Parkinson's disease News

March 21, 2008 (PharmaLive.com). UCB, the company that manufactures rotigotine (Neupro), the transdermal patch treatment that is used to ease the symptoms of Parkinson's disease in its early stages, has announced a recall of all Neupro batches in the United States and some areas of Europe.

The company has assured the public that the recall has been made not because of concern about contamination or toxicity, but because of a deviation from approved product standards that has apparently reduced the effectiveness of the treatment.

Because correction of the problem and replenishment of stocks will take time, patients on Neupro are being advised to contact their health care professionals to arrange for their doses to be reduced slowly over time, as advised on the product label. The company advises strongly against sudden discontinuation.

Dr. Christopher Goetz, Director of the Parkinson's Disease Foundation Research Center at Rush University Medical Center in Chicago, says that for patients now on Neupro, the physician may recommend switching to one of the oral medications known as dopamine agonists that are in the same drug class as Neupro.

Texas doctors test new Parkinson's treatment

February 1, 2008 (KVUE News Austin TX) - Two Austin physicians unveiled a machine Monday that could dramatically improve the life of people with Parkinson's disease. It's a device that sends small electrical currents into the hands and feet of patients.

They say so far it's showing very positive results.

Austin resident Eugene Fairen suffers from Parkinson's disease. He has trouble with his balance and his hands tremble, which makes sleeping difficult.

Fairen says he can now do things he previously was unable to do.

"I can button these two buttons today and that was a triumph. Usually my wife has to do that for me," said Fairen.

Dr. Donald Rhodes is a podiatrist who developed the machine originally for a patient who had a nerve disorder. He wondered whether it could help those with Parkinson's disease.

They began testing it a month ago.

Once a day, patients use his machine to send electrical currents into their bodies.

"It's done through electrodes on the hands and feet, and it stimulates acupuncture points and reflexology points, as well as free nerve endings," said Dr. Rhodes.

Dr. Rob Izor is the Austin neurologist who oversees the tests. He says all five of their patients have shown progress.

"Whenever you hear that something is too good to be true, it probably is, but I am cautiously optimistic that this study has evidence of a trend for therapeutic effect," said Izor.

Another patient with a disease called dystonia, a form of Parkinson's, says the treatment has also brought out really good results for her.

"It's effective for me I found a difference and that's all I can say," said Candyce Drum, dystonia patient.

Doctors Izor and Rhodes say more research is needed before their machine will be available to the public.

New blood test can diagnose Parkinson's

December 26, 2007 (London, UK) - A simple blood test that can diagnose Parkinson's disease could be available from next year, according to scientists.

The test will lead to earlier diagnosis and more effective treatments for patients with the neurological disorder.

Most patients are diagnosed by observing symptoms such as tremors, slow movement and muscular stiffness.

Because of the slow onset of the disease, many sufferers in the early stages are misdiagnosed as having other conditions such as repeated strokes.

This can lead to the use of inappropriate treatments that fail to slow the progression of the disease.

The research, which was funded by the actor Michael J Fox - who was diagnosed with Parkinson's in 1991 at the age of 30 - suggests that genetic alterations caused by the condition can be detected by chemical changes in the blood.

Dr Erik Christensen, the chief executive of DiaGenic, a Norwegian life sciences company that developed the test, said: "Progression of Parkinson's disease has a serious impact on the quality of life of sufferers. The earlier an accurate diagnosis can be made, the earlier treatment can start and the better the prognosis for the patient."

Researchers at DiaGenic announced last year that they had used the same process to develop a blood test that is sensitive enough to pick up early symptoms of Alzheimer's disease.

As part of this work they also discovered 500 genes that are affected by Parkinson's which trigger chemical changes that can also be identified in blood samples.

Dr Clemens Scherzer of the Brigham and Women's Hospital in Boston, Massachusetts, will test DiaGenic's preliminary findings using blood samples already collected from 300 patients.

Dr Christensen said that he expected to be able to apply for a licence so that doctors could use the test by the end of next year.

