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By GINA KOLATA Dr. Bastiaan R. Bloem of the Radboud University Nijmegen Medical Center in the Netherlands thought he had seen it all in his years of caring for patients with Parkinson’s disease. But the 58-year-old man who came to see him recently was a total surprise. A video from the Netherlands of a 58-year-old man with a 10-year history of Parkinson’s disease showed him freezing in his movements after a few steps. Yet he was able to ride a bicycle. The man had had Parkinson’s disease for 10 years, and it had progressed until he was severely affected. Parkinson’s, a neurological disorder in which some of the brain cells that control movement die, had made him unable to walk. He trembled and could walk only a few steps before falling. He froze in place, his feet feeling as if they were bolted to the floor. But the man told Dr. Bloem something amazing: he said he was a regular exerciser — a cyclist, in fact — something that should not be possible for patients at his stage of the disease, Dr. Bloem thought. “He said, ‘Just yesterday I rode my bicycle for 10 kilometers’ — six miles,” Dr. Bloem said. “He said he rides his bicycle for miles and miles every day.” “I said, ‘This cannot be,’ ” Dr. Bloem, a professor of neurology and medical director of the hospital’s Parkinson’s Center, recalled in a telephone interview. “This man has end-stage Parkinson’s disease. He is unable to walk.” Copyright 2010 The New York Times Company

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 13931 - Posted: 06.24.2010

HONG KONG - People of Japanese and European descent who have mutant versions of five genes may be at higher risk of developing Parkinson's disease, two large teams of researchers have found. The two independent studies, published in the latest issue of Nature Genetics, involved more than 25,000 participants in total and are the largest studies to date to try to uncover genetic associations behind Parkinson's disease. A study in Japan looked only at ethnic Japanese while a second study, in the United States, focused only on people of European heritage. In the first study, Tatsushi Toda of Japan's Kobe University and colleagues sequenced the genes of 2,011 participants with the disease and 18,381 others without the disease. They found that those with the disease had variants of the genes PARK16, BST1, SNCA and LRRK2. In the second study, researchers led by Andrew Singleton at the National Institutes of Health's (NIH) laboratory of neurogenetics in the United States analyzed the genes of more than 5,000 patients of European ancestry who suffer from the disease and detected strong links between Parkinson's and variants of the genes SNCA and MAPT. The two teams later compared their data and found that variants of PARK16, SNCA and LRRK2 carry risk of Parkinson's in both Japanese and European populations, while variants of BST1 and MAPT were population-specific. Copyright 2009 Reuters.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 13470 - Posted: 06.24.2010

Researchers funded by the National Institutes of Health have turned simple baker’s yeast into a virtual army of medicinal chemists capable of rapidly searching for drugs to treat Parkinson’s disease. In a study published online today in Nature Chemical Biology, the researchers showed that they can rescue yeast cells from toxic levels of a protein implicated in Parkinson’s disease by stimulating the cells to make very small proteins called cyclic peptides. Two of the cyclic peptides had a protective effect on the yeast cells and on neurons in an animal model of Parkinson’s disease. "This biological approach to compound development opens up an entirely new direction for drug discovery, not only for Parkinson’s disease, but theoretically for any disease where key aspects of the pathology can be reproduced in yeast," says Margaret Sutherland, Ph.D., a program director at NIH’s National Institute of Neurological Disorders and Stroke (NINDS). "A key step for the future will be to identify the cellular pathways that are affected by these cyclic peptides." The research emerged from the lab of Susan Lindquist, Ph.D., a professor of biology at the Massachusetts Institute of Technology (MIT). Parkinson’s disease attacks cells in a part of the brain responsible for motor control and coordination. As those neurons degenerate, the disease leads to progressive deterioration of motor function including involuntary shaking, slowed movement, stiffened muscles, and impaired balance. The neurons normally produce a chemical called dopamine. A synthetic precursor of dopamine called L-DOPA or drugs that mimic dopamine’s action can provide symptomatic relief from Parkinson’s disease. Unfortunately, these drugs lose much of their effectiveness in later stages of the disease, and there is currently no means to slow the disease’s progressive course.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 13051 - Posted: 06.24.2010

