The pharmaceutical company Pfizer announced today that its investigational Alzheimer’s medication, Dimebon, has failed an important test of its effectiveness in the treatment of Alzheimer’s Dementia. A great deal of hope and expectation had been placed in this medication. Its apparent failure has been a disappointment not only for Pfizer, but for many physicians and sufferers of Alzheimer’s Dementia that were expecting Dimebon to be a breakthrough in the treatment of the illness.

Results came from an FDA approved Phase III clinical trial named CONNECTION that was being run by Pfizer and its subsidiary company, Medivation.

Phase III refers to a specific stage in the clinical investigation of new medications for human use. After animal studies have shown a medication to have promise, Phase I trials establish doses and safety of the medication in human beings. Phase II trials then try the medication on small groups of patients to see if the drug shows effectiveness and safety in its use in humans. Phase III trials start after all indications are that the medication is safe and likely to have benefit for patients. Phase III trials involve large numbers of patients in several different clinics or medical centers, and their results are safeguarded by the use of placebos and so-called double blind designs that prevent both the patient and the doctor from knowing who is getting what until the results are determined.

The CONNECTION trial has been a Phase III study looking at the effects of Dimebon in about 600 patients with mild-to-moderate AD in North America, Europe, and South America. The patients in the study had an average age of 74.4 years, and met criteria for the diagnosis of Alzheimer’s Dementia of mild to moderate severity. The patients were randomly assigned to receive either Dimebon or a placebo, i.e., “sugar pill” for six months. During that time their cognitive function was regularly assessed to determine what if any changes were occurring, or if the two treatment groups differed from one another. The finding was that after six months, those patients receiving Dimebon were not at all different from those who merely received the placebo. In other words, the Phase III trial showed that Dimebon was no more effective than a sugar pill. It offered no benefits for patients suffering mild to moderate degree of Alzheimer’s Dementia.

The finding of the apparent ineffectiveness of Dimebon was surprising and disappointing largely because a 2008 clinical trial published in the prestigious journal The Lancet had obtained such positive results with the medication. In that study, 183 patients with mild to moderate Alzheimer’s Dementia appeared to greatly benefit from treatment with Dimebon. I have noted comments in the press that this earlier study was suspect because it was performed in Russian clinics. However, the study was performed as a collaboration of the Russian Academy of Sciences with groups from Baylor, Mount Sinai, UC San Diego, and Georgetown University Colleges of Medicine. Moreover, as I have suggested, the study met the impeccable publication standards of The Lancet. Those remarkable first results with Dimebon were also consistent with what had been learned in animal studies about the effects of this drug on the brain. Dimebon has been found to mimic effects of both of the classes of drugs currently FDA approved to treat Alzheimer’s Disease. That is, it blocks abnormal activity at NMDA receptors in the brain, as does the FDA approved memantine, and it blocks the enzymatic breakdown of the chemical messenger acetylcholine in the same fashion as drugs such as Aricept. In addition, Dimebon may help prevent build up of abnormal tau protein, which causes the neurofibrillary tangles of Alzheimer’s. There are also reports that it can block some of the neurotoxic effects of amyloid, the abnormal protein that accumulates in the brains of sufferers of Alzheimer’s.

Even before any trials in human beings, Dimebon had been found to improve the cognitive function of rats genetically engineered to exhibit changes in the brain and behavior similar to those seen in humans with Alzheimer’s Dementia. Thus, there were compelling reasons to predict that Dimebon would again be shown to be helpful in improving the cognitive function of patients with Alzheimer’s. Sadly, this was not the case.

Some explanation may be found as to why Dimebon may work in some but not other patients with Alzheimer’s Dementia. Moreover, studies are ongoing to see if Dimebon may yet be helpful as an add on to currently approved medications for Alzheimer’s Dementia. Nonetheless, it is now clear that Dimebon is not a miracle cure-all. To quote the great biologist, Thomas Huxely, “A beautiful theory has been destroyed by an ugly fact.”