There are some 10,000 new cases of Parkinson's diagnosed every year in Britain, and about 120,000 people live with the condition, which occurs when cells in the part of the brain that controls movement die.

Dr Kieran Breen, of the Parkinson's Disease Society, said: "The diagnosis of Parkinson's can be difficult, given it has a slow onset and can be mistaken for a number of other conditions, particularly in the early stages.

"There is, therefore, a great need to look for something to measure in the body associated with Parkinson's to be able to develop a test for its diagnosis.

"As blood samples have already been collected, the US researchers can immediately start work on analysing these samples. We look forward to the results."

Last week Opaldia, which provides private health care in Britain, announced that it is expecting to begin offering a blood test to detect breast cancer, also developed by DiaGenic, to its members next year.

Volunteers needed for Parkinson's disease studies

Nov. 8, 2007 (WA University in St. Louis) - Researchers at Washington University School of Medicine in St. Louis are seeking volunteers with Parkinson's disease for two studies. One is investigating the effects of antidepressant drugs on depression and motor function. The second study is assessing the safety and effectiveness of a drug for Parkinson's patients who also have psychotic symptoms.

In the NIH-funded depression study, investigators are evaluating paroxetine (Paxil) and venlafaxine XR (Effexor) for their success in alleviating depression and for their potential effect on motor function in Parkinson's patients.

"Depression is very common in patients with Parkinson's disease," says Kevin J. Black, M.D., associate professor of psychiatry, of neurology, of neurobiology and of radiology and the study's principal investigator. "Doctors frequently prescribe a class of drugs called selective serotonin reuptake inhibitors for these patients. But we don't really know how well these drugs work in this population."

The study will monitor depression levels in participants who receive one of the drugs for 12 weeks. Investigators also will monitor motor function. Neither the researchers nor the study volunteers will know which drug subjects have received or whether they have been given an inactive placebo until the end of the study.

"There have been concerns that this class of drugs, known as SSRIs, might affect motor function," Black explains. "They are known to alleviate depression in otherwise healthy people, but because the drugs interact with some of the same brain structures affected by Parkinson's disease, it is important that we take a closer look at their effects in this population to ensure that in attempting to alleviate depression, we aren't creating other problems."

The study will include 12 weeks of treatment with a four-week follow up. It will involve weekly phone calls as well as in-person visits at two, four, six, eight and 12 weeks.

The second study, supported by Ovation Pharmaceuticals, is testing varying doses of a drug called melperone to treat psychosis in patients with Parkinson's disease. Currently, there are no drugs approved specifically for the treatment of psychosis in Parkinson's patients. Typical antipsychotic drugs often cannot be used because they can exacerbate parkinsonian symptoms such as stiffness and tremors.

Newer, atypical antipsychotic agents have been more successful, and one of those drugs, called clozapine (Clozaril) frequently is prescribed to treat psychosis in Parkinson's patients. Unfortunately, some patients can develop significant complications when taking that drug. Other antipsychotic drugs either are not very effective at reducing psychotic symptoms or they worsen motor symptoms, or both.

"Because melperone seems to work through different mechanisms than other antipsychotic drugs, we want to see whether it can alleviate symptoms of psychosis without exacerbating motor problems," Black says.

Patients in the 10-week study will receive melperone syrup or an inactive placebo in syrup. Again, neither the investigators nor the participants will know whether an individual receives an active drug or a placebo until the study's completion. The study will require seven in-person visits during a 10-week period. If participants' symptoms improve, they will have the option of continuing on the drug longer than 10 weeks as part of an open-label phase of the study.

Certain health problems — such as recent heart attacks, previous treatment with the drugs, and the presence of other medical or psychiatric disorders — may exclude some people from participating. All screening tests, study medications and research-related procedures for these studies are free of charge. For more information, call or e-mail Mary Creech at (314) 362-7651 (maryc@npg.wustl.edu) or Elda Shipley at (314) 362-6514 (shipleye@npg.wustl.edu).

Washington University School of Medicine's 2,100 employed and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children's hospitals. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked fourth in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children's hospitals, the School of Medicine is linked to BJC HealthCare.

