Links for Keyword: Parkinsons

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Fran Lowry Salivary gland biopsy appears to be a diagnostic test for Parkinson's disease, a new study suggests. A biopsy of the submandibular gland that shows the presence of the abnormal protein alpha-synuclein is highly indicative of Parkinson's, as distinct from other neurodegenerative disorders that can mimic the disease, said lead study author, Charles Adler, MD, PhD, from the Mayo Clinic Arizona, Scottsdale, Arizona. "There is currently no diagnostic test for Parkinson's disease in living patients. The only way to make the diagnosis is at autopsy, when you can see an abnormal protein, alpha-synuclein, in certain brain regions," Dr. Adler, a fellow of the American Academy of Neurology, told Medscape Medical News. Their preliminary findings were released January 10; full results will be presented at the American Academy of Neurology's 65th Annual Meeting in San Diego. Dr. Adler and his team have been working on determining whether there is evidence of alpha-synuclein in other organs of the body so that they could develop a diagnostic test in living patients. "We previously published the fact that the submandibular gland has one of the densest concentrations of alpha-synuclein in an organ outside the brain. When we tested this in an autopsy study of 28 Parkinson's disease patients, we found that all 28 of them had alpha-synuclein in the submandibular gland," he said. The discovery led the researchers to biopsy the submandibular gland in living patients with Parkinson's disease to see whether this protein was present. If it was, then the biopsy could potentially be used as a diagnostic test, they reasoned. © 1994-2013 by WebMD LLC

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 17671 - Posted: 01.12.2013

By JAMES GORMAN For the first time, researchers at the Massachusetts Institute of Technology report, brain imaging has been able to show in living patients the progressive damage Parkinson’s disease causes to two small structures deep in the brain. The new technique confirms some ideas about the overall progress of the disease in the brain. But the effects of Parkinson’s vary in patients, the researchers said, and in the future, the refinement in imaging may help doctors monitor how the disease is affecting different people and adjust treatment accordingly. The outward symptoms and progress of Parkinson’s disease — tremors, stiffness, weakness — have been well known since James Parkinson first described them in 1817. But its progress in the brain has been harder to document. Some of the structures affected by the disease have been buried too deep to see clearly even with advances in brain imaging. An important recent hypothesis about how the disease progresses was based on the examinations of brains of patients who had died. Now, a group of scientists at M.I.T. and Massachusetts General Hospital report that they have worked out a way to combine four different sorts of M.R.I. to get clear pictures of damage to two brain structures in people living with Parkinson’s. In doing so, they have added support to one part of the recent hypothesis, which is that the disease first strikes an area involved in movement and later progresses to a higher part of the brain more involved in memory and attention. Suzanne Corkin, a professor emerita of behavioral neuroscience at M.I.T. and the senior author on the paper published online Monday in The Archives of Neurology, said that this progression was part of the hypothesis put forward in 2003 by Heiko Braak, a German neuroscientist, based on autopsies. © 2012 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: 17544 - Posted: 11.27.2012

By Laura Sanders The insidious spread of an abnormal protein may be behind Parkinson’s disease, a study in mice suggests. A harmful version of the protein crawls through the brains of healthy mice, killing brain cells and damaging the animals’ balance and coordination, researchers report in the Nov. 16 Science. If a similar process happens in humans, the results could eventually point to ways to stop Parkinson’s destruction in the brain. “I really think that this model will increase our ability to come up with Parkinson’s disease therapies,” says study coauthor Virginia Lee of the University of Pennsylvania Perelman School of Medicine in Philadelphia. The new study targets a hallmark of Parkinson’s disease — clumps of a protein called alpha-synuclein. The clumps, called Lewy bodies, pile up inside nerve cells in the brain and cause trouble, particularly in cells that make dopamine, a chemical messenger that helps control movement. Death of these dopamine-producing cells leads to the characteristic tremors and muscle rigidity seen in people with Parkinson’s. Lee and her team injected alpha-synuclein into the brains of healthy mice. After 30 days, the protein had spread to connected brain regions, suggesting that rouge alpha-synuclein moves from cell to cell, the scientists found. Months later, the spreading was even more extensive. © Society for Science & the Public 2000 - 2012