The quest for medications that can improve the cognitive function of sufferers of Alzheimer’s dementia continues. It is possible that something will be found to stop or even reverse the degenerative processes of the illness. However, at present the most effective medications only slow the progression of the illness. Some people inherit genes that make it likely they will develop Alzheimer’s Dementia no matter what they do. Thankfully, this is a small minority of people. For most of us, the best approach to Alzheimer’s continues to be to avoid the illness by proper diet, stress reduction, sleeping well, staying active mentally, physically and socially, and by using vitamins, herbs and nutraceuticals that can slow down the neurodegenerative processes that cause damage to the brain. It is important that these steps be initiated in your 40′s and 50′s, when this damage to the brain tends to begin.

http://www.huffingtonpost.com/scott-mendelson-md/alzheimers-drug-dimebon-i_b_485014.html

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The pharmaceutical company Pfizer announced today that its investigational Alzheimer’s medication, Dimebon, has failed an important test of its effectiveness in the treatment of Alzheimer’s Dementia. A great deal of hope and expectation had been placed in this medication. Its apparent failure has been a disappointment not only for Pfizer, but for many physicians and sufferers of Alzheimer’s Dementia that were expecting Dimebon to be a breakthrough in the treatment of the illness.

Results came from an FDA approved Phase III clinical trial named CONNECTION that was being run

by Pfizer and its subsidiary company, Medivation. Phase III refers to a specific stage in the clinical investigation of new medications for human use. After animal studies have shown a medication to have promise, Phase I trials establish doses and safety of the medication in human beings. Phase II trials then try the medication on small groups of patients to see if the drug shows effectiveness and safety in its use in humans. Phase III trials start after all indications are that the medication is safe and likely to have benefit for patients. Phase III trials involve large numbers of patients in several different clinics or medical centers, and their results are safeguarded by the use of placebos and so-called double blind designs that prevent both the patient and the doctor from knowing who is getting what until the results are determined.

The CONNECTION trial has been a Phase III study looking at the effects of Dimebon in about 600 patients with mild-to-moderate AD in North America, Europe, and South America. The patients in the study had an average age of 74.4 years, and met criteria for the diagnosis of Alzheimer’s Dementia of mild to moderate severity. The patients were randomly assigned to receive either Dimebon or a placebo, i.e., “sugar pill” for six months. During that time their cognitive function was regularly assessed to determine what if any changes were occurring, or if the two treatment groups differed from one another. The finding was that after six months, those patients receiving Dimebon were not at all different from those who merely received the placebo. In other words, the Phase III trial showed that Dimebon was no more effective than a sugar pill. It offered no benefits for patients suffering mild to moderate degree of Alzheimer’s Dementia.

The finding of the apparent ineffectiveness of Dimebon was surprising and disappointing largely because a 2008 clinical trial published in the prestigious journal The Lancet had obtained such positive results with the medication. In that study, 183 patients with mild to moderate Alzheimer’s Dementia appeared to greatly benefit from treatment with Dimebon. I have noted comments in the press that this earlier study was suspect because it was performed in Russian clinics. However, the study was performed as a collaboration of the Russian Academy of Sciences with groups from Baylor, Mount Sinai, UC San Diego, and Georgetown University Colleges of Medicine. Moreover, as I have suggested, the study met the impeccable publication standards of The Lancet. Those remarkable first results with Dimebon were also consistent with what had been learned in animal studies about the effects of this drug on the brain. Dimebon has been found to mimic effects of both of the classes of drugs currently FDA approved to treat Alzheimer’s Disease. That is, it blocks abnormal activity at NMDA receptors in the brain, as does the FDA approved memantine, and it blocks the enzymatic breakdown of the chemical messenger acetylcholine in the same fashion as drugs such as Aricept. In addition, Dimebon may help prevent build up of abnormal tau protein, which causes the neurofibrillary tangles of Alzheimer’s. There are also reports that it can block some of the neurotoxic effects of amyloid, the abnormal protein that accumulates in the brains of sufferers of Alzheimer’s.

Even before any trials in human beings, Dimebon had been found to improve the cognitive function of rats genetically engineered to exhibit changes in the brain and behavior similar to those seen in humans with Alzheimer’s Dementia. Thus, there were compelling reasons to predict that Dimebon would again be shown to be helpful in improving the cognitive function of patients with Alzheimer’s. Sadly, this was not the case.