By SANDRA BLAKESLEE By electrically stimulating the spinal cords of rodents, scientists have reversed some of the worst symptoms of Parkinson’s disease. As long as a mild current flows up their spines and into their brains, the animals regain the ability to scamper around their cages, as if they were normal. The therapy, described in Friday’s issue of the journal Science, is a potential alternative to direct stimulation, which requires risky and invasive surgery to implant electrodes deep in the brain, researchers said. Only 30 percent of severely impaired Parkinson’s patients qualify for the operation. Spinal cord stimulation would be less invasive and inherently safer, and it would reduce the amount of drugs needed to treat the disease, said the report’s lead author, Dr. Miguel A. L. Nicolelis, a neuroscientist at Duke. Dr. Nicolelis added that the procedure was now being tested on monkeys, and “if it succeeds, human clinical trials could begin in the next few years.” An expert on stimulation theories who was not involved in the research, Dr. Rodolfo Llinįs, said the treatment “makes good sense,” but he added: “How successfully it will translate to humans is an important issue. The human spinal cord is much more complex than the rodent counterpart, and long-term stimulation might result in nasty secondary effects.” Copyright 2009 The New York Times Company

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 12668 - Posted: 06.24.2010

By Nathan Seppa Brain surgeon Kenneth Follett had never received thank-you cards from his patients after performing an operation — until he started putting electrodes in their brains. Follett, who holds positions at the University of Nebraska Medical Center and the Veterans Affairs Medical Center in Omaha, is among a select group of surgeons who over the past decade have been treating Parkinson’s disease by installing two tiny electrodes in a patient’s brain. The change these devices induce can be astonishing, he says. Parkinson’s is characterized by brain degeneration, marked by a shortage of the neurotransmitter dopamine. That shortage results in movement problems. After surgery, many patients are suddenly able to get around, do household chores and even go shopping, Follett says. “It has the potential to change people’s lives.” Follett’s firsthand observations are now supported by clinical research. He and a team of fellow surgeons and scientists report in the Jan. 7 Journal of the American Medical Association that Parkinson’s patients randomly assigned to get medication plus the surgery show dramatic improvements, whereas patients getting just the best available medication do not. The surgery, called deep-brain stimulation, isn’t new, having been first approved by regulators in 1997. But only one other study — reported by German scientists in 2006 — has tested the surgery against medication in a large, randomized trial. That study also showed benefits in patients who received both surgery and medication (SN: 9/2/06, p. 149). © Society for Science & the Public 2000 - 2009

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 12418 - Posted: 06.24.2010

For many people, our only experience with Parkinson’s disease is that of watching actor Michael J. Fox struggle publicly with the illness as he has campaigned for more research and funding. But as my colleague Karen Barrow notes in the latest “Patient Voices” feature, there are many less-famous faces of Parkinson’s. Parkinson’s disease is a neurologic disorder that occurs as a result of the death of nerve cells in the brain that produce dopamine. The loss of dopamine production in the brain can lead to tremors, balance problems, stiff facial expressions and muffled speech, among other things. In the United States, an estimated 1 million people have the disease, and another 60,000 are diagnosed each year. Although the condition usually develops after the age of 60, 15 percent of those diagnosed are under 50. One of those is runner Alyssa Johnson, 43, who was training for the Boston Marathon in 2003 when she started dragging her leg and developed a shin cramp. After searching for answers, she was finally diagnosed with Parkinson’s. “It’s not something you’d expect with someone my age,'’ she said. “I used to run with my husband all the time. We don’t run together anymore because it’s still too hard for me emotionally. He’s still competitive, and I’m still trying to get from point A to point B.'’ Copyright 2008 The New York Times Company

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 11910 - Posted: 06.24.2010

"I couldn't live the way I was living. It was just too intense," says Nathan Klein. The married freelance television producer and father of two was 45 years old when he found out that that his tremors and loss of motor control were symptoms of Parkinson's disease. He tried various treatments and medications, including dopamine drugs. Explains Klein, "The symptoms don't get better. They get worse. And the pills you take eventually don't help out. So, you know, what's there to look forward to? Nothing." So Klein researched experimental therapies and four years ago decided to enroll in a clinical trial to assess the safety of an experimental gene therapy for Parkinson's. He became the first person in the world to undergo the procedure. Neurosurgeon Michael Kaplitt of Weill Cornell Medical Center operated on Klein. He injected viruses carrying the therapeutic genes directly into the overactive area of his brain, the subthalamic nucleus, that controls movement. Because of the experimental nature of the study, the twelve participants were only treated on one side of the brain. The study was a joint endeavor with The Feinstein Institute for Medical Research in Long Island. © ScienCentral, 2000-2007

