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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 Dimebon Dimebolin Information Availability

]]> http://dimebonalzheimers.com/1238/alzheimers-disease-alzheimers/feed/ 0 http://dimebonalzheimers.com/1213/dimebon-alzheimer%e2%80%99s/ http://dimebonalzheimers.com/1213/dimebon-alzheimer%e2%80%99s/#comments Thu, 26 Apr 2012 11:44:41 +0000 admin http://dimebonalzheimers.com/?p=1213
A new Canada Rx treatment alternative for Alzheimer’s is now available at Big Mountain Drugs, a reputed online Canada pharmacy. Dimebon, or Dimebolin Hydrochloride, as its generic name states, is an antihistamine drug which protects brain cells from continued degeneration and damage. Dimebon is also used to treat Huntington’s disease. As Alzheimer’s is a disease [...]



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A new Canada Rx treatment alternative for Alzheimer’s is now available at Big Mountain Drugs, a reputed online Canada pharmacy. Dimebon, or Dimebolin Hydrochloride, as its generic name states, is an antihistamine drug which protects brain cells from continued degeneration and damage. Dimebon is also used to treat Huntington’s disease. As Alzheimer’s is a disease caused by brain cell death, this drug’s efficacy in slowing down the brain cell damage has proved to be effective in treating AD patients.

As Dimebon is a relatively new drug to aid in Alzheimer’s, it should be mentioned that adverse reactions to the drug that are not established yet may be experienced by some people. Common adverse reactions include depression, diarreah, dizziness, dry mouth, insomnia, nausea, vomiting etc. If experiencing any severe side effects such as chest pain, blurred vision, allergic reactions, hives, severe vomiting and swelling, consulting medical attention is highly recommended.

Alzheimer’s is a slow- progressing disease, which is often, misdiagnosed in its initial stages. However, with knowledge of the symptoms and its causes, individuals stand a better chance of obtaining the correct diagnosis in order to treat Alzheimer’s disease. Dimebon and other Alzheimer’s medication can be ordered from bigmoutaindrugs.com or any other Canadian pharmacy at affordable prices, putting AD treatment within the reach of even the low income retired patients.

http://psychsources.com/new-drug-dimebon-for-alzheimers-disease-2/

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  Dimebon Dimebolin Information Availability

]]> http://dimebonalzheimers.com/1213/dimebon-alzheimer%e2%80%99s/feed/ 0 http://dimebonalzheimers.com/1210/alzheimer%e2%80%99s/ http://dimebonalzheimers.com/1210/alzheimer%e2%80%99s/#comments Sun, 22 Apr 2012 11:43:16 +0000 admin http://dimebonalzheimers.com/?p=1210
Dementia is a brain disorder which severely impairs a person’s memory, thought processes and function. Alzheimer’s is a disease which ranks high in the dementia list. It is believed that Alzheimer’s is a cause of a genetic mutation. This is the increase in beta-amyloid protein, which causes the death of nerve cells in the brain. [...]



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Dementia is a brain disorder which severely impairs a person’s memory, thought processes and function. Alzheimer’s is a disease which ranks high in the dementia list. It is believed that Alzheimer’s is a cause of a genetic mutation. This is the increase in beta-amyloid protein, which causes the death of nerve cells in the brain. There is no exact reason as to why this disease affects only the elderly. The propensity for the elderly people to suffer from AD is linked with the natural degeneration process of brain cells. However, this does not mean that all elderly people are affected with Alzheimer’s. Those with predisposition towards the condition will experience the disease as the natural aging process weakens the brain functioning.