Some explanation may be found as to why Dimebon may work in some but not other patients with Alzheimer’s Dementia. Moreover, studies are ongoing to see if Dimebon may yet be helpful as an add on to currently approved medications for Alzheimer’s Dementia. Nonetheless, it is now clear that Dimebon is not a miracle cure-all. To quote the great biologist, Thomas Huxely, “A beautiful theory has been destroyed by an ugly fact.”

The quest for medications that can improve the cognitive function of sufferers of Alzheimer’s dementia continues. It is possible that something will be found to stop or even reverse the degenerative processes of the illness. However, at present the most effective medications only slow the progression of the illness. Some people inherit genes that make it likely they will develop Alzheimer’s Dementia no matter what they do. Thankfully, this is a small minority of people. For most of us, the best approach to Alzheimer’s continues to be to avoid the illness by proper diet, stress reduction, sleeping well, staying active mentally, physically and socially, and by using vitamins, herbs and nutraceuticals that can slow down the neurodegenerative processes that cause damage to the brain. It is important that these steps be initiated in your 40′s and 50′s, when this damage to the brain tends to begin.

Dimebon

http://www.dimebonalzheimers.com/

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Sphera Global Healthcare Fund, an Israeli hedge fund that’s beaten the market since its founding in 2007, is avoiding shares of local generic-drug maker Teva Pharmaceutical Industries Ltd., which has given investors a 105 percent return over the past five years.

Instead, Sphera is building a stake in Teva’s arch-rival Pfizer Inc., the world’s biggest pharmaceutical company, which has lost 20 percent in that time including dividends. New York- based Pfizer, selling for 7.4 times estimated earnings, is the least expensive of the 10 largest drugmakers. Teva, at 12.6 times profit, is the most expensive.

“As long as something is cheap, we’ll hold it,” said Ori Hershkovitz, 36, who’s a partner in the Tel Aviv-based fund and the head of research, in an interview last month. “As long as something is expensive, we’ll short it.”

That contrarian strategy has paid off. The $120 million fund returned 17 percent since inception in March 2007, compared with a loss of 0.4 percent for a Standard & Poor’s index of global health-care stocks. Now, Hershkovitz and says Pfizer

shares are attractive because of its diversified product portfolio, presence in fast-growing emerging markets and 4.2 percent dividend yield. The New York-based company probably will get positive clinical trial results by September for the tanezumab pain treatment, he said.

Not only is Pfizer a good value now, “but also we have a short-term catalyst,” he said. The fund increased its Pfizer holding this year. The company accounts for 15 percent of Sphera Global Healthcare’s assets, up from 12 percent previously, even as growth for makers of lower-priced generic medicine outpaces that of branded drug companies.

Pfizer’s Forecast

Pfizer shares declined more than warranted because its 2012 forecast in February disappointed investors and because of setbacks with cancer drug Sutent and Alzheimer’s drug Dimebon, he said. Pfizer is “poorly regarded by the market,” said Hershkovitz.

Started with capital from Mori Arkin, the Israeli entrepreneur who led Agis Industries Ltd. until its 2005 takeover by Perrigo Co., the Sphera health fund began accepting external investors in March 2007. The fund taps a network of Israeli doctors for opinions on new drugs and hired a veteran Teva patent lawyer to analyze prospects for generic challengers, said Hershkovitz, who joined at the fund’s inception after working as an analyst for Leader & Co. Investment House Ltd.

Arkin, Hershkovitz and two other partners seek companies whose shares are temporarily depressed by bad news, or whose stock may benefit from catalysts such as drug approvals within two years.

Generic Growth

Sphera Global Healthcare is avoiding Teva, the world’s biggest generic-drug company, even as growth of lower-priced copied medicines outpaces that of branded pharmaceuticals. Pfizer is preparing to lose most of the $11.4 billion in 2009 sales for Lipitor, the top-selling medicine, starting next year when cheaper copies enter the market from companies such as Teva.