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 17499 - Posted: 11.17.2012

By Dan Cossins There’s a new suspect in the search for the causes of Parkinson’s disease—deformities in the nuclear membrane of neural stem cells. Scientists observed the same defects, caused by a single gene mutation, in brain tissue samples from deceased Parkinson’s patients, suggesting that nuclear deterioration—and the mutation that drives it—could play a role in the pathology of the disease. The study, published today (October 17) in Nature, also shows that correcting the mutation reverses this phenotype, pointing to new ways to treat this cause of neurodegeneration. “I don’t recall anyone ever suggesting this as a major phenotype [for Parkinson’s], so that’s really quite a big new direction for the field,” said Mark Cookson, a neuroscientist at the National Institutes of Health in Bethesda, Maryland, who did not participate in the study. Parkinson’s disease has traditionally been attributed to a loss of dopamine-generating neurons, which leads to the degenerative muscle control that is characteristic of the disease. But Parkinson’s also causes many other sensory problems, which cannot be explained by a dopaminergic mechanism. Over the past 5 years, several groups have shown that disruption of the structure of the nuclear envelope—the lipid bilayer that separates nucleus from cytoplasm—is correlated with aging and certain age-related pathologies in the human brain, though the precise role of nuclear defects in the diseases remained unclear. Meanwhile, since 2004 scientists including Cookson have demonstrated that a mutation in the luceine-rich repeat kinase 2 (LRRK2) gene is correlated with Parkinson’s. However, the molecular and cellular mechanisms by which the LRRK2 mutation might drive disease progression remained a mystery. © 1986-2012 The Scientist

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 17392 - Posted: 10.20.2012

COFFEE can give you the shakes, but caffeine seems to have the opposite effect in people with Parkinson's disease, helping to relieve tremors and get them back on the move. In the past, caffeine has been shown to reduce the risk of Parkinson's, but its effects have never been tested in people who already have the disease. Ronald Postuma of McGill University in Montreal, Canada, and colleagues gave 61 people with Parkinson's a 6-week course of pills containing the caffeine equivalent of about three cups of coffee every day, or a placebo. Only people in the caffeine group showed a significant improvement in tests for motor problems, such as the severity of their tremors, and general mobility (Neurology, DOI: 10.1212/WNL.0b013e318263570d). Motor problems associated with Parkinson's are caused by a lack of dopamine in areas of the brain where dopamine-producing cells are destroyed. Adenosine receptors normally inhibit the production of dopamine. Caffeine blocks adenosine receptors and so acts to boost available dopamine. Drugs that target adenosine receptors are already in clinical trials but caffeine could provide a cheaper alternative. © 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: 17123 - Posted: 08.04.2012

By KATE YANDELL When Nancy Mulhearn learned she had Parkinson’s disease seven years ago, she kept the diagnosis mostly to herself, hiding it from friends, colleagues — even, at first, her mother, sister and teenage children. After seven months, she decided she had to tell her family, and they settled into an unspoken agreement not to talk about the disease. She also realized her colleagues already suspected the truth: One asked why she had trouble applying her lipstick. She sometimes could not control her shaking hands. Still, it was years before Ms. Mulhearn, now 51, of Bethlehem Township, N.J., felt she could talk freely about her condition. Ms. Mulhearn, a school secretary, regrets having waited so long. “I didn’t want anybody to feel sorry for me,” she said. “To have people look at you and start crying — that’s not what anyone wants.” In that, Ms. Mulhearn is hardly alone. Doctors and researchers say it’s not uncommon for people with Parkinson’s to conceal their diagnoses, often for years. But the secrecy is not just stressful to maintain; experts fear that it also may be slowing down the research needed to find new treatments. Parkinson’s disease progresses over many years as brain cells that produce dopamine, a neurotransmitter, slowly waste away. Without dopamine, nerves have trouble sending messages; muscle movement becomes erratic and difficult to control. Some patients, though not all, experience memory problems, altered speech, cognitive difficulty, insomnia and depression. Copyright 2012 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: 17019 - Posted: 07.10.2012

