March 5, 2010 by mike.

Newswise — Researchers at the University of Nebraska Medical Center have taken a significant step forward in developing a vaccination approach to reverse the neurological damage seen with Parkinson’s disease.
The findings appear in the March 1 issue of the Journal of Immunology, a leading scientific journal in the field of immunology.
The cause of Parkinson’s disease is the loss of neurons which produce dopamine, a nerve signaling chemical that controls movement and balance. The Parkinson’s Disease Foundation estimates that about 1 million people in the United States and more than 4 million people worldwide have the disease.
Degeneration and loss of these dopamine-producing neurons typically occur after age 60, and it is estimated that one person in 20 over the age of 80 has Parkinson’s.
Neurodegeneration occurs when a normal protein called alpha synuclein clumps, changes shape, then accumulates in the brain. This results in the body attacking it through inflammation and causing destruction of dopamine-producing nerve cells.
In the study, researchers reversed the neurodegenerative effects of alpha synuclein by changing immune responses to it. The vaccine strategy trains the immune system for eliciting neuroprotective responses in damaged brain regions.
In mice with an experimental form of Parkinson’s disease, injection of the vaccine produced cells that were able to reverse the disease. After receiving the treatment, these mice were found to have a similar number of dopamine-producing nerve cells and fibers as mice without Parkinson’s.
“We believe this could be a revolutionary means for Parkinson’s disease therapeutics,” said Howard Gendelman, M.D., who partnered with R. Lee Mosley, Ph.D., to lead the research. “It has been a long journey representing more than 10 years of hard work by our research team.”
The researchers found that the vaccine enabled T cells in the treated mice to migrate to the damaged area of the brain and triggered a neuroprotective response that reduced disease-linked reactions in the brain.
T cells are white blood cells that are of key importance to the immune system and are at the core of adaptive immunity, the system that tailors the body’s immune response to infectious organisms. The T cells act like soldiers who search out and destroy the targeted invaders.
“The identical immune deficits seen in mice are being looked at in humans with Parkinson’s disease,” Dr. Mosley said. “Early results are encouraging. This should pave the way for researchers to begin follow-up studies on the Parkinson’s treatments and open up new opportunities to realize an immunization approach for other neurodegenerative disorders such as Alzheimer’s disease and amyotrophic lateral sclerosis (Lou Gehrig’s disease).”
Dr. Gendelman said additional work is needed to determine how to translate the study results into a therapy for humans and to make sure the treatment is safe for patients.
Human studies are being conducted at the University of Alabama-Birmingham and within the next month at UNMC to determine if the immune deficits seen in mice also are present in humans with Parkinson’s disease. Such studies are required before vaccine trials are performed in humans, Dr. Gendelman said. This phase of the research is being made possible through funding from the Shoemaker Foundation in Nebraska.
James Linder, M.D., CEO of UNeMed, UNMC’s technology transfer company, said UNeMed has filed a patent application on the vaccine and will soon commence discussions with commercial partners on bringing the vaccine to the clinical setting.
Dr. Gendelman is professor and chairman of the UNMC Department of Pharmacology and Experimental Neuroscience (PEN). Dr. Mosley is associate professor in the PEN department. They teamed with three graduate students, Ashley Reynolds, Ph.D., David Stone and Jessica Hutter, who were responsible for performing the study and analyzing its results.
What others are saying:
“Dr. Gendelman and his team are to be congratulated for their important insights as to why dopamine-producing cells die and how to rescue these cells, which are the pathological hallmark in Parkinson’s disease. This seminal work is extremely significant since it provides a cogent rationale for immune-based strategies in human Parkinson’s disease and a unique and important opportunity to develop novel neuroprotective therapies.” — Stanley Appel M.D., chairman, neurology, Methodist Neurological Institute, Houston
“I think this work is really important. The studies in this new report, along with other data from the Gendelman group, our own lab, and others are leading to a completely new way of thinking about the role of immunity in PD. The new information points to a central role of the immune system as a causative element of the Parkinson degenerative process.
“This work leads to the idea that it might be possible to develop a vaccine which could alter immune responses in human PD and slow or prevent the progression of Parkinson’s disease. This concept would most likely have been dismissed as a ‘crazy idea’ just a few years ago, but these studies put the proposal on solid scientific footing. If we can confirm Dr. Gendelman’s findings in humans, this would open the door to an important new class of therapies for Parkinson’s disease.” — David Standaert, M.D., Ph.D., professor and vice chair, neurology, University of Alabama at Birmingham (UAB), who is collaborating with Dr. Gendelman by studying T cell functions in Parkinson’s patients
“This discovery has the potential to impact millions of people affected by Parkinson’s disease. We are very enthusiastic about finding a company to help bring this technology through the clinic.” — Michael Dixon, Ph.D. president, UNeMed Corporation, technology transfer company for UNMC
“As a treating physician, using medications or surgical interventions to manage the disabling symptoms of Parkinson’s disease is rewarding. But having the possibility to alter the course of the disease would be revolutionary. The successful approach to a vaccine in a mouse model of Parkinson’s disease opens new treatment horizons. If eventually proven to have similar effectiveness in humans, such a vaccine could dramatically change what can be done about Parkinson’s disease. I am proud of our efforts at UNMC to treat and find a cure for Parkinson’s disease and other movement disorders.” ¬Diego Torres-Russotto, M.D., assistant professor, neurological sciences, and director of UNMC Movement Disorders Program