Symptoms of Alzheimer’s

The most common symptom of Alzheimer’s is memory lapse. Most often memory lapse is dismissed as normal behaviour of the elderly. However, the severity of memory loss associated with AD is much greater than age related memory loss. People with AD will keep forgetting their names, where they live, the incidents and activities they just encountered minutes ago, and even the names of family members. Personality changes and the inability to interact socially are other symptoms of Alzheimer’s. The memory lapse continues as the disease progresses and the degeneration of the brain accelerates. After a while, a person with Alzheimer’s disease will be unable to function in the normal world. Confusion, disorientation and total inability to care for themselves is common when the disease is at its zenith. If neglected, aggravated health conditions resulting from pneumonia or another form of debilitating state of health is the conclusion to this disease as persons become home bound due to the illness.

http://psychsources.com/new-drug-dimebon-for-alzheimers-disease-2/

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  Dimebon Dimebolin Information Availability

About the study

HORIZON was a phase 3 clinical trial primarily looking at the effect of dimebon (latrepirdine) on cognitive function in mild-to-moderate Huntington’s disease. It was the first large clinical trial to focus on the cognitive aspects of HD and was a global collaboration between the European Huntington’s Disease Network (EHDN) and Huntington Study Group (HSG), supported by Medivation Inc, and Pfizer Inc.

Latrepirdine (dimebon) is an antihistaminic drug that was first used to treat allergies in the 1980’s. Recently, latrepirdine has been shown to enhance sur­vival of brain cells and improve learning and memory in early phase studies of Alzheimer’s disease (AD) and Huntington’s disease (HD).

The HORIZON trial aimed to compare dimebon 20mg three times daily with placebo (no drug) and was double-blind, so neither investigator or participating subjects knew which treatment arm they were assigned to. The following global regions took part in the HORIZON trial:

• North America (30 sites)
• Australia (3 sites)
• Europe (26 sites; 8 countries)

Unfortunately in April 2011, it was announced that Dimebon had failed to demonstrate improvement in thinking and memory among study participants taking Dimebon 60 mg/day.

http://hdresearch.ucl.ac.uk/all-studies/horizon-dimebon-trial/

For Sale

Dimebon

A potential Alzheimer’s drug that had seemed to perform spectacularly well in a medium-scale clinical trial has now been shown in a larger and more conclusive trial to have no apparent effect on the disease.

The surprising failure of the drug, known as dimebon, is yet another disappointment for Alzheimer’s researchers as well as patients and their families. It also raises questions about the conduct and design of Alzheimer’s clinical trials, particularly in Russia where the initial dimebon trial took place.

“The prior doubts about the Russian trial appear to have been borne out,” says Sam Gandy, an Alzheimer’s researcher at Mount Sinai School of Medicine.

Dimebon (generic name latrepirdine) was originally developed and briefly used as an antihistamine in Russia in the 1980s. It began to be re-evaluated as a potential Alzheimer’s drug in the 1990s, after Russian researchers reported that it seemed to boost the levels of memory-related neurotransmitters in lab tests on brain cells.

A San Diego-based company, Medivation, Inc., eventually began clinical trials of dimebon in Russia, where the drug was already approved for use. In 2008, astounding results were reported in 183 Russian patients whose Alzheimer’s dementia was classified as “mild-to-moderate.” Half had received dimebon at a dose of 20 mg thrice daily, and half had received a thrice-daily placebo. After six months, the dimebon group scored much higher on standard tests of cognition and quality of life, and follow-up studies suggested that the progression of the disease had been stopped. The apparent “treatment effect” was the largest ever reported for an Alzheimer’s drug trial.

Some researchers expressed concern that such a powerful result was too good to be true, particularly since no one really knew how dimebon worked against Alzheimer’s. However, several well-known U.S. clinical trial experts had observed the Russian study and vouched for its validity. Other researchers soon reported evidence from laboratory studies that dimebon might be able to boost the general survival ability of neurons in a way that could make them resistant to other neurodegenerative diseases too (see “Hope and Caution on Russian Antihistamine Drug for Alzheimer’s”).

Unfortunately, dimebon seemed only weakly effective in a small-scale clinical trial in people with Huntington’s disease; its results were reported in February. And on March 3, dimebon’s candidacy as an Alzheimer’s drug was most likely terminated.