Teva, based in the Tel Aviv suburb of Petah Tikva, was the fund’s biggest holding when it started four years ago, and comprised as much as 15 percent of its holdings until Sphera sold the shares in 2008. The drugmaker in January told investors it’s aiming to more than double sales to $31 billion by 2015, and last month agreed to buy Germany’s Ratiopharm GmbH, snatching it away from Pfizer in an auction.

While Sphera missed out on Teva’s last rally, the company’s American depositary receipts probably won’t budge much from about $65 in the next several months, said Hershkovitz. Teva has advanced 41 percent in the past year to close yesterday at $63.51 on the Nasdaq Stock Market.

“Looking back I think of course we could have done it differently,” the fund manager said. “Right now, if you look long term, you can find opportunities that are 20 percent to 30 percent cheaper.”

Sanofi Slump

Sanofi-Aventis SA is one of them, he said. The fund added to its stake in the Paris-based company this year as the shares slumped on the prospect of a generic competitor in the U.S. to Sanofi’s Lovenox anti-clotting drug, he said. Sanofi fell from a 52-week high of 58.90 euros on Jan. 20 to as low as 51.68 euros two weeks later after Novartis AG said Jan. 22 it planned to sell a version of the drug as soon as it obtains U.S. Food and Drug Administration approval.

The sell-off wiped 9.52 billion euros ($12.7 billion) off Sanofi’s market capitalization, more than Lovenox contributes in earnings, he said. “The stock grossly overreacted,” said Hershkovitz. Sanofi now sells for 8.5 times this year’s estimated earnings, compared with an average price-earnings ratio of 11 for the 10 largest drugmakers.

Sphera added to its stake in Pfizer and Sanofi this year after selling U.S. drugmaker Merck & Co. when shares peaked above $40 in January, Hershkovitz said.

Twelve percent of the fund is in Basel, Switzerland-based Novartis, which Sphera regards as the “best-managed company in our universe,” said Hershkovitz. Ten percent is invested in Novartis’s cross-town competitor Roche Holding AG, which he said has the best science.

California-based biotechnology companies Onyx Pharmaceuticals Inc. and NeurogesX Inc. account for about 9 percent of the fund. Onyx is working with Germany’s Bayer AG on the tumor-fighting drug Nexavar, while NeurogesX is developing a pain-treating patch. The fund views both companies as takeover targets, Hershkovitz said.

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Dimebon Online

http://www.dimebonalzheimers.com/

The pharmaceutical company Pfizer announced today that its investigational Alzheimer’s medication, Dimebon, has failed an important test of its effectiveness in the treatment of Alzheimer’s Dementia. A great deal of hope and expectation had been placed in this medication. Its apparent failure has been a disappointment not only for Pfizer, but for many physicians and sufferers of Alzheimer’s Dementia that were expecting Dimebon to be a breakthrough in the treatment of the illness.

Results came from an FDA approved Phase III clinical trial named CONNECTION that was being run by Pfizer and its subsidiary company, Medivation. Phase III refers to a specific stage in the clinical investigation of new medications for human use. After animal studies have shown a medication to have promise, Phase I trials establish doses and safety of the medication in human beings. Phase II trials then try the medication on small groups of patients to see if the drug shows effectiveness and safety in its use in humans. Phase III trials start after all indications are that the medication is safe and likely to have benefit for patients. Phase III trials involve large numbers of patients in several different clinics or medical centers, and their results are safeguarded by the use of placebos and so-called double blind designs that prevent both the patient and the doctor from knowing who is getting what until the results are determined.

The CONNECTION trial has been a Phase III study looking at the effects of Dimebon in about 600 patients with mild-to-moderate AD in North America, Europe, and South America. The patients in the study had an average age of 74.4 years, and met criteria for the diagnosis of Alzheimer’s Dementia of mild to moderate severity. The patients were randomly assigned to receive either Dimebon or a placebo, i.e., “sugar pill” for six months. During that time their cognitive function was regularly assessed to determine what if any changes were occurring, or if the two treatment groups differed from one another. The finding was that after six months, those patients receiving Dimebon were not at all different from those who merely received the placebo. In other words, the Phase III trial showed that Dimebon was no more effective than a sugar pill. It offered no benefits for patients suffering mild to moderate degree of Alzheimer’s Dementia.