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February 25, 2010 by mike.

BY TOM BLACKWELL, NATIONAL POST WITH FILES FROM CANWEST NEWS SERVICE

A decade ago, Michael J. Fox predicted Parkinson’s — the disease that has afflicted him for 17 years — would be cured in 10 years. No such breakthrough is close, but new research at the University of Windsor could halt its advance.

Each time University of Windsor graduate student Katie Facecchia sees the B.C-raised actor on television, talking about his life-and-death battle with Parkinson’s disease, she “can’t help but think — just hang on, there’ll be something soon.”

Ms. Facecchia is part of a team of researchers from the school’s biochemistry and psychology departments, led by Prof. Siyaram Pandey, who believe they have made a research breakthrough that laboratory tests have proven halt the advance of Parkinson’s.

Prof. Pandey said the treatment is a water-soluble formulation of the natural chemical compound — coenzyme Q10 — that stops further degeneration of neurons in the brains of lab rats.

The currently non-curable neurodegenerative disease is caused by the death of brain cells that produce dopamine, a chemical that carries signals between the nerves in the brain that control movement.

The “Co-Q10” compound cannot reverse the damage, cautioned Prof. Pandey, but he said it can halt its progression.

“As the disease progresses, the neurons die at a faster rate,” said Prof. Pandey, “Usually, by the time it’s diagnosed, 50 per cent of the neurons are gone. The only treatment now is for the symptoms, but the dosage has to always be increased, because the neurons continue to die. If we can protect those neurons that are left over, it could lead to a normal life.”

He said the research so far has “shown amazing results . . . the near-complete protection of brain cells.”

The findings have been published in the academic journal BMC Neuroscience, and the team has begun collaborating with a pharmaceutical company based in New Jersey, Zymes LLC.

Prof. Pandey said he hopes their research will proceed to clinical testing soon.

“We’re still at the pre-clinical stage,” he said. “But the results are promising.”

Mr. Fox officially launched his research foundation in Canada on Thursday, saying he still wakes up every day believing the illness will be beaten during his lifetime, but now recognizes the advances will come in small, often unspectacular steps.

“I have learned that 99% of progress is failure,” said the 47-year-old former star of TV and movies.

“You’re not so much proving things as disproving things, and that is a fundamental part of it,” he said. “The brain is like space, like the depths of the ocean: it’s this frontier we just don’t understand … I’d love to get the answers, but if we can find the right questions, that’s just as important for me and just as exciting.”

He later suggested that scientists will have figured out the disease within 30 or 40 years, “if not a lot sooner,” but said he was not driven by a desire to find a cure for himself.

“People have a hard time believing this — [but] I sometimes forget that I’m even affected by this,” he said. “I want to enable and empower those who have the intelligence and the knowledge and the wherewithal to solve the problem .”

Throughout a 20-minute news-conference appearance in Toronto, Mr. Fox swayed back and forth under the disorder’s influence, his hands clenching the table in front of him and his voice faltering at times, but kept his audience rapt with often-witty responses.