On that day, Medivation reported results from a large, apparently definitive trial of dimebon in 598 people with Alzheimer’s in North America, South America, and Europe. Those results suggest that dimebon, while safe, is completely ineffective against Alzheimer’s disease. The data failed to show even a hint of a consistent impact on patients’ cognition and quality of life, compared to a placebo.

In recent years, a number of Western drug companies have used Russian hospitals as a relatively inexpensive proving ground for early-stage drug development. However, in at least one other case, a positive result from a Russian trial has failed to translate to a larger, more rigorous Western trial.

Gandy says he wonders whether “something is systematically wrong over there.”

In the case of dimebon, not only the early clinical trial results but also a significant amount of laboratory work appears to be of questionable value. Over the past few years, researchers who were eager to find dimebon’s mechanism of action against dementia have reported, for example, that it blocks the toxicity of amyloid beta aggregates found in Alzheimers, or that it enhances the survival of mitochondria. If nothing else, the case underscores the weakness of such laboratory evidence in the absence of data in people that confirms it.

“At the moment I don’t think that any of these effects is clinically important,” said Gandy, whose own research group recently found that dimebon actually increases amyloid beta levels outside cells, in lab dish and animal experiments.

To some researchers, the dimebon failure, and the failure of many other Alzheimer’s drug candidates to date, points to a larger problem:  The treatments are started too late in the course of the disease.

“What you want in such trials are people who are just starting to lose neurons, but typically by the time an Alzheimer’s patient goes to see a neurologist, his or her brain has already been severely damaged,” says Jeffery Kelly, an investigator at the Scripps Research Institute in La Jolla, California, whose work has focused on amyloid-associated conditions. “Considering the way the Alzheimer’s trials are being done now, I’m not sure that even a great drug could be discerned as such.”

Gandy agrees:  “I think that our best chance for impact on this disease is presymptomatic intervention and prevention.”

http://www.dana.org/news/features/detail.aspx?id=25798

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We now know that even old people continue to create new brain cells. But these new neurons die off as we age. Scientists may be on the brink of discovering a compound to prevent brain cell death, offering the promise of treatment for Alzheimer’s.

Or, to be precise, the so-called dentate gyrus in the hippocampus region of their brains.

The hippocampus is associated with memory, and the dentate gyrus is one part of the brain that generates new neurons, or nerve cells — the little building blocks that get wired into the mind’s complicated circuitry.

Pieper, a biochemist at the University of Texas Southwestern Medical Center, had the “very tedious” task of detecting those new neurons, employing a series of antibodies to help amplify their telltale signal.

He found a great many nascent neurons, and this is very good news.

Until the 1960s, the received wisdom was that once you became an adult, you had your full complement of brain cells. Hence your mother’s stern warnings about protecting the only brain cells you’d ever have.

We’ve since learned that all mammals, including humans, give birth to new brain cells throughout their lifespan. But not all of those cells survive to become fully fledged neurons.

Somewhere along their journey to getting wired into the brain, they essentially commit suicide, a process called apoptosis, or programmed cell death.

For the most part, this is just the natural state of affairs. Biology isn’t always efficient, discarding much of what it builds. Human embryos, for instance, wouldn’t develop fingers if the cells between their digits didn’t go through apoptosis.

The trouble is, as we age, the rate of programmed cell death in the brain increases. More and more of those new cells simply don’t make it through the 30-day process of becoming fully connected neurons.

In effect, our brains lose some of their ability to repair themselves.

This, however, wasn’t what Pieper was seeing in Room K3.406.

The relative multitude of new neurons that he eventually detected were the product of mice whose brains had been treated with a chemical compound dubbed P7C3 or, in subsequent tests, a derivative of P7C3 that proved even more effective.

The drug wasn’t making the mice produce more cells, but it was somehow protecting more of those cells from apoptosis.

“Instead of 70 or 80 per cent dying along the route, only 40 or 50 per cent are dying,” says Steven McKnight, another University of Texas biochemist who worked on the study, published last month in the journal Cell.

