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.

(HealthNewsDigest.com) - ST. PAUL, Minn., — New research shows people who regularly take ibuprofen may reduce their risk of developing Parkinson’s disease, according to a study released today that will be presented at the American Academy of Neurology’s 62nd Annual Meeting in Toronto April 10 to April 17, 2010.

The research involved 136,474 people who did not have Parkinson’s disease at the beginning of the research. Participants were asked about their use of non-steroid anti-inflammatory drugs (NSAIDs), including aspirin, ibuprofen and acetaminophen. After six years, 293 participants had developed Parkinson’s disease.

The study found regular users of ibuprofen were 40 percent less likely to develop Parkinson’s disease than people who didn’t take ibuprofen. Also, people who took higher amounts of ibuprofen were less likely to develop Parkinson’s disease than people who took smaller amounts of the drug. The results were the same regardless of age, smoking and caffeine intake.

“Ibuprofen was the only NSAID linked to a lower risk of Parkinson’s,” said Xiang Gao, MD, with Harvard School of Public Health in Boston. “Other NSAIDs and analgesics, including aspirin and acetaminophen, did not appear to have any effect on lowering a person’s risk of developing Parkinson’s. More research is needed as to how and why ibuprofen appears to reduce the risk of Parkinson’s disease, which affects up to one million people in the United States.”

The study was supported by the National Institute of Neurological Disorders and Stroke.

The American Academy of Neurology, an association of more than 22,000 neurologists and neuroscience professionals, is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Parkinson’s disease, ALS (Lou Gehrig’s disease), dementia, epilepsy and migraine. For more information about the American Academy of Neurology and the AAN Annual Meeting, visit http://www.aan.com/.

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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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January 28, 2010 by mike.

The largest epidemiological study of Parkinson’s disease in the United States has found that the disease is more common in the Midwest and the Northeast and is twice as likely to strike whites and Hispanics as blacks and Asians.

The study, based on data from 36 million Medicare recipients, is both the first to produce any significant information on patterns of Parkinson’s disease in minorities and to show geographic clusters for the condition.
“Finding clusters in the Midwest and the Northeast is particularly exciting,” says lead author Allison Wright Willis, M.D., assistant professor of neurology at Washington University School of Medicine in St. Louis. “These are the two regions of the country most involved in metal processing and agriculture, and chemicals used in these fields are the strongest potential environmental risk factors for Parkinson’s disease that we’ve identified so far.”
The results appear online in the journal Neuroepidemiology.
Parkinson’s disease is a common neurodegenerative condition that causes tremor, stiffness, slowness, mood and behavioral disorders, sleep problems and other symptoms. The disease is characterized by loss of dopamine, a compound involved in communication between brain cells.
According to Willis, genetic factors explain only a small percent of cases. Environmental factors are likely more common contributors and may include prolonged exposures to herbicides and insecticides used in farming or to metals such as copper, manganese and lead.
For the new study, Willis analyzed data on more than 450,000 cases of Parkinson’s disease per year over six years, 1995 and 2000-2005. Collectively, that data included information from more than 98 percent of all Americans 65 and older.
Willis found Asians and blacks developed Parkinson’s disease at half the rate of whites and Hispanics.
“We are going to try to learn more about why this is the case,” says Willis. “It could be that those with Asian or African ancestry have genes that help protect them from exposure to environmental factors that cause Parkinson’s disease, or they may have fewer exposures to those factors.”
Epidemiologists have long debated whether Parkinson’s disease is more prevalent in rural or urban areas, with some studies showing higher rates in cities and some in the countryside. Willis found the condition is more common in urban areas but concluded the comparison between the two rates offered little potential for insight into the disease.
“It’s always been an open question as to how to best define the terms ‘urban’ and ‘rural,’” she says. “Urban and rural is defined in many different and relatively arbitrary ways, and we came away convinced by our results that these distinctions have little to do with what is causing the disease.”
Willis and her colleagues plan further studies of how exposure to single or combined environmental factors influences disease risk.
“This was the largest descriptive epidemiological study yet to be conducted of Parkinson’s disease in the United States, and it has both given us some interesting new leads for the future research and reinforced some ideas we already had,” she says.
More information: Wright Willis A, Evanoff BA, Lian M, Criswell SR, Racette BA. Geographic and ethnic variation in Parkinson disease: a population-based study of US Medicare beneficiaries. Neuroepidemiology, 2010;34:143-151
Provided by Washington University School of Medicine (news : web)

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January 23, 2010 by mike.