The Michael J. Fox Foundation — which has dispersed $150-million in the United States, Canada and elsewhere since its founding in 2000 — has just been given charitable status in Canada, a fact that Mr. Fox said meant a lot to him as a Canadian.

He and the foundation’s CEO, Katie Hood, heaped praise on the event’s co-hosts, the McEwan Centre for Regenerative Medicine — cutting-edge stem-cell researchers — and Toronto Western, which Ms. Hood called one of the world’s hotbeds of Parkinson’s science.

The Fox foundation itself has earned positive reviews for its focused, aggressive approach to funding research, designed to ensure scientists share information and quickly pounce on any breakthroughs.

The actor, who first found fame in the 1980s NBC series Family Ties, and later in movies such as Back to the Future, played a much different role in recent years as a high-profile opponent of George W. Bush’s decision to bar U.S. government funding of research on embryonic stem cells.

That funding decision has since been overturned by Barack Obama, who succeeded Mr. Bush as president. And scientists at Thursday’s event suggested stem cells — with their ability to convert into other types of cells — may help them understand how Parkinson’s affects the brain, but are unlikely to be developed into a “magical” cure.

Meanwhile, Mr. Fox dismissed complaints that his research-focused charity will sap donor dollars from the Parkinson’s Society, a Canadian group dedicated to supporting and advocating for the country’s 100,000 patients, stressing that the foundation is not launching an “invasion” of this country.

“I really feel that a rising tide lifts all boats,” he said. “I think in the 10 years we’ve been doing this, we’ve raised Parkinson’s awareness to the point where most organizations and most people endeavouring to help the Parkinson’s community are getting more attention than they did.”

Mr. Fox was to appearing at a fundraising dinner later on Thursday with ’80s rock star Bryan Adams.

National Post

tblackwell@nationalpost.com

© Copyright (c) National Post

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November 13, 2009 by mike.

Simvastatin, a commonly used, cholesterol-lowering drug, may prevent Parkinson’s disease from progressing further. Neurological researchers at Rush University Medical Center conducted a study examining the use of the FDA-approved medication in mice with Parkinson’s disease and found that the drug successfully reverses the biochemical, cellular and anatomical changes caused by the disease.

“Statins are one of the most widely used cholesterol-lowering drugs throughout the world,” said study author Kalipada Pahan, PhD, professor of neurological sciences at Rush University Medical Center. “This may be a safer approach to halt the disease progression in Parkinson’s patients.”

Pahan and colleagues from Rush, along with researchers at the University of Nebraska Medical Center in Omaha published these findings in the October 28 issue of the Journal of Neurosciences.

The authors have shown that the activity of one protein called p21Ras is increased very early in the midbrain of mice with Parkinson’s pathology. Simvastatin enters into the brain and blocks the activity of the p21Ras protein and other associated toxic molecules, and goes on to protect the neurons, normalize neurotransmitter levels, and improves the motor functions in the mice with Parkinson’s.

“Understanding how the disease works is important to developing effective drugs that protect the brain and stop the progression of Parkinson’s,” said Pahan. “If we are able to replicate these results in Parkinson’s patients in the clinical setting, it would be a remarkable advance in the treatment of this devastating neurodegenerative disease.”

The study was supported by grants from National Institutes of Health and Michael J. Fox Foundation for Parkinson’s Research.

Parkinson’s is a slowly progressive disease that affects a small area of cells within the mid-brain known as the substantia nigra. Gradual degeneration of these cells causes a reduction in dopamine, which is a vital chemical neurotransmitter. The decrease in dopamine results in one or more of the classic signs of Parkinson’s disease that includes, resting tremor on one side of the body, generalized slowness of movement, stiffness of limbs, and gait or balance problems. The cause of Parkinson’s disease is unknown. Both environmental and genetic causes of the disease have been postulated.

Parkinson’s disease affects about 1.2 million patients in the United States and Canada. Although 15 percent of patients are diagnosed before age 50, it is generally considered a disease that targets older adults, affecting one of every 100 persons over the age of 60. This disease appears to be slightly more common in men than women.

Source: Deborah Song
Rush University Medical Center

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September 25, 2009 by mike.

By John Gever, Senior Editor, MedPage Today

Final results from a closely watched trial of rasagiline (Azilect) in Parkinson’s disease suggested the drug slowed the illness’s progression, study leaders said, but outside experts voice doubts.