This could have profound implications in treating what for many is the most terrifying brain disease associated with old age: Alzheimer’s.

And if there’s a research community that could use a dose of very good news, it’s the Alzheimer’s crowd.

Roughly 500,000 Canadians over the age of 65, about one in 11, now suffer from dementia, more than half of those as a result of Alzheimer’s disease.

By 2038, the number of people with dementia is projected to more than double as the huge baby boom generation moves squarely into its sunset years. (In Canada, the oldest baby boomers turn 63 this year, while those at the absolute peak of the boom are turning 49 and 50.)

Put another way, within a generation, roughly one in three Canadian households will have an extended family member suffering from dementia.

Progressive and ultimately fatal, Alzheimer’s can be as emotionally draining for family members as it is confusing and debilitating for those afflicted with the disease.

The other dispiriting fact is how research into Alzheimer’s is so far adhering to the old undergraduate mantra: the more we discover, the more we realize how much we don’t know.

First described in 1906 by a German psychiatrist Alois Alzheimer, the disease kills off neurons and the connections between them, resulting in the familiar loss of memory and language skills.

As Alzheimer’s moves to other parts of the brain, confusion, mood swings, irritability and social withdrawal often ensue.

Two proteins, beta amyloid and tau, have so far been identified as the leading culprits in bringing about the death of cells. Both proteins occur naturally in healthy brains — even if the precise role of beta amyloid is uncertain — but something happens to tilt the balance.

Enzymes normally help clear away excess beta amyloid. In the brains of Alzheimer’s patients, however, beta amyloid molecules start sticking together to form toxic clumps and, eventually, larger agglomerations called plaques.

Tau is a bit trickier in that it normally performs some essential tasks, such as maintaining what amounts to the transport system that ferries needed chemicals between the body of the cell and its nerve endings.

With Alzheimer’s, the tau instead starts to pile up in thread-like tangles, effectively choking the cell to death.

Many researchers believe beta amyloid also plays a role in developing these tangles, that it has a sort of cascading effect.

But with Alzheimer’s, things can get complicated in a hurry.

For instance, a vaccine now in trials may help reduce the amount of beta amyloid, but past research has already thrown up a maddening paradox. Some otherwise normal elderly people have just as many plaques as Alzheimer’s patients but show no signs of dementia.

Conversely, the march of dementia can continue unabated even in cases where the beta amyloid has been successfully reduced.

“We’re at a crossroads in our understanding,” says Dr. Jack Diamond, scientific director at the Alzheimer Society of Canada and a professor emeritus in psychiatry and behavioural neuroscience at McMaster University. “This has opened up areas that we didn’t know about before.”

Diamond now believes that the emphasis on beta amyloid may have been too great — that the death of neurons is ultimately caused by a far more complex array of factors, a lot of which have to do with something called oxidative stress.

Just as any engine produces heat as a by-product, a cell’s natural metabolism produces oxygen radicals — molecules dubbed “reactive oxygen species,” or ROS.

Sometimes, ROS is used by the immune system to kill off invading organisms, but mostly ROS gets flushed from the system by enzymes and anti-oxidants.

The bad news happens when ROS starts to accumulate much faster than the body can dispose of it, overwhelming the body’s natural ability to repair and heal itself.

The risk factors thought to bring an overabundance of ROS are many and varied. But they just happen to overlap with what we know to be the risk factors for Alzheimer’s itself, from diet and lifestyle to the effects of menopause (see sidebar).

If that’s the case, then there is no single “cause” of Alzheimer’s, but instead an array of risks that eventually pass some crucial threshold and start killing off neurons in the brain.

The corollary is that treating and preventing Alzheimer’s will have to involve just as many fronts.

“We’re pretty sure that, in the end, it’s going to be a combination therapy,” says Diamond. “There isn’t one magic bullet here.”

But, just maybe, part of the needed arsenal may flow from what Andrew Pieper was spying in that little cubbyhole in Dallas.