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 11151 - Posted: 06.24.2010

In 2003, ScienCentral interviewed researcher Michael Kaplitt, assistant professor of neurological surgery at New York-Presbyterian/Weill Cornell Medical Center, and co-founder of Neurologix, Inc. Kaplitt and his team had gotten approval for a Phase 1 study to determine the safety of gene therapy in patients with Parkinson's disease and had performed the world's first gene therapy surgery on a patient with the disease. The findings of the completed study are published in the June 23 issue of the British medical journal The Lancet. The video to the right includes excerpts from our 2003 interview with Kaplitt. For more information on the newly published study, read on. The study reported positive results from the first ever gene therapy trial for Parkinson's disease. The clinical trial studied 12 patients, 11 men and one woman, ranging in age from 50 to 67, who had advanced Parkinson's disease. It was a "Phase 1" study, meaning it was designed primarily to test and prove that the therapy is safe. Kaplitt and his team used a harmless virus called an adeno-associated virus (AAV) as a sort of cargo ship for the corrective gene they wanted to deliver to the patient's brains. The virus carrying the gene called "GAD" (glutamic acid decarboxylase) was injected into a part of the brain called the subthalamic nucleus (STN), which usually has abnormally high activity in Parkinson's patients. This heightened activity leads to the loss of muscle control that is a hallmark of Parkinson's. © ScienCentral, 2000-2007

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 10419 - Posted: 06.24.2010

By CLAUDIA DREIFUS CAMBRIDGE, Mass. — Short of a Nobel Prize, there are few scientific honors that the biologist Susan L. Lindquist has not won. In The Lab Susan Lindquist and her team tested 5,000 genes to find a few that express a protein capable of saving a yeast cell from the Parkinson’s gene. Among other accolades, she is a Howard Hughes Medical Investigator, a member of the National Academies of Science and the American Academy of Arts and Sciences, and the 2006 recipient of the Sigma Xi William Procter Prize for Scientific Achievement. It has all come her way because of her imaginative research into how proteins function. Dr. Lindquist, the former director of the Whitehead Institute for Biomedical Research at the Massachusetts Institute of Technology, studies how molecular proteins change shape in cell division. The process, called protein folding, can— when it goes wrong — lead to diseases like Alzheimer’s and Parkinson’s. Last June, Dr. Lindquist and a group of colleagues published a paper in the journal Science reporting new clues about how Parkinson’s develops and how it might be treated. Copyright 2007 The New York Times Company

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 10210 - Posted: 06.24.2010

In humans, a dearth of the neurotransmitter dopamine has long been known to play a role in Parkinson's disease. It is also known that mutations in a protein called parkin cause a form of Parkinson's that is inherited. Now, UCLA scientists, reporting in the Jan. 31 issue of The Journal of Neuroscience, have put the two together. Using a new model of Parkinson's disease they developed in the simple Drosophila (fruit fly), the researchers show for the first time that a mutated form of the human parkin gene inserted into Drosophila specifically results in the death of dopaminergic cells, ultimately resulting in Parkinson's-like motor dysfunction in the fly. Thus, the interaction of mutant parkin with dopamine may be key to understanding the cause of familial Parkinson's disease — Parkinson's that runs in families. Conventional wisdom has held that parkin is recessive, meaning that two copies of the mutated gene were required in order to see the clinical signs of Parkinson's disease. But the researchers, led by George Jackson, M.D., Ph.D., UCLA associate professor of neurology and senior scientist at the Semel Institute for Neuroscience and Human Behavior at UCLA, wanted to see if they could get the protein to act in a dominant fashion, so they put only one copy of the mutation into their fly model. The result was the death of the neurons that use dopamine, the neurotransmitter long implicated in Parkinson's disease. "We put the mutant parkin in all different kinds of tissues and in different kinds of neurons, and it was toxic only to the ones that used dopamine," Jackson said. "No one's shown this degree of specificity for dopaminergic neurons."