by Liz Else THOUSANDS of people may soon be making a very important three-minute phone call - to a computer. It could tell them whether or not they have Parkinson's disease. Technology has long promised a revolution in "smart medicine", allowing painful pokes and prods to be replaced with faster, more accurate and non-invasive ways of diagnosing a range of diseases. That vision took a big step forward last week, when Max Little of the Massachusetts Institute of Technology's Media Lab appealed for people worldwide to test a voice-based system he helped develop for diagnosing Parkinson's. The software uses a speech-processing algorithm to identify telltale changes in the voice of a person with the disease. Parkinson's affects some 6 million people worldwide. Although surgery and drugs can hold back its progression, there is no cure. Diagnosing it and tracking its course usually relies on an assessment of someone's symptoms using the Unified Parkinson's Disease Rating Scale, which involves tests of motor skills, for example. The process is time-consuming, expensive and requires people to attend a clinic for the tests to be carried out. It is partly because of this that it is thought that around a fifth of cases of Parkinson's are never diagnosed. But the disease often manifests early on in the voice, as it affects the ability to control the vocal cords and soft palate. Common signs include a quaver in the voice, softer speech and breathiness or hoarseness, though they can be subtle at first. This makes Parkinson's a perfect candidate for diagnosis over the phone. © 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: 17018 - Posted: 07.10.2012

By Jane Wakefield Technology reporter, Parkinson's is a devastating disease for those living with the condition and currently there is no cure. Diagnosis can also be slow as there are no blood tests to detect it. But now mathematician Max Little has come up with a non-invasive, cheap test which he hopes will offer a quick new way to identify the disease. He will be kicking off the TEDGlobal conference in Edinburgh calling for volunteers to contribute to a huge voice database. Mr Little has discovered that Parkinson's symptoms can be detected by computer algorithms that analyse voice recordings. In a blind test of voices, the system was able to spot those with Parkinson's with an accuracy of 86%. Mr Little was recently made a TED Fellow. The non-profit organisation behind the TED (Technology, Entertainment and Design) conference creates 40 such fellowships each year. The programme aims to target innovators under the age of 40 and offers them free entry to conferences and other events. Mr Little became interested in understanding voice from a mathematical perspective while he was studying for a PhD at Oxford University in 2003. BBC © 2012

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 16976 - Posted: 06.27.2012

By Scicurious A colleague handed me this paper, not just as an interesting aspect of Parkinson’s, but as somewhat supportive paper for the role of serotonin in depression. I have said before that I think the serotonin theory of depression (as depicted in Zoloft commercials) is probably wrong, but my views are actually a bit more nuanced than that. The serotonin theory is probably wrong, but not because it is wrong, rather, it is oversimplified. I think that low serotonin levels on their own probably don’t cause depression, but it looks like there may still be a role for serotonin in depressive symptoms, and this paper seems to agree. Science, it’s always more complicated than you think at first. Parkinson’s is something that no one wants to get. It’s a degenerative disorder of the nervous system, which results in a wide variety of symptoms. Most people think of Parkinson’s and picture a shuffling gait, severe hand tremor, slowness of movement and rigidity. But there are other symptoms as well, include depression, hallucinations, fatigue, sleep disturbances, and cognitive deficits as the disease progresses. And when most people think of potential causes for Parkinson’s, they think of a deficit in dopamine, the neurotransmitter that I usually think of with regard to reward and reinforcement, but which is extremely important in motor systems as well. In Parkinson’s patients, you see a striking loss of dopamine neurons in motor areas like the substantia nigra (it’s easy to see because the melanin in the substantia nigra, which is latin for “black substance” dyes the cells black, and when those cells die, the stubstantia nigra becomes a lot less substantia and nigra). But again, it’s not just dopamine in the substantia nigra, there are other systems involved and differences in signaling that also play a role as the disease progresses. © 2012 Scientific American,

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 16970 - Posted: 06.26.2012

by Peter Aldhous If ever we develop a DeLorean-based time machine, it would be handy to send information into the past revealing what kind of medical research to focus on. For years, actor Michael J. Fox was on the front line of the US's "stem cell wars", arguing that embryonic stem cells could cure conditions like his own – Parkinson's disease. Last week Fox revealed he now believes that other lines of research hold more promise. "There have been some issues with stem cells, some problems along the way," Fox told ABC News. "An answer may come from stem cell research but it's more than likely to come from another area." Complicated business The Michael J. Fox Foundation, based in New York City, is still backing stem cell research, says its chief scientific adviser, Gene Johnson of Washington University in St Louis, but has shifted its emphasis in recent years. "Using stem cells as therapeutic agents is a very complicated business," Johnson says. Obstacles include working out how to get transplanted cells to integrate into the brain, and developing "off-the-shelf" cell lines that can be used for any recipient. Meanwhile, other avenues are speeding towards clinical trials. These include neurotrophic factors – proteins that promote the survival of nerve cells – as well as antibodies that target the alpha-synuclein protein, which may be a cause of the brain damage seen in Parkinson's. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory, Learning, and Development
Link ID: 16833 - Posted: 05.23.2012