That the promise of P7C3 would surface at the University of Texas involves a kind of poetry, gleefully defying the odds.

Dallas is slightly off the beaten track, at least compared with the massive medical clusters in places like Toronto and Boston. But more than anything, it’s the way Pieper and McKnight went about their studies, which is nothing short of retro.

Most drugs these days get developed through a highly rational process that essentially takes what we know about existing chemicals and how they operate, and then refines that to hit a certain target in a specific way.

You come up with a hypothesis based on what you know, then you test it.

Pieper and McKnight didn’t work that way. Theirs wasn’t so much a leap of faith as a kind of blind leap to a more or less unknown destination.

Over the years, the University of Texas has built up a library of roughly 200,000 chemical compounds. So, within certain parameters, McKnight and Pieper simply asked their chemist colleagues to come up with a representative sample of 1,000 compounds.

Then they bunched the chemicals together in batches of 10 and started injecting them into the brains of lab mice to see what effect they had on neurogenesis, the development of neurons.

If a batch showed promise, then they’d test again with the individual chemicals.

In other words, they did old-fashioned in vivo screens, running tests on whole, living organisms, in this case mice and later rats.

“I guarantee you, people were laughing at us,” says McKnight. “I mean, our own colleagues.”

“Not even behind our backs,” adds Pieper.

As it happens, the pair stumbled on the effects of P7C3 early on. It was compound 63, showing up first in mice 13 and 14, since two mice received each batch of 10 chemicals.

This was a kind of double bonus, since the odds of P7C3 showing up at all in the representative sample — and then being singled out early on — were slight to vanishing. It was a needle in a haystack.

Nor did P7C3 (an aminopropyl carbazole for the chemists keeping score at home) have precisely the desired effect.

They were actually hoping to find a drug that would increase the creation of new cells. “That was our bias,” says McKnight. “And yet, in the end, the compound doesn’t affect the rate of birth at all.”

Instead, it greatly improves the life expectancy of whatever new cells are created. There is, curiously, an upside to this unexpected result.

“Usually, if you get what you’re not looking for, the likelihood that it’s right is better,” says McKnight. “If you get what you’re looking for, you gotta worry as scientists.”

The drug world, after all, does have a minor tradition of discovering unexpected benefits. What we now know as Viagra started out as a drug directed at the heart to lower blood pressure, but it had an embarrassing effect on patients taking it in trials.

Or, as McKnight likes to say, the researchers “missed by about a foot and a half.”

He and Pieper didn’t get exactly what they were looking for, either, but turning their discovery into a useable drug may require another dose of luck. Pharmaceutical companies tend to like certainty, and some big unknowns still surround P7C3.

For starters, precisely how P7C3 manages to protect newly forming neurons is a mystery.

McKnight and Pieper suspect the chemical preserves the integrity of mitochondria, which are sort of little organs or “organelles” inside the cell.

Mitochondria are akin to power plants, since they generate most of a cell’s chemical energy. They also control a cell’s growth cycle and, ultimately, give the signal that initiates apoptosis, or programmed cell death.

But figuring out exactly how P7C3 affects mitochondria at a molecular level could take months, or years.

Nor do Pieper and McKnight know whether P7C3 can stop an existing neuron from dying, although experiments are underway to test that. “It would be wonderful if it did,” says McKnight.

This could have implications well beyond Alzheimer’s, and include potential treatments for Huntington’s disease, Lou Gehrig’s disease and even the effects of traumatic head injuries.

But there is only so much McKnight and Pieper can do in an academic setting to push P7C3 toward becoming a drug that humans can take. And they’ve already spent somewhere between $5 million and $7 million working on the chemical.

“We want to hand it off to a pharmaceutical company, but we’re not in the charity business,” says McKnight. “We’d like to have the school compensated if anything came out of it.”

Ironically, though, one of the biggest stumbling blocks is something that, until earlier this year, was being hailed as the most promising drug in the treatment of Alzheimer’s: Dimebon.

