If you don’t know someone directly or indirectly that is suffering from Alzheimer’s you will soon. It might have happened while you were reading this article.

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Why Can’t I Buy Dimebon for Alzheimer’s?

admin — Thu, 17 Nov 2011 06:11:56 +0000

Why can’t, I, WE, buy Dimebon for Alzheimer’s disease?

TERMINATED. That is the word they used when the Dimebon clinical trial that my mother was enrolled in was abruptly canceled on May 7, 2010.

The termination was caused by the failure of the Dimebon Connection Study. My mother was not enrolled in the that study. But, because the study failed to produce the necessary results for potential FDA approval the rug was pulled from under our feet.

We weren’t the only ones. There were more than 2,000 patients enrolled in Dimebon clinical trials. This means at least 1,000 participants received Dimebon. The other participants received a placebo.

The study was not terminated due to any safety findings. Dimebon was well-tolerated in clinical trials.

Safety was not an issue. The problem was efficacy. In other words, the drug did not provide enough benefit to participants. From a statistical standpoint it did not stop memory loss. There was some benefits registered on the behavior scale.

Now to my point.

Dotty did benefit. While on Dimebon, she was more alert and her behavior was dramatically improved over what I had come to expect.

Keep in mind here, Dotty was diagnosed before entering the clinical trial as being in the moderate to severe stage of Alzheimer’s. She scored 14 on the MMSE. She also scored 16 during the trial.

I did ask the personnel at the clinical trial site if they thought that Dotty was showing any improvement. They told me yes. I asked how?

Here is an example. At the outset of the clinical trial they showed Dotty a picture of a fork. Then asked, what do you with this? She could not say or demonstrate how you use a fork. When they put a fork in her hand she could demonstrate what you do with a fork.

Later in the study, they did the same test over. Sure enough, Dotty looked at the picture of the fork and then demonstrated what you do with a fork.

By the way, by the point in the clinical trial I didn’t have to ask anyone anything. I saw with my own eyes, ears, and brains that Dotty was a different person.

How much better?

Hold on tight. Better than she had been in many years. Let me set this straight. I couldn’t tell if there was any improvement in Dotty’s memory, and if you would like to know the truth, I didn’t care.

What I did care about was that Dotty seemed to be more interested in living her life. She was a fuller, better person.

My point. I can accept memory loss. I don’t spend much time thinking about Dotty’s memory, or what she can or can’t remember. What I do care about is the look on Dotty’s face, and how she responds to activity.

Dotty clearly looked more there, and was clearly experiencing “more enjoyment”.

As my close friends know, I was “dancing on the ceiling”.

We are not the only one’s that saw benefits from Dimebon. There are several articles and stories on this website from other caregivers that were enrolled in the Dimebon clinical trials.

I know they want an answer to this question.

Why Can’t We Buy Dimebon in the United States?

The drug is safe. The drug has been used in Russia since 1983.

And, Dimebon was proven to be safe in the clinical trials.

http://www.alzheimersreadingroom.com/2011/11/why-cant-i-buy-dimebon-for-alzheimers.html

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Alzheimer’s Association statement on negative Phase III trial results for latrepirdine (Dimebon)

admin — Tue, 09 Aug 2011 15:15:39 +0000

“The Alzheimer’s Association is disappointed to learn of the negative results from the Phase III clinical trial of latrepirdine (Dimebon),” said William Thies, Ph.D., Alzheimer’s Association chief medical and scientific officer. “People with Alzheimer’s, their families and caregivers desperately need more and better treatment options for this devastating, fatal brain disease.”

Nonetheless, the Alzheimer’s Association remains optimistic about the future prospects for better Alzheimer treatments and prevention strategies. Several dozen other compounds are in the pipeline for Alzheimer’s disease. We remain encouraged by the fact that drugs in the pipeline for Alzheimer’s attack the disease from a variety of angles.

“The population is aging, and we need to make significant advances soon in the treatment and prevention of Alzheimer’s. It is an overwhelming epidemic, already claiming millions of individuals, and it is on track to deplete our healthcare resources and devastate Medicare,” Thies said. “The current level of federal research funding for Alzheimer’s is unacceptable considering the many millions of people this disease affects and the huge financial impact on our economy and society. And, these numbers will grow exponentially with the aging of our population.”

According to the Association, in order to get better diagnosis, treatments and prevention for Alzheimer’s, we must address two important issues:

(1) We must address the chronic underinvestment in research to ultimately solve the Alzheimer crisis. We need to get more Alzheimer drugs in the pipeline. To do this, we must increase the research investment in Alzheimer’s to levels similar to other leading causes of death, such as cancer and heart disease. Only then will we have the chance to see the same type of progress — such as declining death rates, and viable lifestyle-based prevention strategies — and stop this epidemic. If we do not invest now, the cost of Alzheimer’s disease to taxpayers in Medicare and Medicaid costs will be $20 trillion dollars over the next 40 years — equal to 25 economic stimulus bills.

