Links for Keyword: Parkinsons

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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

National Institutes of Health researchers have found that Parkin, an important protein linked with some cases of early-onset Parkinson’s disease, regulates how cells in our bodies take up and process dietary fats. Parkinson’s disease is a complex, progressive, and currently incurable neurological disorder characterized by shaking, stiffness, slowed movement, and impaired balance. Parkinson’s primarily affects people over 50, but in about 5 to10 percent of cases it occurs in people as young as their 20s. This form of the disease, which affects actor, author, and Parkinson’s activist Michael J. Fox, is known as early-onset Parkinson’s. Parkin mutations are present in as many as 37 percent of early-onset Parkinson’s cases. However, laboratory mice with defective Parkin do not display obvious signs of the disease. This preliminary study, which will appear online in the Journal of Clinical Investigation on Aug. 25, suggests defective Parkin may indirectly contribute to the development of some early-onset Parkinson's by changing the amount and types of fat in people’s bodies. The research team, composed of scientists from the NHLBI and the NIH’s National Institute of Neurological Disorders and Stroke, observed that mice with defective Parkin did not gain weight in response to a high-fat laboratory diet, as regular mice typically do. When the researchers examined several organs of the Parkin-defective mice, they noticed that the cells contained low levels of certain proteins that transport fat in the body. In contrast, normal mice that were fed the same high-fat diet had high levels of these fat-carrying proteins, as well as high levels of Parkin, suggesting that Parkin is involved in fat transportation.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 15724 - Posted: 08.27.2011

By Tina Hesman Saey Stabilizing the ties that bind a protein important in Parkinson’s disease to its buddies might help fend off the disease, a new study of the protein’s structure suggests. Alpha-synuclein builds up in tough aggregates in the brains of patients with Parkinson’s disease. Researchers thought that this protein was normally a floppy, snakelike molecule. But now, neuroscientist and neurologist Dennis Selkoe of Brigham and Women’s Hospital and Harvard Medical School and his colleagues show that alpha-synuclein normally forms bands of four molecules in living cells. These quartets (scientists call them tetramers) of alpha-synuclein molecules resist the clumping that leads single molecules of the protein down the path to brain cell destruction, Selkoe and colleagues report online August 14 in Nature. Discovering that alpha-synuclein works in groups of four could be important in treating or preventing Parkinson’s disease, says Patrik Brundin, a neuroscientist at Lund University in Sweden. The findings suggest that loner alpha-synuclein molecules could be “part of the ‘bad guy’ pathway, and stabilizing it as a tetramer might help avoid the disease,” he says. No one yet knows whether quartets of alpha-synuclein disintegrate into single molecules in the brains of people with Parkinson’s disease, leading to big brain-cell-killing plaques. Studies comparing normally aging brains with those of people with the disease may help answer those and other questions raised by the study, Brundin says. © Society for Science & the Public 2000 - 2011

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 15681 - Posted: 08.16.2011

Alla Katsnelson Peggy Willocks was 44 when she was diagnosed with Parkinson's disease. It progressed quickly, forcing her to retire four years later from her job as a primary-school principal in Elizabethton, Tennessee. Soon, her condition had deteriorated so much that she was often unable to dress and feed herself, take care of basic hygiene or walk unaided across a room. Willocks enrolled in a trial for an experimental therapy called Spheramine, developed by Titan Pharmaceuticals, a biotechnology company in South San Francisco, California. Spheramine consists of cultured human retinal epithelial cells bound to specialized man-made carrier molecules. The cells are implanted into the brain, where it is hoped that they will produce the dopamine precursor levodopa, which can reduce the symptoms of Parkinson's disease. In August 2000, Willocks became the second person ever to receive the treatment. After having a steel halo — a stereotactic frame — bolted to her skull, she was put under general anaesthesia. Surgeons then used the frame and coordinates obtained from numerous magnetic resonance imaging (MRI) scans to pinpoint the location at which to drill. They then snaked a catheter through her brain's white matter to deliver the cells into the striatum. At first there was no effect, but Willocks says that after 6–8 months she began to feel better. The changes were always moderate and gradual, except for once, about nine months after her surgery, when she showed what her doctor called a "radical" improvement in balance. By a year after the treatment, she and the five other patients in the phase I trial showed an improvement in motor ability of 48%, and those gains largely held 4 years later1. © 2011 Nature Publishing Group,