Dimebon started life as an everyday antihistamine in Russia, used to treat allergies and hay fever. Until, that is, people started noticing how Dimebon seemed to help Alzheimer’s patients, apparently by enhancing the survival of brain cells.

Such was the drug’s promise that Medivation Inc., backed by the pharmaceutical giant Pfizer Inc., has been busy nursing it through all the tests and trials needed for approval by the U.S. Food and Drug Administration.

Then, last March, came Medivation’s announcement that in advanced trials, Dimebon had proved no more effective than a placebo. The company’s shares tanked 68 per cent on the news.

Further trials are underway, but the word Dimebon has itself become toxic, which is highly problematic for McKnight & Co.

Their own tests have shown P7C3 (and a stronger derivative) to be vastly more effective than either Dimebon or another compound developed by an affiliate of Merck KGaA.

The trouble is, all three are chemically similar.

“Some people have told us, ‘You don’t want to mention that you’re anything like Dimebon,’ ” says McKnight. “But as scientists, we can’t do anything like that. That’s stupid.”

Which leaves him in the odd position of rooting for Dimebon, even though he says its effectiveness is “borderline” and only a fraction of that achieved by P7C3.

“My hope is that the Dimebon story holds water, that it’s right, because that’s what we need to get the pharmaceutical companies to go and improve (P7C3),” says McKnight.

“Once they know how to turn the crank, they can dial it up as high as they want.”

And that, metaphorically at least, is just what Alzheimer’s patients and their families have been so desperately awaiting.

Dimebon

http://www.dimebonalzheimers.com/

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Researchers have found a drug that can help the brain grow new cells, and they said their study may lead to ways to improve experimental Alzheimer’s drugs.

The researchers’ work, done on rodents, builds on findings that all mammals, including humans, make brain cells throughout their lives. Most of these die, but this drug helps more of the baby cells survive and grow to become functioning brain cells.

“We make new neurons every day in our brain,” Andrew Pieper of the University of Texas Southwestern Medical Center in Dallas who worked on the study, said in a telephone interview. “What our compound does is allow more of them to survive.”

The compound is called P7C3 for now, and the researchers have already started tweaking it to make it more effective. They said it seems safe and appears to work even when taken as a pill.

The compound is similar to Medivation and Pfizer experimental Alzheimer’s drug, Dimebon, and may provide ways to improve its effects, Pieper and colleagues reported in the journal Cell.

It is also similar to some compounds owned by Serono, the researchers said.

Dimebon, originally a Russian-made antihistamine also known as latrepirdine, failed in a clinical trial for Alzheimer’s disease in March.

“For the sake of patients suffering from Alzheimer’s disease, it is hoped that the apparently marginal clinical utility of Dimebon might be enhanced by improvements in both its potency and ceiling of proneurogenic, neuroprotective efficacy,” the researchers wrote.

“If so, our work offers concrete assays for the development of improved versions of these neuroprotective drugs.”

Alzheimer’s gradually destroys the brain and affects 26 million people globally. Drugs, such as Pfizer’s Aricept, improve symptoms only minimally.

The researchers went through 1,000 representative compounds from 300,000 chemicals, pooled them, and administered them to mice. They then dissected the brains to see whether any of the mice had made new cells in the hippocampus, a region of the brain associated with learning and memory.

They eventually narrowed the field to P7C3.

When they gave it to old rats for two months, the elderly rodents did far better than other old rats in learning their way around a water maze.

When dissected, the treated rats turned out to have three times the usual number of newborn neurons in a brain region called the dentate gyrus.

They made a derivative of P7C3 called A20 that worked even better

When the researchers tested Dimebon and the Serono compounds, they found these drugs also stimulated the growth of new brain cells. Being able to target their effects could lead to better drugs to treat Alzheimer’s and perhaps other diseases that destroy brain cells like strokes and amyotrophic lateral sclerosis, also known as ALS or Lou Gehrig’s disease.