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 9916 - Posted: 06.24.2010

Roxanne Khamsi, Atlanta Initial results from the first human clinical trial of gene therapy treatment for Parkinson’s disease suggest the approach can significantly reduce symptoms of the disease. After a year, the 12 patients in the trial showed an average 25% improvement in motor control. The researchers say the new treatment shows no signs of reducing immunity – gene therapy for other illnesses has caused fatal immune-system complications. There is currently no cure for Parkinson’s disease, a fatal degenerative brain condition that causes tremors, speech difficulties and progressive loss of mobility, among many other symptoms. Sufferers can take medications such as levodopa, which helps by elevating levels of the chemical messenger dopamine in the brain. But people respond less to the drug over time and can experience side effects such as jerky movements. Researchers hoping to develop a cure for Parkinson’s have now turned to gene therapy. They developed the treatment by engineering a harmless virus to carry genes that encode a protein called glutamic acid decarboxylase, or GAD. The protein helps make a key nerve signalling chemical called GABA (gamma aminobutyric acid), which inhibits a brain region known as the subthalamic nucleus. This is important because the subthalamic nucleus is typically overactive in Parkinson’s disease due to a loss of dopamine-producing cells elsewhere in the brain. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 9490 - Posted: 06.24.2010

New research suggests that nicotine treatment protects against the same type of brain damage that occurs in Parkinson’s disease. The research was conducted in laboratory animals treated with MPTP, an agent that produces a gradual loss of brain function characteristic of Parkinson’s. Experimental animals receiving chronic administration of nicotine over a period of six months had 25 percent less damage from the MPTP treatment than those not receiving nicotine. This protective effect may explain the lower incidence of Parkinson’s disease among smokers. The results also suggest that nicotine may be useful as a potential therapy in the treatment of early-stage Parkinson’s patients. The five-year study was conducted by researchers at The Parkinson’s Institute, an independent, non-profit research institute located in Sunnyvale, California. The study results are published in an on-line early release in the Journal of Neurochemistry (doi:10.1111/j.1471-4159.2006.04078.x) Parkinson’s disease is a progressive, neurodegenerative disease caused by the death of small clusters of cells in the midbrain. The gradual loss of these cells results in reduction of a critical transmitter called dopamine, the chemical messenger responsible for normal movement. “While we would never recommend that people smoke, these results suggest that nicotine promotes the survival of dopamine-producing cells in animals with no overt Parkinson’s symptoms,” said David A. Schwartz, M.D., director of the National Institute of Environmental Health Sciences, the federal agency that provided funding for the study.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 9218 - Posted: 06.24.2010

A National Institutes of Health-sponsored clinical trial with 200 Parkinson's disease patients has shown that creatine and minocycline may warrant further consideration for study in a large trial, according to Karl Kieburtz, M.D., M.P.H., University of Rochester, who spoke today at the World Parkinson Congress on behalf of the trial investigators. Study investigators caution that while the news is encouraging, the results do not demonstrate that these agents are effective in Parkinson's disease. Before these interventions can be recommended as a treatment they must be tested in a larger trial with hundreds of patients. Study findings are available online and will be published in the March 14 issue of Neurology.* Parkinson's disease is a degenerative disorder of the brain in which patients may develop progressive tremor, slowness of movements, and stiffness of muscles. It affects approximately 1 percent of Americans over the age of 65. Although certain drugs, such as levodopa, can reduce the symptoms of Parkinson's, no treatment has been shown to slow the progressive deterioration in function. The National Institute of Neurological Disorders and Stroke (NINDS) of the National Institutes of Health (NIH) has organized a nationwide multi-center effort called NET-PD (Neuroprotection Exploratory Trials in Parkinson's Disease), a randomized, double-blind futility trial, to study compounds that may slow the clinical decline of Parkinson's disease. As the initial step in these efforts, creatine and the antibiotic minocycline were identified as agents worthy of preliminary study. Patients very early in the disease course who did not yet need medications typically used to treat their Parkinson's symptoms were included in the study.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 8575 - Posted: 06.24.2010