Chemical That Triggers Parkinson's Disease Discovered

Oct. 31, 2007(Science Daily) - Researchers at the Saint Louis University School of Medicine have discovered the key brain chemical that causes Parkinson's disease - a breakthrough finding that could pave the way for new, far more effective therapies to treat one of the most common and debilitating neurological disorders.

Currently, the main approach for treating Parkinson's disease, which afflicts more than 1.5 million Americans, is to replace dopamine that's lost when the cells that produce it die off and cause the disorder. With this new research, however, scientists can better work toward 'neuroprotective' therapies - those that actually block dopamine cells from dying off in the first place.

"We believe this work represents a very significant breakthrough in understanding the complicated chemical process that results in Parkinson's disease," said William J. Burke, M.D., Ph.D., professor of neurology at the Saint Louis University School of Medicine and the study's lead author.

"For the first time, we've identified the chemical that triggers the events in the brain that cause this disorder," Burke added. "We believe these findings can be used to develop therapies that can actually stop or slow this process."

Parkinson's disease occurs when some nerve cells in a part of the brain called the substantia nigra die or become impaired. Normally, these cells produce dopamine - a vital chemical that allows smooth, coordinated function of the body's muscles and movements.

When about 80 percent of these dopamine-producing cells die or are damaged, the symptoms of Parkinson's disease begin to appear. These include tremors and shaking, slowness of movement, rigidity and stiffness, and difficulty with balance.

Scientists have long known that a key protein called alpha-synuclein plays a role in the development of Parkinson's disease. Alpha-synuclein is found throughout the brain - but in some people, the protein clumps together. This causes the death of the dopamine-producing cells, which in turn causes Parkinson's to develop.

The SLU researchers discovered that dopamine itself actually plays a role in destroying the cells that produce it.

In the process that leads to Parkinson's disease, dopamine is converted into a highly toxic chemical called DOPAL. Using test-tube, cell-culture and animal models, the researchers found that it is DOPAL that causes alpha-synuclein protein in the brain to clump together, which in turn triggers the death of dopamine-producing cells and leads to Parkinson's.

"This is very exciting," Burke said. "This is the first time that anyone has ever established that it is a naturally occurring byproduct of dopamine that causes alpha-synuclein to aggregate, or clump together. It's actually DOPAL that kicks this whole process off and results in Parkinson's disease."

Ibuprofen may curb risk of Parkinson's disease

September 7, 2007 (SpiritIndia.com) – In 1992, subjects provided information on four types of commonly used analgesics. In 2001, they provided information on the occurrence of Parkinson's disease. The researchers detected 413 cases of Parkinson's disease during follow up.

"We found that individuals who regularly used ibuprofen had about a 35 percent lower risk of developing Parkinson's disease than non-users," Dr. Alberto Ascherio, of Harvard School of Public Health in Boston, Massachusetts, told.

Specifically, compared to those who did not use NSAIDs, users of 2 to 7 ibuprofen tablets per week had about a 28 percent reduced relative risk of developing Parkinson's disease, while those who reported using 1 or more tablets per day had a 38 percent reduced risk of Parkinson's.

No associations were observed between the risk of PD and the use of aspirin, other NSAIDs, or acetaminophen.

"These findings suggest that ibuprofen could contribute to the prevention of Parkinson's disease," Ascherio said. "Because of the progressive nature of the degenerative process, it is also possible that this drug could be beneficial for individuals with Parkinson's, but this should be tested in randomized clinical trials."

"It would be premature for people with Parkinson's disease to start taking ibuprofen or other anti-inflammatory drugs," Ascherio cautioned. "Albeit promising, these findings are insufficient to support a change in current therapeutical practice."

First gene therapy clinical trial for Parkinson's disease improves patients' motor skills with no major side effects

Aug. 8, 2007(Cornell University) - In what could be a breakthrough in treating Parkinson's disease, researchers at NewYork-Presbyterian Hospital/Weill Cornell Medical Center improved the motor function of 12 patients over the course of one year by injecting a harmless gene-bearing virus into their brains.

