Ten years ago people talked confidently of stopping Alzheimer’s disease in its tracks. Now, they realise they have no idea how to do that

DRUG companies are notoriously secretive. The clock starts running on a patent when it is filed, so the longer something can be kept under wraps before that happens, the better for the bottom line. You know something is up, then, when a group of these firms announce they are banding together to share the results of abandoned drug trials. And on June 11th several big companies did just that. They publicised the profiles of 4,000 patients from 11 trials so that they could learn from each other’s failures. An act of selflessness, perhaps, but also one of desperation.

Alzheimer’s disease is one of those things that policymakers would rather hide from. It is, perhaps, the classic illness of old age. Physical frailty is expected, and can be coped with. Mental frailty is much scarier for the sufferer and more demanding for those who have to look after him. It is expensive, too. Alzheimer’s is estimated to cost America alone some $170 billion a year. And it is getting commoner as average lifespans increase. The number of people suffering from the disease is expected to triple by 2050. Effective treatments would thus be embraced with enthusiasm by sufferers and society alike. The right Alzheimer’s drug could earn a drugmaker a lot of money. The incentives are there. But the science has still failed to deliver.

At the turn of the century, Alzheimer’s research seemed promising. A flurry of drugs which treated symptoms of the disorder had just hit the market and researchers were setting out confidently on a deeper investigation of its causes. Understanding those, they felt sure, would result in a cure. It still might, but the truth is that the hoped-for understanding has not come. As a consequence, a long list of would-be cures have failed in late-stage clinical trials, at enormous cost to the companies producing them. The latest of these, Dimebon, made by Pfizer, was abandoned as recently as March, after $725m had been spent on research and development.

Beta testing

The problem of what causes Alzheimer’s is profound. The physical manifestations of the disease that Alois Alzheimer noticed in 1906 are sticky plaques of one type of protein, now known as beta-amyloid, and nerve-cell-engulfing tangles of a second type, called tau protein. Since 1991 the smart money has been on the hypothesis that the disease is caused by the plaques, and that the tangles are mere consequence. For the past two decades, therefore, most attention has been given to developing drugs that will remove amyloid plaques from an affected brain. Five drugs that do this are on the market, but they only delay the onset of dementia. Once their effectiveness has run its course, memory loss and cognitive decline progress unimpeded, and sometimes even accelerate.

Partly as a consequence of this, the plaque theory is waning. Most researchers still believe beta-amyloid is the culprit, but the idea that free-floating protein molecules, rather than the proteins in the plaques, are to blame is gaining ground. This idea is supported by a study published in April in the Annals of Neurology, which showed that mice without plaques, but with floating beta-amyloid, were just as weakened by the disease as mice with both. If that is true in people, too, many more drugs now in clinical trials may prove to be ineffective.

Another fundamental problem is that, whatever is causing the damage, treatment is starting too late. By the time someone presents behavioural symptoms, such as forgetfulness, his brain is already in a significant state of disrepair. Even a “cure” is unlikely to restore lost function. A biochemical marker that indicates the progress of the disease would thus help identify those for whom early action would be advisable, and might help to distinguish people with Alzheimer’s from those with the less hostile forms of forgetfulness that tend to come with old age. Such a marker would also benefit the organisers of clinical trials. They would be able to see more easily whether a drug was working.

To this end, the Alzheimer’s Disease Neuroimaging Initiative (ADNI), established by America’s National Institutes of Health (NIH) in 2004, is measuring the levels of certain proteins in the cerebrospinal fluid of people who may have Alzheimer’s or may go on to develop it. Though the project still has a long way to go, it has already helped develop a test to diagnose the early stages of the disease.

ADNI’s anagram DIAN, the Dominantly Inherited Alzheimer Network, based at Washington University in St Louis, is taking another approach to the biomarker question. Its researchers are studying families with a genetic mutation that triggers the early onset of Alzheimer’s. That terrible knowledge means it is possible to predict which members of a family are destined to get the disease, and compare their biochemistry with that of relatives who do not have the mutation.

It is hard pounding, however, and—as the drug companies’ confession suggests—it is the “R” rather than the “D” of research and development that needs to be emphasised at the moment. A bad time, then, to be cutting back on “R”. That tripling of future sufferers is going to be expensive. Yet Alzheimer’s research, on which the NIH spent $643m in 2006, is to receive only $480m in 2011. It has not been singled out for these cuts. They are part of a general belt-tightening at the agency. But in this as in everything, you get what you pay for. And that might, in the future, be an awful lot of witless, wandering elderly.

http://www.dimebonalzheimers.com/

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Pfizer announced Wednesday that Dimebon, a drug that had initially proven promising in treating Alzheimer’s, failed in its latest study.  Pfizer partnered with Medivation Inc. to develop the drug.

