Links for Keyword: Parkinsons

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By Dina Fine Maron All eyes were on Perry Cohen when he froze at the microphone. His voice failed him. He couldn’t read his notes. Eventually, the once-powerful Parkinson’s disease speaker had to be helped off the stage halfway through his speech. That was in February 2012, but the memory of that day is emblazoned in his mind. “It was the adrenaline and the pressure of speaking — it drained all the dopamine out,” Cohen says, referring to the brain chemical that is found lacking in the neurodegenerative disorder. “That’s why my symptoms got worse.” When Cohen learned he had Parkinson’s disease 17 years ago his symptoms were subtle. In the past couple years, however, the deterioration of his nervous system has become increasingly obvious, ultimately threatening to silence one of the most prominent voices in the Parkinson’s patient community. Cohen is now first in line to try a novel treatment he hopes will halt or even reverse the symptoms of his Parkinson’s disease. Two months ago he became the inaugural patient to undergo a gene therapy treatment led by the National Institutes of Health. The trial attempts to devise an intervention for Parkinson’s disease at the root of the problem: protecting dopamine in the brain. Researchers in this trial are attempting to surgically deliver a gene into the body that will make a natural protein to protect dopaminergic neurons, the brain cells attacked by the disease. To date no Parkinson’s treatment is geared toward reversing the progression of Parkinson’s disease. © 2013 Scientific American

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 18410 - Posted: 07.27.2013

By Melinda Wenner Moyer Many studies over the past decade have pointed to pesticides as a potential cause of Parkinson's disease, a neurodegenerative condition that impairs motor function and afflicts a million Americans. Yet scientists have not had a good idea of how these chemicals harm the brain. A recent study suggests a possible answer: pesticides may inhibit a biochemical pathway that normally protects dopaminergic neurons, the brain cells selectively attacked by the disease. Preliminary research also indicates that this pathway plays a role in Parkinson's even when pesticides are not involved, providing an exciting new target for drug development. Past studies have shown that a pesticide called benomyl, which lingers in the environment despite having been banned in the U.S. in 2001 because of health concerns, inhibits the chemical activity of aldehyde dehydrogenase (ALDH) in the liver. Researchers at the University of California, Los Angeles, U.C. Berkeley, the California Institute of Technology and the Greater Los Angeles Veterans Affairs Medical Center wondered whether the pesticide might also affect levels of ALDH in the brain. ALDH's job is to break down DOPAL, a naturally forming toxic chemical, rendering it harmless. To find out, the researchers exposed different types of human brain cells—and, later, whole zebra fish—to benomyl. They found that it “killed almost half of the dopamine neurons while leaving all other neurons tested intact,” according to lead author and U.C.L.A. neurologist Jeff Bronstein. When they zeroed in on the affected cells, they confirmed that the benomyl was indeed inhibiting the activity of ALDH, which in turn spurred the toxic accumulation of DOPAL. Interestingly, when the scientists lowered DOPAL levels using a different technique, benomyl did not harm the dopamine neurons, a finding that suggests that the pesticide kills these neurons specifically because it allows DOPAL to build up. © 2013 Scientific American,

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 18396 - Posted: 07.20.2013

It only takes one bad apple to spoil the bunch, and the same may be true of certain proteins in the brain. Studies have suggested that just one rogue protein (in this case, a protein that is misfolded or shaped the wrong way) can act as a seed, leading to the misfolding of nearby proteins. According to an NIH-funded study, various forms of these seeds — originating from the same protein — may lead to different patterns of misfolding that result in neurological disorders with unique sets of symptoms. “This study has important implications for Parkinson’s disease and other neurodegenerative disorders,” said National Institute of Neurological Disorders and Stroke (NINDS) Director Story Landis, Ph.D. “We know that among patients with Parkinson’s disease, there are variations in the way that the disorder affects the brains. This exciting new research provides a potential explanation for why those differences occur.” An example of such a protein is alpha-synuclein, which can accumulate in brain cells, causing synucleinopathies, multiple system atrophy, Parkinson’s disease, Parkinson’s disease with dementia (PDD), and dementia with Lewy bodies (DLB). In addition, misfolded proteins other than alpha-synuclein sometimes aggregate, or accumulate, in the same brains. For example, tau protein collects into aggregates called tangles, which are the hallmark of Alzheimer’s disease and are often found in PDD and DLB brains. Findings from this study raise the possibility that different structural shapes, or strains, of alpha-synuclein may contribute to the co-occurrence of synuclein and tau accumulations in PDD or DLB.

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: 18346 - Posted: 07.04.2013

By PAULA SPAN It was supposed to be a short stay. In 2006, Roger Anderson was to undergo surgery to relieve a painfully compressed spinal disk. His wife, Karen, figured the staff at the hospital, in Portland, Ore., would understand how to care for someone with Parkinson’s disease. It can be difficult. Parkinson’s patients like Mr. Anderson, for example, must take medications at precise intervals to replace the brain chemical dopamine, which is diminished by the disease. “You don’t have much of a window,” Mrs. Anderson said. “If you have to wait an hour, you have tremendous problems.” Without these medications, people may “freeze” and be unable to move, or develop uncontrolled movements called dyskinesia, and are prone to falls. But the nurses at the Portland hospital didn’t seem to grasp those imperatives. “You’d have to wait half an hour or an hour, and that’s not how it works for Parkinson’s patients,” Mrs. Anderson said. Nor did hospital rules, at the time, permit her to simply give her husband the Sinemet pills on her own. Surgery and anesthesia, the disrupted medications, an incision that subsequently became infected — all contributed to a tailspin that lasted nearly three months. Mr. Anderson developed delirium, rotated between rehab centers and hospitals, took a fall, lost 60 pounds. “People were telling me, ‘He’s never going to come home,’” Mrs. Anderson said. He did recover, and at 69 is doing well, his wife said, though his disease has progressed. But his wasn’t an unusual story, neurologists say. © 2013 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: 18054 - Posted: 04.22.2013

Nearly half of those with Parkinson's face regular discrimination, such as having their symptoms mistaken for drunkenness, a survey suggests. The survey of more than 2,000 people was commissioned by charity Parkinson's UK. One person in 500 people is affected by the condition in Britain. Parkinson's sufferer Mark Worsfold was arrested during last year's Olympics because police thought he looked suspicious. He was detained during the cycling road race in Leatherhead, Surrey, reportedly because he was not smiling - the condition means his face can appear expressionless. Parkinson's is a progressive neurological condition that attacks the part of the brain that controls movement. The main symptoms of Parkinson's are tremors or shaking that cannot be controlled, and rigidity of the muscles, which can make movement difficult and painful. Speech, language and facial expressions can also be affected. Most people who get it are aged 50 or over but younger people can have it too. The survey found that one in five people living with Parkinson's had been mistaken for being drunk, while one in 10 had been verbally abused or experienced hostility in public because of their condition. Around 62% said they thought the public had a poor understanding of how the condition affects people. BBC © 2013

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 18035 - Posted: 04.15.2013

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