“This striking demonstration of a treatment that stems age-related cognitive decline in living animals points the way to potential development of the first cures that will address the core illness process in Alzheimer’s disease,” said Dr. Thomas Insel, director of the National Institute on Mental Health, which helped pay for the study.

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Alzheimer’s patients, brain injury patients, and dementia sufferers may benefit from a newly discovered pill that grows brain cells. The drug, currently labeled P7C3 while it undergoes continued study, appears to provide a safe and effective option that helps support developing brain cells to become viable. Testing done on rats demonstrated that the older rats who had been dosed with P7C3 were capable of learning their way

through a maze when other rats, who had not received the drug, could not. The researchers hope the drug can be used to increase the effectiveness of Alzheimer’s drugs like Dimebon, which recently failed in clinical trials.

“For the sake of patients suffering from Alzheimer’s disease, it is hoped that the apparently marginal clinical utility of Dimebon might be enhanced by improvements in both its potency and ceiling of proneurogenic, neuroprotective efficacy,” the researchers wrote. “If so, our work offers concrete assays for the development of improved versions of these neuroprotective drugs.”

More than 25 million people currently suffer from Alzheimer’s disease, which is a progressive disease that destroys the brain until autonomic functions cease and the sufferer dies. P7C3 represents a hopeful breakthrough in research that could lend itself to other areas of brain trauma treatment, including helping people with ALS (also known as Lou Gehrig’s disease).

Dr. Thomas Insel, director of the National Institute on Mental Health, said, “This striking demonstration of a treatment that stems age-related cognitive decline in living animals points the way to potential development of the first cures that will address the core illness process in Alzheimer’s disease.” The National Institute on Mental Health helped fund the study.

The rats that were treated with the drug had three times as many developing brain cells. Researchers have since used P7C3 to create a derivative drug called A20 that shows even more promise. When the derivative was combined with Dimebon and Sereno, two test-phase Alzheimer treatments, it caused new brain cell growth stimulation.

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A pill that reverses age-related mental decline that affects three-quarters of a million people in the UK may be on the horizon as a result of research on new nerve drugs.

The studies raise the possibility of a cure for memory loss and fading mental faculties in an ageing population, according to experts who stress that a lot more work is needed to develop the early animal research.

Alzeheimer Scotland says about 65,000 people have the condition in Scotland and the number of people affected will pass 100,000 by 2029.

Scientists in the US screened thousands of compounds for their brain-protective properties. They identified one called P7C3 that had dramatic effects on ageing rats and genetically engineered mice.

The molecule spurred on the growth of new neurons in a part of the brain vital to memory, according to the research, which has been reported in the journal Cell.

It significantly improved the ability of ageing rats to swim through a water maze – a standard test of memory-dependent learning – and assisted the birth of brain cells in mice.

Further research showed that a derivative of the compound, called A20, had an even bigger impact on the brain.

The scientists are still trying to find out how the drugs work. They appear to prevent a process called apoptosis, which causes cells to self-destruct.

Thomas Insel, director of the US body that funded the work, the National Institute of Mental Health (NIMH), said: “This striking demonstration of a treatment that stems age-related cognitive decline in living animals points the way to potential development of the first cures that will address the core illness process in Alzheimer’s disease.”

A key factor is that P7C3 can be swallowed, rather than having to be injected.

Dr Steven McKnight, one of the research leaders from the University of Texas Southwestern Medical Centre in ­Dallas, said: “The neuroprotective compound, called P7C3, holds special promise because

of its medication-friendly properties.

“It can be taken orally, crosses the blood-brain barrier with long-lasting effects, and is safely tolerated by mice during many stages of development.”

The “blood-brain barrier” is a biological wall designed to prevent potentially harmful substances entering the brain.

Drugs that target the brain have to overcome this obstacle if they are to be effective.

Scientists now know that the adult brain is “plastic” and capable of regenerating itself under the right conditions.