Patients receiving 1 mg/day of rasagiline for 72 weeks showed a mean 2.82-point worsening of symptoms compared with a 4.52-point change among patients in a “delayed start” group who received placebo for 36 weeks followed by rasagiline for 36 weeks (P=0.02), according to a report in the Sept. 24 issue of the New England Journal of Medicine.

The difference is an indication that rasagiline did not merely alleviate Parkinson symptoms, but actually slowed the loss of neuronal function that causes the disease, wrote C. Warren Olanow, MD, of Mt. Sinai School of Medicine in New York City, and colleagues.

In a press release issued by Mt. Sinai, Olanow said the findings, if confirmed, would be “one of the biggest advances made in Parkinson’s in six years.”Action Points
Explain to interested patients that there is currently no treatment known to delay progression of the underlying pathology of Parkinson’s disease, although several therapies are available to relieve symptoms.

Explain that rasagiline is FDA-approved for symptomatic treatment of Parkinson’s disease. However, the findings of this study that it may modify the underlying pathology need confirmation in additional studies.

Explain, too, that the potential disease-modifying effect was measured indirectly and was not apparent with a higher drug dose.
The study, called ADAGIO, had strength of numbers — 1,176 patients with untreated, early-stage Parkinson’s disease. The delayed-start trial design is an attempt to detect a disease-modifying effect for a condition that doesn’t lend itself to direct measures — which in this case would likely require brain biopsies.

Because this approach is relatively new, the NEJM included a primer on the delayed-start design by Ralph B. D’Agostino Sr., PhD, a statistician at Boston University.

He wrote that Olanow and colleagues achieved “some success” with ADAGIO.

But the investigators themselves cautioned that the results were somewhat ambiguous, as no disease-modifying effect was seen with a higher rasagiline dose. Patients taking 2 mg/day in the early- and delayed-start groups had nearly identical changes on the Unified Parkinson’s Disease Rating Scale (UPDRS) scores — 3.47 points with the early start versus 3.11 points with the delayed start (P=0.60).

“Given the negative findings for the 2-mg dose, we cannot definitively conclude that rasagiline at a dose of 1 mg per day has disease-modifying effects,” Olanow and colleagues conceded.

Some of the data had been presented earlier at scientific meetings, priming the Parkinson’s disease research community for responses — much of which was critical.

Peter LeWitt, MD, a neurologist at Henry Ford Hospital in Detroit, questioned whether the disase-modifying effect seen in the trial was clinically significant, even if it was real.

On the basis of early presentations of the trial data, LeWitt wrote in Neurology in April that the reported effect barely made a dent in the expected disease progression.

“The small clinical improvements . . . need to be contrasted with the typical rate of progression in early Parkinson’s disease, whose annual mean change ranges from 6.31 to 10.46 UPDRS units,” LeWitt wrote.

Other experts contacted by MedPage Today and ABC News generally agreed.

“I would be reluctant to accept the conclusion that this provides compelling evidence of slowed Parkinson’s disease progression,” said J. Eric Ahlskog, MD, PhD, of the Mayo Clinic in Rochester, Minn.

Even one investigator in the trial cast doubt on the study’s importance.

William Weiner, MD, chairman of neurology at the University of Maryland, said he disagreed with the NEJM report’s emphasis on the possible disease-modifying effect.

“I was never given the opportunity to review the article and I would not have agreed to stressing the neuroprotection angle so strongly,” he wrote in an e-mail.

He said the primary outcome ended up as less than two points’ difference on the 176-point UPDRS scale. “[It is] maybe statistically significant, but it is surely not clinically meaningful,” Weiner said.

Joanne Wojcieszek, MD, of Indiana University in Indianapolis, noted that rasagiline — a monoamine oxidase B inhibitor — involves dietary precautions and a long list of other medications to avoid. “It takes a lot of time to explain this med to patients,” she said.

She also said the drug is expensive. The online pharmacy Drugs.com lists a price of $311 for a month’s supply of the 1-mg dose.

In the ADAGIO trial, patients with at least two of the three major symptoms of Parkinson’s disease — resting tremor, bradykinesia, and rigidity — not previously receiving chronic treatments were eligible to participate.