Disease nosed its way into David Eger's life gradually. At first, he couldn't raise his elbow as high as usual. He brushed it off as a possible gym injury. But soon, his left fist would clench and go rigid. "My family began to notice it and observe it, so I decided I'd better go and have somebody look at it," says Eger, a 60-year old clinical psychologist. After testing, Eger's was diagnosed with Parksinson's disease, a brain disorder that whittles away the brain's ability to make a key chemical called dopamine that controls body movement. Now, researchers working on a study in mice have found that a popular dance club drug — the amphetamine, ecstasy — might help patients like Eger combat the physical decline that accompanies Parkinson's. "We went and tested as many as 70 drugs total, belonging to 20 different pharmacological groups," explains Raul Gainetdinov, a neuroscientist who was part of the Duke University team that studied the effects of amphetamines in lab mice that have Parkinson's-like symptoms. "To our surprise, not many things really worked. When we tried with ecstasy it was the first drug that we discovered working... It was amazingly effective," he says. "[The mice] went from a situation where they were completely frozen to ability to move quite a significant distance, and pretty much normally." © ScienCentral, 2000-2005

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 8197 - Posted: 06.24.2010

Symptoms in mice that mimic Parkinson’s disease are reversed by treatment with amphetamines, including Ecstasy, according to a new study. The drugs seem to work through a pathway not involving the chemical dopamine, which surprised the researchers since dopamine deficiency is the cause of Parkinson’s. These results may lead to the discovery of “other systems that can replace or substitute for the very important action of dopamine”, says study author Marc Caron of Duke University, US. Dopamine transmission in a region of the brain called the striatum is essential for normal movement. Parkinson’s results when dopamine-producing neurons in this region die. The best current treatment for the condition is a chemical called L-Dopa – a natural precursor to dopamine. L-Dopa works well for patients in the early stages of the disease, but its effectiveness diminishes with time, and it can actually cause involuntary movements. To screen for other types of drugs, Russian scientists Tatyana Sotnikova and Raul Gainetdinov, working with the team at Duke University, studied mice altered to possess no brain dopamine. They show classic symptoms of Parkinson’s disease including muscle rigidity, problems initiating movement, and resting body tremor. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 7722 - Posted: 06.24.2010

The human brain is a complicated organ and the last to be deciphered by medicine. Although we are continually gaining new understanding about the intricacies of how the brain works ? especially what happens in the brain when things stop working and how to treat those issues ? but science still has a long way to go. The tremors that Steve Tarence, from Milford, Connecticut, suffered in his right arm because of Parkinson's Disease became so severe there was little he could still do by himself. "It's what they call flapping, where? the hand just takes off on you," he explains. "I couldn't go out, I couldn't turn around? life was changed completely because of it. It was really bad." He says deep brain stimulation (DBS) gave him back much of the life Parkinson's had taken away. "I am not afraid to go out, I'm not afraid to eat soup, I'm not afraid to do so many things? it's really, really wonderful," says Tarence. It was so successful in calming the tremors in his right arm that he plans to have it done for the tremors that have now begun on his left side. In DBS, surgeons implant electrodes ? with millimeter precision ? into the brain to stimulate the areas causing the tremors. But how pulses of electrical stimulation relieve the uncontrolled movement, why it doesn't help some patients, and what the long-term consequences of it might be, are not fully understood. © ScienCentral, 2000-2005.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 7532 - Posted: 06.24.2010

Pope John Paul II was one of the most vigorous, well-traveled popes in history. But in his last years, Parkinson's disease made him frail and weak. People with Parkinson's often experience muscle rigidity, trembling, difficulty walking, and problems with balance and coordination. There is no cure for this progressive neurological disorder. Parkinson's disease is caused by a loss of the brain cells called neurons that produce a chemical called dopamine. Without enough of this important neurotransmitter, parts of the brain become overactive and sufferers lose control of their muscle activity. "We really don’t understand what dopamine does in the normal situation," says Mark West, a psychology professor at Rutgers University. "We know what happens when dopamine's been lost—movement becomes very difficult. In some way then, dopamine helps the brain’s motor system function smoothly. "The typical drug given is L-Dopa, which the brain converts into dopamine, and thus, some of the dopamine that's been lost is replaced," says West. The drug, developed more than 30 years ago, remains the most effective treatment. But doctors admit L-Dopa is only a bandaid for the symptoms and for some patients, it works only temporarily. "It was pretty clear over time," explains Michael Kaplitt, a professor of neurological surgery at New York Presbyterian-Weill-Cornell Medical Center. "Parkinson’s disease patients will suffer with this disorder for a long period of time—for 15, 20, 30 years or more. And after they've taken these drugs for a long period of time, a lot of things can happen. For some patients, they can become increasingly resistant to the medication after years of taking it, so they will require increasing doses of the medication, or they'll require more numerous doses throughout the day. But even with that they continue to worsen." (C) ScienCentral, 2000-2005.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 7135 - Posted: 06.24.2010