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 15666 - Posted: 08.11.2011

by Andy Coghlan People with Parkinson's disease might one day be treated with brain cells made from their own skin. Two teams of researchers have independently worked out how to turn skin cells into specialised neurons that make dopamine. This neurotransmitter, which is vital for mobility, is depleted in the brains of people with Parkinson's. The studies raise the possibility of improving mobility in people with Parkinson's by restoring dopamine production to normal. At present, most patients take a drug called L-dopa to readjust levels, but with varying levels of success. Both techniques avoid the initial step of converting skin cells into embryo-like pluripotent cells – a technique which poses a possible cancer risk. Vania Broccoli of the San Raffaele Scientific Institute in Milan, and colleagues, first reprogrammed mouse skin cells using three transcription factors – proteins previously linked with the development of the neurons. The same trio of factors transformed skin cells taken from human embryos, healthy adults and people with Parkinson's. The only drawback is that Broccoli's team first had to infect the skin cells with viruses carrying genes to make the transcription factors, although the viruses used are not ones that might disrupt DNA and cause cancer. © 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: 15536 - Posted: 07.07.2011

By Nathan Seppa A nutritional supplement that is free of charge, offers a wide range of health benefits and poses little risk sounds like fodder for a late-night TV commercial. But proponents of vitamin D are increasingly convinced that the sunshine vitamin delivers the goods, no strings attached. It offers a safe route to better health, these advocates say, by promoting proper function of the bones, heart, brain, immune system, you name it. Yet, the proponents claim, most people don’t get enough. Whereas humans’ pre­historic ancestors lived outdoors and made oodles of vitamin D in their sun-exposed skin, people today have become shut-ins by comparison — and scant sun exposure means low vitamin D. Of course, not everyone sees such a grand reach for the vitamin. While scientists concur that it is essential for bone maintenance, some stop right there. The skeptics note that vitamin D’s other promising qualities have shown up largely in studies that fall short of the gold standard of medicine — the randomized controlled trial, in which groups of people get either a placebo or the real thing. While a handful of randomized trials have shown additional benefits, others have not, leaving a gap in the vitamin’s otherwise sterling reputation. This debate came to a head last November, when an Institute of Medicine panel of scientists announced new vitamin D recommendations. The old intake levels were barely high enough to prevent rickets, a bone condition associated with the Industrial Revolution. The IOM panel boosted the recommended daily intake of the vitamin from 200 to 600 international units per day for most of the population. The new dose is about 15 micrograms, in the range of vitamin D found in most multivitamins. © Society for Science & the Public 2000 - 2011

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 8: Hormones and Sex
Link ID: 15531 - Posted: 07.05.2011

By Stephen Adams, Medical Correspondent The research, which follows studies indicating that it slows the progress of Alzheimer's, suggests lithium could be a cheap therapy to combat a range of brain disorders common in the elderly. Scientists at the Buck Institute for Ageing in San Francisco made the finding in a study of mice. They hope to conduct their first trials in humans soon. Compounds of lithium - itself a soft alkali metal - have been used for over 50 years to treat mania and mood swings. But its effect on a range of neuro-degenerative diseases is only starting to be appreciated. Earlier this year a small-scale study of people with mild cognitive impairment -trouble with memory and thinking - found it delayed the onset of full-blown Alzheimer's. Psychiatrists believe it slows the formation of amyloid plaques and brain cell tangles thought to cause the disease. The American researchers think lithium works in a similar way to prevent Parkinson's, which is caused because specific brain nerve cells die. They said their study - the first in animals - showed it stopped the build up of toxic proteins and cell death. Prof Julie Andersen, of the Buck Institute, said trials in people to determine the correct dosage could start soon. © Copyright of Telegraph Media Group Limited 2011

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 15483 - Posted: 06.25.2011