A Glasgow-based doctor is to lead the world's biggest research study into the cause of Parkinson's disease. The brain condition affects almost 130,000 people in the UK. Dr Donald Grosset, a neurologist at Glasgow University, said he hoped to find better ways of both diagnosing and treating the disease. Charity Parkinson's UK is looking for 3,000 volunteers with the condition - and their siblings - to take part in the study. Parkinson's is a debilitating condition with symptoms which include tremors, mood changes, movement difficulties, loss of smell and speech problems. The charity said it was investing more than £1.6m in the Tracking Parkinson's study with the long-term aim of boosting the chances of finding a cure. The study will follow 3,000 volunteers - people recently diagnosed with the disease, people diagnosed aged under 50 and their brothers and sisters. The aim is to identify markers in the blood which could be used to create a simple diagnostic test for the disease, something which does not yet exist. Parkinson's UK said early diagnosis is crucial if doctors are to be able to prescribe the right drugs for people with the condition. BBC © 2012

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 16657 - Posted: 04.16.2012

By Phyllis Richman, Parkinson’s disease is a thief. It robbed me of the ability to turn over in bed. I can no longer take a long walk. Opening a plastic bag or turning a newspaper page has become a challenge. We PWPs (Persons With Parkinson’s) become familiar with loss. In my case, though, Parkinson’s has also granted one of my keenest desires. After decades of hopelessly wishing on birthday candles and turkey collarbones that I could carry a tune, suddenly I can unashamedly join in family singalongs. I can sing. That’s thanks to fellow PWP Judy Dodge. A retired church music director and organist, she arranged with the Parkinson Foundation of the National Capital Area to lead a weekly PWP choir class. I would never have signed up, but she persuaded me that the voice exercises would be good for my stiffening vocal cords, and my tunelessness would not be a drag on the group. While some had signed up simply for a chance to do choral singing, the class was designed to be therapeutic as well, to counterbalance Parkinson’s softening our voices and flattening our tone, to strengthen our lungs and our enunciation. Mine wasn’t the worst among the hesitant and scratchy voices, and there were some talented singers to drown us out. But even they needed to practice projecting their voices and keeping their muscles supple. Every Wednesday afternoon for about a year now, a dozen or more PWPs gather in a Chevy Chase church hall where the heating system breathes more loudly than we do. We warm up our throats by humming and singing scales. We try to breathe slowly and project strongly. We massage our cheeks, stretch out our tongues and read poetry. We belt out folk songs, gospel and show tunes. It isn’t always tuneful, but it is fun. © 1996-2012 The Washington Post

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 16616 - Posted: 04.05.2012

MONKEYS with Parkinson's disease-like symptoms have had their suffering eased by an injection of human embryonic stem cells (hESCs) into their brain. Jun Takahashi of Kyoto University in Japan and colleagues injected these cells into monkeys whose brains had been damaged by a chemical that destroys dopamine-producing neurons and so causes Parkinson's symptoms. Two monkeys received hESCs that had been matured into an early form of neural cell. Six months later, the monkeys had recovered 20 to 45 per cent of the movement they had lost before treatment. Post-mortems a year after treatment showed that the cells had developed into fully functioning dopamine-secreting neurons. Another monkey that received less-mature neural cells also showed improvements (Stem Cells, DOI: 10.1002/stem.1060). "Monkeys starting with tremors and rigidity [began] to move smoothly, and animals originally confined to sitting down were able to walk around," says Takahashi. The team says it will probably be four to six years before clinical trials in humans begin. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory, Learning, and Development
Link ID: 16538 - Posted: 03.19.2012