(2) In addition to increasing funding, it is imperative that people volunteer for Alzheimer clinical trials. Later this year, at the Alzheimer’s Association 2010 International Conference on Alzheimer’s Disease (ICAD), the Association is planning to launch a first of its kind tool to help match people with Alzheimer’s and caregivers with Alzheimer clinical trials.

Next week, the Alzheimer’s Association is bringing together advocates from across the country at the Alzheimer’s Action Summit to encourage legislators to increase funding for Alzheimer’s disease. Join us in Washington, D.C. or take action virtually at alz.org.

The Alzheimer’s Association
The Alzheimer’s Association is the leading voluntary health organization in Alzheimer care, support and research. Our mission is to eliminate Alzheimer’s disease through the advancement of research; to provide and enhance care and support for all affected; and to reduce the risk of dementia through the promotion of brain health. Our vision is a world without Alzheimer’s.

http://www.maganj.com/?p=573

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Amyloid Theory in Alzheimer's Takes Another Hit

admin — Thu, 21 Oct 2010 07:33:54 +0000

Clinical trials of a drug aimed at reducing beta-amyloid plaque accumulation in Alzheimer’s disease have been stopped because of lack of efficacy, striking another blow against the amyloid theory of the disease.

Eli Lilly announced that it was halting development of a drug called semagacestat, an inhibitor of the gamma-secretase enzyme that produces beta-amyloid protein, after preliminary results from two large placebo-controlled trials indicated no benefit from the treatment.

“It did not slow disease progression and was associated with worsening of clinical measures of cognition and the ability to perform activities of daily living,” according to a Lilly press release.

The trials had a total of more than 2,600 participants with mild to moderate Alzheimer’s disease. Patients receiving the drug showed greater declines in these measures than did those in the placebo groups.

Lilly said it had instructed site investigators to stop dosing patients as soon as possible but to continue following participants for at least six months to collect cognitive function scores and safety data.

“These additional follow-up visits will help to answer a number of important questions, including whether the differences between patients who received semagacestat and those who received placebo will continue after semagacestat has been discontinued,” the company indicated.

The two trials began in 2008; one was scheduled to run until June 2011 and the other until March 2012.

Lilly is also halting other, smaller, short-term studies of semagacestat.

The drug is the latest anti-amyloid agent to fail in late-stage, placebo-controlled trials, casting more doubt on whether this approach can ever work in established Alzheimer’s disease.

Negative clinical results have also been found for tarenflurbil, latrepirdine (Dimebon), and bapineuzumab, which target beta-amyloid protein production or the sticky plaques that form when soluble beta-amyloid changes shape to become fibrous and insoluble.

But development of bapineuzumab is continuing, with preliminary PET scan data indicating that the drug successfully breaks up amyloid plaques in Alzheimer’s patients as intended. Clinical results from the phase III study are now eagerly awaited in the Alzheimer’s community.

The Lilly trials of semagacestat also included PET scans to measure effects on plaque burden. The company’s announcement did not include those results; a Lilly spokesman said the PET data were still blinded and would not be available for analysis for at least six months.

Those data could be critical in determining whether beta-amyloid is a worthwhile target for Alzheimer’s drugs, as well as what went wrong with semagacestat specifically.

A finding that semagacestat treatment did reduce plaque accumulation, yet failed to show clinical benefit, might suggest that this approach will not work in patients with established symptoms.

But Samuel Gandy, MD, of Mount Sinai School of Medicine in New York City, told MedPage Today that it might only cast doubt on gamma-secretase as the specific target.

“There are new data suggesting that some of the gamma-secretase genes that cause familial Alzheimer’s also lower enzyme activity,” Gandy wrote in an e-mail.” This could be the explanation for the Lilly drug: i.e., that low gamma-secretase activity can be part of the disease and therefore using an inhibitor might be very challenging.”

He agreed that the PET data would be important in figuring out what happened.

“If the amyloid burden got worse, that means that low gamma-secretase activity can increase amyloid buildup like in familial AD. If the amyloid burden got better, that could suggest that some other gamma secretase substrate (e.g., Notch) was also inhibited and caused side effects,” Gandy said.

Lilly emphasized that it was not giving up yet on beta-amyloid as a target. The company is continuing development of an anti-amyloid monoclonal antibody, solanezumab, with two phase III trials now underway.