Participants were rated on the UPDRS at baseline and 10 subsequent visits during the 72-week trial.

Three primary endpoints were evaluated: average weekly change in UPDRS score over weeks 12 to 36, showing slower change in the early-start group versus placebo; less change in the early-start group in total UPDRS change from baseline to week 72, which would reflect a disease-modifying effect; and noninferiority of the early-started treatment to delayed start in the rate of change in UPDRS scores over weeks 48 to 72, when all patients were taking rasagiline.

The researchers said the 1-mg dose met all three endpoints, but the 2-mg dose met only the first and third.

Olanow and colleagues offered a possible explanation for the lack of disease-modifying effect with the 2-mg dose. They suggested it may have been so effective at reducing Parkinson symptoms in both treatment groups that the slowed progression in the underlying pathology was masked.

They said the results with the 1-mg dose “cannot be readily explained by an effect on symptoms alone, since both groups received the same treatment for the last nine months of the study.”

The possibility of a disease-modifying effect was supported by laboratory studies showing that rasagiline and its primary metabolite protect neurons from various toxins.

The researchers said they had avoided at least some of the pitfalls involved with delayed-start trials identified by D’Agostino:

Dropout rates remained low during the placebo phase, reducing the bias that dropouts introduce.
Randomization should have minimized problems associated with misdiagnosis of early-stage patients.
Although average weekly change in UPDRS score is not a standard measure of disease progression, the findings were confirmed with categorical analyses.
The finding of an apparent disease-modifying effect with the 1-mg dose provided assurance that the placebo phase was not too short.
Despite the skepticism voiced by others, one prominent neurologist told MedPage Today and ABC News that the ADAGIO results were persuasive and immediately practice-changing.

“I do believe that this constitutes a major advance in Parkinson’s,” wrote Daniel Kremens, MD, of Thomas Jefferson University in Philadelphia, in an e-mail. “From this study alone and the use of this drug, the paradigm of Parkinson’s treatment really should shift.”

He said it was no longer appropriate to initiate drug treatment only after symptoms become disabling.

“We should no longer be waiting. We should consider starting [patients] on treatment as soon as diagnosis is made with hope that we can modify the disease course. And that’s a major change in how Parkinson’s is treated currently,” Kremens wrote.

Teva supported the ADAGIO study.

Olanow and colleagues reported relationships with Teva, Lundbeck, Boehringer Ingelheim, Novartis/Orion, Solvay, Ceregene, Merck Serono, Ceregene, Eisai, Eutherapie, GlaxoSmithKline, Osmotica, Schering-Plough, Pierre Fabre, Allergan Neuroscience, Alphamedica, ApotheCom, Axis Healthcare, Bayer Schering, CNS Schering-Plough, Centopharm, Embryon, Genzyme, Impax, Ipsen, Kyowa, Merck, Ortho-McNeil, Pfizer, Prestwick, Quintiles, Santhera, Schwarz Pharma, Valeant Pharm, Vernalis, Acadia, SkyePharma, UCB Pharma, INC Research, Mentor, Asubio, i3 Research, Chelsea Therapeutics, Advanced Neuromodulation Systems, Medtronic Neurological, Neurogen, and Orion.

D’Agostino reported being a special employee of the FDA, but had no relationships with industry.

Lewitt reported relationships with Allergan, Boehringer-Ingelheim, GlaxoSmithKline, Novartis, Schwarz Pharma (now UCB), Solstice, Vernalis, Asubio, Brittania, Eisai, Impax, Kyowa, Neurim, Neuroderm, Neurologix, Orion, Prestwick, Spherics, XenoPort, Merck & Co., Santhera, Schering-Plough, Supernus, Valeant, and Chelsea Therapeutics.

Wojcieszek reported a relationship with Teva.

Ahlskog reported no potential conflicts.

Weiner reported relationships with Teva, Boehringer Ingelheim, Santhera, Biogen Idec, and Novartis.

Kremens reported a relationship with Teva.

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February 8, 2009 by mike.

By Rick Nauert, Ph.D.
Senior News Editor
Reviewed by John M. Grohol, Psy.D. on January 27, 2009

A new study offers tantalizing hope that the drug rasagiline can do what no other medication for Parkinson’s disease does — slow the progression of the devastating degenerative brain disease.