By Nathan Seppa Twice-a-week tai chi lessons can help people with Parkinson’s disease maintain their footing and lessen the risk of falls, a new study finds. Training in the Chinese martial art seems to improve ankle stability, posture control and walking ability in these patients. Tai chi includes exercises and posture changes by which the body flows slowly from one position into another, with heightened awareness of balance, coordination and weight shifting. “We’re hoping that physical therapy will pick up some of these movements” for Parkinson’s patients, says study coauthor Fuzhong Li, a behavioral researcher at the Oregon Research Institute in Eugene. “They are very easy to incorporate into PT sessions.” The study appears in the Feb. 9 New England Journal of Medicine. Parkinson’s disease gradually destroys brain cells that produce dopamine, a neurotransmitter essential for delivering brain signals that control muscle movement. People with the disease risk falling every day as they struggle to maintain balance in walking and performing common tasks. Many Parkinson’s patients improve with medication or brain surgery (SN: 9/2/2006, p. 149). But those benefits have limits. “Surgical treatment and drugs make a person more mobile but don’t improve the ability to control balance,” says Lee Dibble, a physical therapist and Parkinson’s researcher at the University of Utah. The new report suggests that tai chi and to some extent resistance training do aid balance and limit falls. “You really need an intervention like this to improve and maintain function,” Dibble says. © Society for Science & the Public 2000 - 2012

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 16368 - Posted: 02.11.2012

By Laura Sanders After surviving a bout of virulent bird flu, mice’s brains show short-term reductions of a key brain chemical and long-lasting signs of infection, a new study finds. The research suggests this type of flu might leave people more vulnerable to brain disorders such as Parkinson’s disease. While most people think of influenza as a disorder of the body, certain kinds of flu also infect the brain. Recent studies have found that the bird flu virus known as H5N1, which kills about half the people it infects, can set up shop in the brain. But exactly what happens next has been a mystery. In the new study, scientists at St. Jude Children’s Research Hospital in Memphis, Tenn., examined the brains of mice that had survived an initial H5N1 infection. As in people, the virus kills about half of mice affected. “The first goal with H5N1 was to characterize the neurological effects,” says study coauthor Richard Smeyne. After being infected with H5N1 isolated from a Vietnamese boy who died from the flu, some mice initially got very sick, but then seemed to recover completely after about 21 days. Yet the story wasn’t so simple in the brain, the team reports in the Feb. 1 Journal of Neuroscience. Nerve cells that make one of the brain’s key messengers — the neurotransmitter dopamine, which helps regulate movement — shut down production about 10 days after infection. These nerve cells, which are the same cells that degenerate in people with Parkinson’s disease, “basically take a time out,” Smeyne says. “All efforts are to survive.” © Society for Science & the Public 2000 - 2012

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 16332 - Posted: 02.02.2012

By Alice Reid Well before sunup, Chuck Linderman launches his daily workout at the Alexandria boat house: 30 minutes pulling hard on a Concept 2 rowing machine, an equal stint lifting free weights and 30 minutes pedaling a stationary bike. He drives himself to sweaty, breathless exhaustion, for Linderman is training for the race of his life — a race against Parkinson’s disease. Linderman is one of a million Americans afflicted by this neurodegenerative disease that kills off the brain cells responsible for the body’s ability to move. His diagnosis came six years ago, when his wife noticed that his right arm was moving weirdly and that he was having trouble fastening the top button on his dress shirts. His doctor recommended seeing a neurologist. “It took the guy less than 15 minutes to make the diagnosis,” said Linderman, 64. Rowing already played a role in his life. For nearly a decade, he had been active in Alexandria Community Rowing’s masters program. So his response to Parkinson’s was immediate. Fight back with what he knew best: strenuous exercise. “What is the alternative? A descent into invalidism?” said Linderman, who retired two years ago from his job as director of a power company association. Exercise of any sort has long been known to be helpful for Parkinson’s. Before the development of effective drug therapy in the ’60s, patients often improved with any exercise, even the act of folding laundry, according to Michael Okun, national medical director of the Parkinson’s Foundation, which emphasizes exercise as an important tool to fight the disease. © 1996-2012 The Washington Post