The research, which marks the first phase 1 clinical trial using gene therapy to battle the progressive neurodegenerative illness, is published in the June 23 issue of The Lancet.

"These exciting results need to be validated in a larger trial, but we believe this is a milestone -- not only for the treatment of Parkinson's disease, but for the use of gene-based therapies against neurological conditions generally," said lead researcher Michael Kaplitt, the Victor and Tara Menezes Clinical Scholar in Neurological Surgery at Weill Cornell Medical College and director of Movement Disorders Surgery at New York-Presbyterian Hospital/Weill Cornell Medical Center.

"Viruses exist in nature mainly to transfer their own genes to the host cell," he explained. "So, we modify the AAV (adeno-associated virus) in such a way that the only gene it carries is the one we want to deliver to the therapeutic site."

In this case, the "gene of interest" is the glutamic acid decarboxylase (GAD) gene. "GAD makes a chemical called GABA, a major inhibitory neurotransmitter in the brain that helps 'quiet' excessive neuronal firing," said Matthew During, professor of molecular biology and cancer genetics at Ohio State University, the senior author of the study, who worked on this research while at Weill Cornell.

"In Parkinson's disease, not only do patients lose many dopamine-producing brain cells, but they also develop substantial reductions in the activity and amount of GABA in their brains. This causes a dysfunction in brain circuitry responsible for coordinating movement," During explains.

Thus, the researchers inserted the GABA-producing gene GAD back into an area of the brain called the subthalamic nucleus, a key regulatory center within this motor circuit, via the AAV.

"We saw no adverse events related to the treatment, no immunological changes or infections over the year of the study, no imaging evidence of toxicity whatsoever," Kaplitt said.

Three months, as well as one year, after treatment, the patients as a group showed a 25 percent to 30 percent improvement in motor function when they had been off their medications for 12 hours (the off state), and up to 65 percent improvement in some patients while they were on medication.

"That was really surprising and heartening, because traditional Parkinson's surgeries improve patients in the off state but not as frequently in the on-medication state," said Kaplitt, noting that the next step is a larger, more definitive efficacy-centered study. "We've now shown that the genetic modification of the patient's own brain cells can be done safely, and it appears to have enough effectiveness in this case to justify further exploration -- potentially opening up gene therapy for a host of brain disorders," he said.

About 1.5 million Americans have Parkinson's disease, which is characterized by a steady loss in brain cells producing the neurotransmitter dopamine, which alters the function of brain networks controlling motor function. Medications, as well as surgery, can treat some of the symptoms, but there is no cure.

This work was funded by Neurologix of Fort Lee, N.J., which is developing the AAV-GAD agent. Kaplitt and During are co-founders of the company and remain consultants. Additionally, Kaplitt's father, Dr. Martin Kaplitt, is chairman of the board of Neurologix and, as such, has stock ownership and receives salary.

Test drug seen as best hope in decades for tackling Parkinson's

June 10, 2007(The Nation - 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."

Parkinson's Drug Patch Gets the Green Light

May 10, 2007 (Sci-Tech Today)- Parkinson's disease results from the loss of dopamine-producing brain cells. Dopamine is crucial for the communication between cells that control muscle movement, which explains the trembling commonly seen in Parkinson's patients. The new drug Neupro (rotigotine transdermal system) works by activating dopamine receptors in the brain, mimicking the neurotransmitter's effect.

The treatment options for patients with early Parkinson's expanded Wednesday with the approval of a new drug in patch form – a first for medicines to treat symptoms of the disease. The once-daily Neupro patch contains a drug called rotigotine, which has not been sold before in the United States, the Food and Drug Administration said. The drug patch, made by Schwarz Pharma AG, is the first for the treatment of symptoms of Parkinson's disease.

Parkinson's disease results from the loss of dopamine-producing brain cells. Dopamine is crucial for the communication between cells that control muscle movement, which explains the trembling commonly seen in Parkinson's patients.

Rotigotine works by activating dopamine receptors in the brain, mimicking the neurotransmitter's effect.

The most common side effects for Neupro include skin reactions at the patch site, dizziness, nausea, vomiting, drowsiness and insomnia, the FDA said. Most are typical with this class of drugs.