The study investigated the long-term effects of rasagiline (Azilect) on newly diagnosed patients and discovered people who began the drug earlier continued to do better than those for whom treatment was delayed six months.

A research paper, “Long-term Outcome of Early Versus Delayed Rasagiline Treatment in Early Parkinson’s Disease” was recently published in the journal Movement Disorders.

“Patients who received rasagiline right from the beginning rather than after a six-month delay experienced less progression of the clinical signs and symptoms of Parkinson’s disease that interfere with activities of daily living such as eating, walking and dressing,” said the study’s lead author Robert A. Hauser, MD.

“This is potentially consistent with a slowing of underlying disease progression, although other possible mechanisms also need to be considered.”

The study, sponsored by Teva Pharmaceutical Industries Ltd. (Israel), Teva Neuroscience, Inc. (USA) and H. Lundbeck A/S (Denmark), was a long-term open label extension of the multisite trial known as TEMPO.

In TEMPO, more than 400 untreated patients with early Parkinson’s disease were randomly assigned to rasagiline for a year (1 mg daily or 2 mg daily) or to placebo for six months followed by rasagiline for six months (2 mg daily).

At the end of a year, patients receiving rasagiline from the start fared better as measured by the Unified Parkinson’s Disease Rating Scale. They experienced less worsening of motor symptoms, such as rigidity and tremor, and had fewer problems with activities of daily living than patients who began rasagiline six months later.

The open-label extension study followed more than 300 patients from the TEMPO study for up to 6.5 years. In this extension study, all patients continued on rasagiline (1 mg. daily) and could take other Parkinson’s disease medications as needed.

The researchers found those who started rasagiline right from the beginning of the TEMPO study continued to fare better than patients in the delayed-start group. Over the course of the entire study, the early-start group had 16 percent less progression of the signs and symptoms of Parkinson’s disease, and this greater clinical benefit was observed even as patients received conventional Parkinson’s disease medications in addition to rasagiline.

Rasagiline appeared to be well tolerated in this long-term study.

If the clinical outcomes from the TEMPO and extension study hold up under further scrutiny, it may indicate that early initiation of rasagiline confers a protective effect against disease progression, Dr. Hauser said.

If this is the case, it reinforces the importance of individuals being diagnosed and treated as soon as possible.”

The study authors point out that early initiation of any drug to relieve symptoms of Parkinson’s disease may lead to a better clinical outcome compared to delayed administration — something that will be elucidated as more delayed-start studies are performed with other Parkinson’s medications.

Source: University of South Florida Health

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January 11, 2009 by mike.

AFFiRiS has started pre-clinical development of a Parkinson’s vaccine. The vaccine, known as PD01, can be used to target a specific protein that is closely associated with the causes of this degenerative neurological disease. Excellent product candidates from discovery studies have prompted the company to file a patent application and proceed immediately with development.

Similarly positive results from external assessments impelled the Austrian Research Promotion Agency (FFG) to provide considerable financial funding for the project. The vaccine is based on the company’s AFFITOME technology, which, among other things, has already been used to develop two Alzheimer’s vaccines, which are currently both in phase I clinical testing.

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November 18, 2007 by mike.

Los Angeles — A U.S. study suggests over-the-counter medicines called non-steroidal anti-inflammatory drugs, or NSAIDs, may reduce a person’s risk of Parkinson’s disease.

The study involved 579 men and women, half of whom had Parkinson’s. The participants were asked if they had taken aspirin and if they had taken non-aspirin NSAIDs, such as ibuprofen, once a week or more at any point in their life for at least a month.

The study found regular users of non-aspirin NSAIDs reduced their risk of Parkinson’s disease by as much as 60 percent compared with non-regular users and non-users. Women who were regular users of aspirin reduced their risk of Parkinson’s disease by 40 percent.

“Our findings suggest NSAIDs are protective against Parkinson’s disease, with a particularly strong protective effect among regular users of non-aspirin NSAIDs, especially those who reported two or more years of use,” said study author Angelika Wahner of the UCLA School of Public Health. “Interestingly, aspirin only benefited women. It may be that men are taking lower doses of aspirin for heart problems, while women may be using higher doses for arthritis or headaches.”

The study is reported in the journal Neurology.

© 2007 United Press International.