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 16238 - Posted: 01.10.2012

By Ingrid Wickelgren Peter West makes his living working with explosives, but for a long time he did his job despite a terrifying handicap: tremors. His hands would twitch and shake, his head would bob, his speech would become garbled. Sometimes he could barely pour milk from a pitcher—the milk slopping over the side of the glass. “At that time, I was mixing high explosives,” West says. “I knew it was a matter of time before I dropped one.” Luckily the most significant thing West, 54, dropped was his golf ball. In 2003, while on the links, a doctor in West’s party noticed he was having trouble balancing the ball on the T. One thing led to another, and West was diagnosed with essential tremor, a neurological disorder characterized by shaking of the hands and other body parts. The main treatment option was drugs that would make him sleepy—a hazardous side effect in his line of work. West, however, hooked up with doctors at Rhode Island Hospital who performed deep brain stimulation. In 2004, they opened West’s skull and implanted an electrode in his thalamus, a structure in the center of the brain just above the brainstem. They ran a wire to another device, inserted under the skin of his collarbone, that generated pulses of electrical current. The treatment reduced West’s tremors to manageable levels, and allowed him to continue his work. © 2011 Scientific American,

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 16157 - Posted: 12.17.2011

By Neil Bowdler Health reporter, BBC News An international study has linked an industrial solvent to Parkinson's disease. Researchers found a six-fold increase in the risk of developing Parkinson's in individuals exposed in the workplace to trichloroethylene (TCE). Although many uses for TCE have been banned around the world, the chemical is still used as a degreasing agent. The research was based on analysis of 99 pairs of twins selected from US data records. Parkinson's can result in limb tremors, slowed movement and speech impairment, but the exact cause of the disease is still unknown, and there is no cure. Research to date suggests a mix of genetic and environmental factors may be responsible. A link has previously been made with pesticide use. 'Significant association' The researchers from institutes in the US, Canada, Germany and Argentina, wanted to examine the impact of solvent exposure - specifically six solvents including TCE. They looked at 99 sets of twins, one twin with Parkinson's, the other without. Because twins are similar genetically and often share certain lifestyle characteristics, twins were thought to provide a better control group, reducing the likelihood of spurious results. BBC © 2011

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: 16030 - Posted: 11.14.2011

by Jessica Hamzelou How well can you control your thoughts? Mind-control training could improve symptoms of Parkinson's disease. Deep brain stimulation, which involves implanting electrodes in the brain, helps to alleviate problems with movement experienced by people with Parkinson's disease. "If putting in an electrode works, we thought training brains to self-regulate might work as well," says David Linden at Cardiff University, UK. To find out, Linden's team asked 10 people with Parkinson's to think about moving while having their brains scanned by fMRI for 45 minutes. Five were given real-time neurofeedback showing how well they activated a brain region that controls movement. Each participant was then told to practice such thoughts at home. Two months later, movement problems including rigidity and tremor had improved by 37 per cent in the group that received feedback compared with no change in the rest. "Sending signals to brain areas normally deprived of input could be reshaping neural networks," says Linden. Roger Barker, a neuroscientist at the University of Cambridge, points out that the treatment would not work for everyone with Parkinson's disease. "If the person has a bad tremor then it would be difficult to get an image, while others don't like being inside the scanners," he says. © 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: 16001 - Posted: 11.08.2011

By GRETCHEN REYNOLDS Scientific discoveries can be serendipitous, and so it was when Jay L. Alberts, then a Parkinson’s disease researcher at Emory University in Atlanta, mounted a tandem bike with Cathy Frazier, a Parkinson’s patient. The two were riding the 2003 RAGBRAI bicycle tour across Iowa, hoping to raise awareness of the neurodegenerative disease and “show people with Parkinson’s that you don’t have to sit back and let the disease take over your life,” Dr. Alberts says. But something unexpected happened after the first day’s riding. One of Ms. Frazier’s symptoms was myographia, a condition in which her handwriting, legible at first, would quickly become smaller, more spidery and unreadable as she continued to write. After a day of pedaling, though, she signed a birthday card with no difficulty, her signature “beautifully written,” Dr. Alberts says. She also told him that she felt as if she didn’t have Parkinson’s. Impressed, Dr. Alberts, who now holds an endowed research chair at the Cleveland Clinic in Ohio, embarked on a series of experiments in which he had people with Parkinson’s disease ride tandem bicycles. The preliminary results are raising fascinating questions not only about whether exercise can help to combat the disease but also — and of broader import — whether intense, essentially forced workouts affect brains differently than gentler activity, even in those of us who are healthy. Scientists have known for some time that, in lab animals, forced and voluntary exercise can lead to different outcomes. Generally, mice and rats enjoy running, so if you put a running wheel in a rodent’s cage, it will hop aboard and run. © 2011 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: 15903 - Posted: 10.13.2011