The finding of the apparent ineffectiveness of Dimebon was surprising and disappointing largely because a 2008 clinical trial published in the prestigious journal The Lancet had obtained such positive results with the medication. In that study, 183 patients with mild to moderate Alzheimer’s Dementia appeared to greatly benefit from treatment with Dimebon. I have noted comments in the press that this earlier study was suspect because it was performed in Russian clinics. However, the study was performed as a collaboration of the Russian Academy of Sciences with groups from Baylor, Mount Sinai, UC San Diego, and Georgetown University Colleges of Medicine. Moreover, as I have suggested, the study met the impeccable publication standards of The Lancet. Those remarkable first results with Dimebon were also consistent with what had been learned in animal studies about the effects of this drug on the brain. Dimebon has been found to mimic effects of both of the classes of drugs currently FDA approved to treat Alzheimer’s Disease. That is, it blocks abnormal activity at NMDA receptors in the brain, as does the FDA approved memantine, and it blocks the enzymatic breakdown of the chemical messenger acetylcholine in the same fashion as drugs such as Aricept. In addition, Dimebon may help prevent build up of abnormal tau protein, which causes the neurofibrillary tangles of Alzheimer’s. There are also reports that it can block some of the neurotoxic effects of amyloid, the abnormal protein that accumulates in the brains of sufferers of Alzheimer’s.

Even before any trials in human beings, Dimebon had been found to improve the cognitive function of rats genetically engineered to exhibit changes in the brain and behavior similar to those seen in humans with Alzheimer’s Dementia. Thus, there were compelling reasons to predict that Dimebon would again be shown to be helpful in improving the cognitive function of patients with Alzheimer’s. Sadly, this was not the case.

Some explanation may be found as to why Dimebon may work in some but not other patients with Alzheimer’s Dementia. Moreover, studies are ongoing to see if Dimebon may yet be helpful as an add on to currently approved medications for Alzheimer’s Dementia. Nonetheless, it is now clear that Dimebon is not a miracle cure-all. To quote the great biologist, Thomas Huxely, “A beautiful theory has been destroyed by an ugly fact.”

The quest for medications that can improve the cognitive function of sufferers of Alzheimer’s dementia continues. It is possible that something will be found to stop or even reverse the degenerative processes of the illness. However, at present the most effective medications only slow the progression of the illness. Some people inherit genes that make it likely they will develop Alzheimer’s Dementia no matter what they do. Thankfully, this is a small minority of people. For most of us, the best approach to Alzheimer’s continues to be to avoid the illness by proper diet, stress reduction, sleeping well, staying active mentally, physically and socially, and by using vitamins, herbs and nutraceuticals that can slow down the neurodegenerative processes that cause damage to the brain. It is important that these steps be initiated in your 40′s and 50′s, when this damage to the brain tends to begin.

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Dimebom is a new pharmaceutical treatment alternative for patients suffering from Alzheimer’s Disease.   Dimebon is an older medication that has recently been discovered to be most helpful in treating patients with Alzheimer’s disease.   Dimebom (the actual drug is known chemically as Dimebolin) is an older  Russian antihistamine drug.  It was popularly used in Russia as an antihistamine for hayfever, allergies and the like.  In fact the drug was sold as an easy to obtain antihistamine – sold over the counter without a prescription.

Dimebom is currently in clinical trials in the United States by a company named Medivation .    The website for Medivation, the pharmaceutical company involved with the clinical development and testing of Dimebom in the United States? Can be found at link   www.medivation.com .   To learn more about Medivation’s clinical trials of Dimebom the link is

http://www.medivation.com/pipeline_dimebontrials.html#p3

For more information on CONNECTION study locations, eligibility and enrollment, please visit www.connectionstudy.com or call toll-free 1-877-888-6386

At this point in time Dimebom is not available in any manner to Alzheimer Patients or their families, outside of the study material afforded by the Medivation Company and the Medivation clinical trials themselves.

Dimebon Alzheimer?s Disease

http://www.dimebonalzheimers.com