Other potential safety concerns include sudden onset of sleep while engaged in activities such as driving or operating machinery, hallucinations and decreased blood pressure when standing up, the agency said.

Neupro has been available in Europe since 2006.

Parkinson's patients may benefit from treadmill exercise

May 16, 2007 (NewKarala.com) - University of Southern California (USC) researchers have shown that patients with Parkinson's disease and similar movement disorders may benefit from treadmill exercises.

Dr. Michael Jakowec, Assistant Professor of Neurology at the Keck School of Medicine, studied the effects of treadmill exercise between animal models with and without a loss of certain cells that are similar to what Parkinson's patients might suffer.

Since Parkinson's results from the loss of nerve cells in the brain that produce dopamine, which is critical as a stimulator of motor system nerves in the body, the researchers looked at changes in dopamine levels.

They observed that the subjects with cell loss had an effect on dopamine levels after they exercised, while normal subjects showed less of a difference in levels.

"Our study shows that the beneficial effects of exercise in Parkinson's Disease may be due to a more efficient use of dopamine," says first study author Dr. Giselle Petzinger, Assistant Professor of Neurology.

"Surviving dopamine cells in our animal models- made to simulate what Parkinson's patients suffer with- subjected to intensive treadmill exercise appear to work harder," adds the researcher.

The study indicates that the benefits of treadmill exercise on motor performance may be accompanied by changes in dopamine neurotransmission that are different in the injured subjects compared to the non-injured.

"Studies in our animal model of Parkinson's disease support the fact that exercise is beneficial for patients with Parkinson's. Exercise may help the injured brain to work more efficiently by allowing the remaining dopamine producing neurons to work harder and in doing so may promote stronger connections in the brain," says Jakowec.

High-Frequency Stimulation Provides Long-Term Efficacy for Parkinson's Symptoms: Presented at AANS

May 4, 2007 (Drs. Guide) - High-frequency stimulation (HFS) of the subthalamic nucleus (STN) is a safe, effective, and stable treatment for patients with advanced Parkinson's disease, according to a retrospective evaluation of this technique.

Lead author Alim L. Benabid, MD, PhD, director, department of neurosurgery, Centre Hospitalier Universitaire A. Michallon, Grenoble, France, discussed the study's results here at the American Association of Neurological Surgeons (AANS) annual meeting.

Currently, STN-HFS is the treatment of choice for treating patients with advanced Parkinson's disease. Dr. Benabid and colleagues studied the evolution of the cardinal features of this technique in a 14-year series that included 304 patients.

Enrolled patients underwent surgery in the STN since 1993 (296 bilaterally, 600 electrodes). The researchers retrospectively analyzed the duration of benefit, active contact coordinates, complications, and long-term changes in the nature of the disease.

Improvement in major symptoms was an average of 65% for the major Parkinson's symptoms as evaluated using the Unified Parkinson's Disease Rating Scale, Hoehn and Yahr Staging of Parkinson's Disease, and quality-of-life scales. Improvement in speech was an average of 35%.

Drug dosages, and subsequently the levodopa-induced dyskinesias, were decreased by an average of 65%. This was linearly correlated to the preoperative levodopa-induced improvement and was strictly dependent on the accurate placement of the leads, according to the researchers.

The benefit of STN-HFS persisted in levodopa-sensitive symptoms such as tremor, akinesia, and rigidity, but not for midline symptoms such as balance and gait. Patients' baseline condition (off medication, off stimulation) worsened in 25% of patients, was stable in 36% of patients, and improved in 38%. Improvements continued over 5 years in 19% of patients.

The researchers determined that mild and transient complications were due to pretargeting (5.7%), implantation (30%), stimulation (19.6%), and hardware failure (16.7%). Complications decreased by a ratio of 2.3 with the learning curve of operators who performed the procedure.

There were psychic disorders in 8.3%, one procedure-related death, and one suicide.

The researchers concluded that STN-HFS is safe, effective, and stable over time. "Careful surgical practice and patient selection improve the outcome," the noted.