Dimebon trial failed to effectively treat Alzheimer’s

Dimebon was studied to see if it could improve patients’ ability to think and operate on a daily basis.  The drug was tested over a 6 month period, and it was tested on patients with mild to moderate Alzheimer’s disease. The trial studied 598 patients from multiple countries.  When compared with the placebo, the drug showed no significant benefits.

Dimebon proved promising in previous, smaller trials

Dimebon proved successful in earlier, smaller trials conducted with Russian patients.  Pfizer hoped that further tests would result in an effective drug that could not just treat symptoms, but either stop or reverse the mind crippling disease.

Effective Alzheimer’s drug remains elusive

Finding an effective Alzheimer’s drug has proven elusive for drug makers.  Myriad Genetics and Neurochem have also worked to develop Alzheimer’s drugs.  Within the last three years, those drugs also failed in late stage trials.

Pfizer, which has offices in New York and New Jersey, says that Dimebon has not been fully discounted. Currently, the pharmaceutical is conducting four other Dimebon trials.

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The medication? Razadyne was originally made from daffodil flowers using the very same extract that soldiers in ancient Greece used to stay alert on the battlefields.?? The drugs commercially available of Razadyne currently use a synthetic version or variant of this initial compound.

Radazyne not only blocks cholinesterase in the same way that the Alzheimer’s drug Aricept does but also and in addition stimulates the brain’s? nicotine and nicotinic receptors.? The nicotinic receptors in the brain serves the brain functioning and are involved in attention and learning facilities and functions and functioning.

Originally researchers had hoped that this double pharmacological actions would serve to double the drug’s benefits in treatment as well.

However clinical trials of Rasadyne ( chemically or generically galantamine) have not borne this out as well.

As a general guideline and measure Razadyne is generally held to be as effective in the ranges as that of Aricept.

Dimebon Alzheimer?s Disease

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Aricept was approved by the FDA for treating severe Alzheimer’s patients making it one of the few drugs indicated for all three stages of Alzheimer’s disease

Three preliminary studies have indicated and reported that patients who take Aricept have slightly less Alzheimer’s related loss in brain volume and volumes than those not being prescribed and taking the medication

A major three year study by the National Institutes of Health found that Aricept helped delay dementia for about eighteen months in patients with MCI.? At thirty six months, only a small subset of participants maintained these benefits. those with APOE4 gene , which increases a person’s risks of developing Alzheimer’s.

Aricept is one of the few CHeI studied exclusively in elderly African Americans with Alzheimer’s who had a similar response to others.? But because ethnic groups metabolize some drugs differently scientists view drugs in diverse ethnic groups more favorably.? At present most of the FDA approved meditations have been studied in Asians as well as Latin American ethnic groups.

Dimebon Alzheimer?s Disease

http://www.dimebonalzheimers.com

Aricept can be said to have been studied longer , and in more patients two similar medications or so that are in present medical and pharmaceutical use.? Aricept is the easiest to use of the pharmaceutical choices and is often noted as being the best tolerated by patients over the alternative treatments.?? Aricept clears more slowly than the other drugs from the body.? Shorter half lives or longer half lives for drugs have both good and bad points in consideration of the treatment choice for the specific patient and treatment plan in view.

Compliance ( the percent of the time that patients take the medication as prescribed or recommended? properly as described is estimated generally at 50 %).??? The “studies”? show and demonstrate that little can be done to improve compliance levels of drugs, other than making the treatment regime easier? and less complex , or to tie in the taking of the pills , tablets , liquid or whatever the form the medication is in? with a daily habit of the patient – say a meal or shaving time in the morning.?? The other way to enhance compliance is to make the regimen simpler – say for example by making the medicine choice 2 times a day instead of 4 times a day.

With medications with a longer half life if the patient does mean taking a dose, there is still some drug or drug levels left in the body.Hence the drug will stay be in the body and serum to some level .? This is an advantage for the drug Aricept.? On the other side of the fence if side effects are a problem these side effects will last longer and take a longer time to clear.? Often though one way of dealing with this is to start with lower dosages initially in the first time periods.? On top of that patients can often get “used to a drug”? taken this way , starting off with lower dosages rather than blasting the patient from the beginning.? Started at lower levels and dosages initially patients can often be treated with medications and medication dosages that side effects would limit otherwise. On top of that most Alzheimer patients are being treated with a range of multitude of different drugs and medications already whose side effect interactions are often unstudied or unknown or both.

Only one dose of the drug Aricept is needed as a standard dose per day.? Its a fairly simple regimen.? Aricept as a result is widely used for Alzheimer’s patients.? Its benefits for Alzheimer’s patients can last up to a year.

Dimebon Alzheimer?s Disease

http://www.dimebonalzheimers.com