The following statement is being released by the Parkinson’s Disease Foundation, located at 710 West 168th Street, New York City. It follows the announcement, earlier today, of a decision by Amgen Incorporated, manufacturer of GDNF, an experimental neural growth factor, to forgo the offer of reinstatement of GDNF to patients who were involved in recent clinical trials of the treatment. The authors of the PDF statement are Stanley Fahn, M.D., the Foundation’s Scientific Director, and Robin Anthony Elliott, its Executive Director. "The Amgen announcement, which followed a resolution by the PDF Board of Directors urging the company to permit patients who participated in the company’s clinical trials the option of continued access to GDNF, is deeply disappointing to PDF, to the Parkinson’s community, and to the participating patients," the statement reads. "However well-intentioned the company may have been in wrestling with this issue, we believe it has reached the wrong decision – whether judged in terms of science, or the desires of the people who participated in the clinical trials, or the issues of safety." "In terms of the science, we would argue that the reinstatement of GDNF, if accompanied by the continuing collection of efficacy and safety data, would enable scientists and regulatory authorities to monitor the long-term aspects of safety and efficacy of the treatment. Furthermore, the observation of increased fluorodopa uptake in PET scans needs to be carefully followed over time to determine if this will eventually translate into clinical improvement. Giving up this opportunity to learn is, in our view, a mistake." © 2005 The Parkinson’s Disease Foundation

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 6872 - Posted: 06.24.2010

Scientists who developed the first yeast model of Parkinson’s disease (PD) have been able to describe the mechanisms of an important gene’s role in the disease. Tiago Fleming Outeiro, Ph.D., and Susan Lindquist, Ph.D., of the Whitehead Institute for Biomedical Research in Cambridge, Massachusetts, studied the gene’s actions under normal conditions and under abnormal conditions to learn how and when the gene’s product, alpha-synuclein, becomes harmful to surrounding cells. The scientists created a yeast model that expresses the alpha-synuclein gene, which has been implicated in Parkinson’s disease (PD). Yeast models are often used in the study of genetic diseases because they offer researchers a simple system that allows them to clarify how genes work. The National Institute of Neurological Disorders and Stroke, part of the National Institutes of Health, funded the study, which appears in the December 5, 2003, issue of Science. ¹ The alpha-synuclein protein, which is found broadly in the brain, has been implicated in several neurodegenerative disorders. Sometimes a mutation or a misfolding of the protein causes the problems; other times there are too many copies of the normal gene. A study earlier this year reported that patients with a rare familial form of PD had too many normal copies of the alpha-synuclein gene, which resulted in a buildup of protein inside brain cells, causing the symptoms of PD.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 4653 - Posted: 06.24.2010

St. Paul, MN – Excessive gambling could be an unfortunate yet rare side effect in Parkinson’s patients who take certain dopamine agonists, according to a study in the August 12 issue of Neurology, the scientific journal of the American Academy of Neurology. Researchers at Muhammad Ali Parkinson Research Center in Phoenix, Ariz., examined the data of 1,884 Parkinson’s patients who were seen during a one-year period. Nine patients – seven men and two women – were identified with pathological gambling. “The risk of gambling problems in a Parkinson’s patient is very small,” said study author Mark Stacy, MD, who is now the medical director of the Parkinson’s Disease and Movement Disorders Center at Duke University Medical Center, Durham, N.C. “However, it may be appropriate for doctors to inform patients of this potential risk, particularly in their patients taking relatively high dosages of a dopamine agonist, and with a documented history of depression or anxiety disorder.”

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 4151 - Posted: 06.24.2010