Nerve growth in the hippocampus, the brain’s memory ­centre, can potentially stave off mental decline.

However, even in a normal brain most of the newborn neurons die during the month or more it takes them to develop and become “wired in”.

Newborn hippocampus neurons are known to fare much worse in people with age-related disorders such as Alzheimer’s, which cause the runaway death of nerve cells.

The scientists set about trying to find compounds that might protect vulnerable growing neurons in the dentate gyrus, a key area of the hippocampus.

They found that giving P7C3 to the genetically engineered adult mice reduced the death of newborn cells.

It prevented the stunted growth of branch-like neuronal extensions, and thickened an abnormally thin layer of cells by 40%.

When the compound was fed to ageing rats, they outperformed other rodents in the water maze test.

This was traced to a level of newborn neurons in the dentate gyrus of the treated animals, which was three times higher than normal.

Other compounds with structural similarities to P7C3 may also be worth investigating, said the scientists.

At least two of these have already been looked at as potential Alzheimer’s treatments. The P7C3 derivative A20 was 300 times more potent than one of these drugs, Dimebon, which failed in a Phase III patient trial, the researchers said.

They wrote: “The speculative idea that these chemicals share a common mode of action will only be rigorously tested upon identification of their molecular target.”

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A single daily pill that stops Alzheimer’s in its tracks is being developed by scientists.

The drug, discovered by sheer luck according to researchers, stops brain cells from dying, boosting their numbers and sharpening memory.

Given early enough, it could prevent sufferers from reaching the devastating final stages of the disease, in which they lose the ability to walk, talk and even swallow.

Some experts believe it could even be a cure.

Alzheimer’s and other forms of dementia blight the lives of more than 800,000 Britons, and the number of cases is expected to double within a generation.

With the death of brain cells at the core of Alzheimer’s, the breakthrough brings fresh hope.

U.S. researchers found the drug after testing more than 1,000 chemicals on mice. Dr Steven McKnight said: ‘We really didn’t know if the screen would turn up a favourable compound or not. It was blind luck.’ In tests, the drug, known only as P7C3, boosted the production of cells in a part of the brain critical to memory.

Dr McKnight, of the University of Texas Southwestern, said: ‘These mice are bad at making new neurons. The question was, “Can you fix that?” And the answer to that was “yes”.’ Not only did the new brain cells form, but they also worked properly, the journal Cell reports.

In other experiments, the drug improved memory in ageing rats, making it easier for them to find their way through a maze. Further research showed that a derivative of the compound, called A20, had an even bigger impact on the brain.

Dr McKnight and colleague Dr Andrew Pieper are still trying to find out how the drug works.

It appears to prevent a process called apoptosis, which causes cells, including many newly-formed brain cells, to self-destruct.

It also seems to give a boost to the mitochondria, the tiny batteries that power cells.

The research team hope the chemical can be turned into a once-a-day pill. Those with multiple sclerosis, Huntington’s disease and schizophrenia might also benefit. Dr McKnight said: ‘The neuroprotective compound P7C3 holds special promise because of its medicationfriendly properties.

‘It can be taken orally, crosses the blood-brain barrier with long-lasting effects, and is safely tolerated by mice during many stages of development.’

The blood-brain barrier is a biological ‘wall’ designed to prevent potentially harmful substances entering the brain.

Thomas Insel, director of the U.S. body that funded the work, the National

Institute of Mental Health, said: ‘This striking demonstration of a treatment that stems age-related cognitive decline in living animals points the way to potential development of the first cures that will address the core illness process in Alzheimer’s disease.’

But the development of an effective pill does not bring with it a guarantee of treatment on the NHS, with current drugs severely rationed.

One, Aricept, costs just £2.50 a day but is rationed to those with ‘ moderate’ illness.

Rebecca Wood, of the Alzheimer’s Research Trust, said: ‘Any research that moves us towards a way of preserving the life of cells in the brain is worthy of attention. Steps must now be taken to research whether the compound can be used beneficially and safely in people.’

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