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August 25, 2007 by mike.

Merck KGaA and its development partner, Newron, say that a late-stage study of their experimental therapy for Parkinson’s failed to demonstrate any significant effect. But the two developers refuse to walk away from safinamide. Researchers are planning to mount new trials with lower doses to find the right formula.

“The primary endpoint, time to intervention, did not reach statistical significance when data from both safinamide dose groups were pooled,” the companies said, after reviewing 18 months of combined data from patients taking the 50-100 mg and 120-200 mg doses. But researchers said that a lack of response among patients taking the highest dose could have skewed the data. Adding safinamide to dopamine agonist therapy at 50-100 mg daily could delay the time to therapeutic adjustment.

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July 15, 2007 by mike.

Scientists have discovered a protein which may help to slow, or even reverse symptoms of Parkinson’s disease.

Parkinson’s destroys nerve cells that produce the brain chemical dopamine, causing movement and balance problems.

Finnish researchers found the new molecule can prevent degeneration of these cells - and help damaged cells start to recover.

Their paper, featured in Nature, showed symptoms eased in rats given injections of the protein…

BBC NEWS

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June 15, 2007 by mike.

http://nationmultimedia.com:80/world…ewsid=30036474

PARIS - A drug tested on lab mice slows and may even halt the progress of Parkinson’s, offering the brightest pharmacological hope in decades of rolling back this tragic disease, US researchers report on Sunday.

Isradipine, already licensed for treatment for high blood pressure, rejuvenated ageing dopamine cells, the brain cells whose death causes Parkinson’s, they say.

The outcome among mice was so promising that the team now plan on conducting trials on human volunteers.

“Our hope is that this drug will protect dopamine neurons, so that if you began taking it early enough, you won’t get Parkinson’s disease, even if you were at risk,” said lead researcher James Surmeier, professor of physiology at Northwestern University in Chicago.

“It would be like taking a baby aspirin every day to protect your heart.”

Parkinson’s is an incurable, degenerative disease of the central nervous system that causes uncontrollable shaking, along with impaired speech and movement. In approximately one third of cases it also results in dementia.

Estimates of its prevalence vary between 0.1 and 0.3 per cent of the population, meaning that approximately one in 500 people contract the disease.

The cause is a loss of dopamine, a chemical messenger that helps direct movement. The substance is provided in a part of the brain called the substantia nigra.

Most pacemaking neurons use sodium ions to produce a regular electrical signal.

But the new research unexpectedly found that dopamine cells, when they reached adulthood, start to depend more and more on calcium ions.

This discovery is important, because calcium ions are far more troublesome to control than their placid sodium counterparts: the cell uses up lots of energy, either to round up and sequester the calcium or pump it out.

As a result, the dopamine cells become stressed on reaching their calcium-addicted adulthood and die prematurely.

Surmeier’s hunch was to try isradipine, a well-tolerated hypertension and stroke drug commercialised under the name of DynaCirc, which blocks the channels in the cell surface that admit calcium.

Tested on lab-dish cells and then on mice which had been genetically engineered to have Parkinson’s, the team found that within a few hours of being exposed to the drug, the neurons reverted to their youth-like state, of using sodium.

This lowered the cells’ stress level, making them less vulnerable to the toxins, still poorly understood, that kills them.

“They start acting like they’re youngsters again,” Northwestern quoted Surmeier as saying.

The study is published online on Sunday by Nature, the British science journal.

So far the work has only been carried out on animals, and more needs to be done to assess the drug’s effect on humans.

But Surmeier voiced cautious hopes it could be the first treatment to prevent or slow the progression of this devastating disease.

The mainstay treatment for Parkinson’s is L-DOPA, a drug that the brain converts into dopamine.

At first, L-DOPA has a seemingly miraculous effective on symptoms. The problem, though, is that it becomes less and less effective as time wears on and the disease progresses. That forces doctors to raise the dose of this drug, which induces unwanted side-effects, including spastic, jerky movements.

So, if isradipine can slow the death of dopamine neurons, the L-DOPA “honeymoon” could be significantly extended.

“If we could double or triple the therapeutic window for L-DOPA, it would be a huge advance,” said Surmeier. “There has not been a major advance in the pharmacological management of Parkinson’s in 30 years.”

Agence France-Presse

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