By Branwen Jeffreys Health correspondent, BBC News Combining exercise with conventional treatments for depression does not improve recovery, research suggests. In the NHS-funded study - published in the British Medical Journal - some patients were given help to boost their activity levels in addition to receiving therapy or anti-depressants. After a year all 361 patients had fewer signs of depression, but there was no difference between the two groups. Current guidelines suggest sufferers do up to three exercise sessions a week. The National Institute for Health and Clinical Excellence (Nice) drew up that advice in 2004. At the time it said that on the basis of the research available, increased physical activity could help those with mild depression. The latest study, carried out by teams from the Universities of Bristol and Exeter, looked at how that might actually work in a real clinical setting. All 361 people taking part were given conventional treatments appropriate to their level of depression. But for eight months some in a randomly allocated group were also given up advice on up to 13 separate occasions on how to increase their level of activity. BBC © 2012

Keyword: Depression
Link ID: 16877 - Posted: 06.06.2012

By Ferris Jabr The rat stood on its hind limbs at one end of a narrow runway. It wore a tiny black vest attached to a robotic arm that hovered above its head. Without such mechanical support, the rat would have fallen over—its spinal cord had two deep cuts, rendering its back legs useless. Rubia van den Brand, then a doctoral candidate at the University of Zurich, stood at the other end of the runway, urging the animal to walk. Although the robotic arm kept the rat upright, it could not help the creature move; if the rodent were ever to walk again, it would have to will its feet forward. For the first time since van den Brand began her experiments, the rat moved one of its back legs on its own—a small, effortful step. She ran to her boss's office with the news and a crowd immediately gathered in the lab to watch what many had deemed impossible. Van den Brand and Grégoire Courtine, now at the École Polytechnique Fédérale de Lausanne (E.P.F.L.), along with their colleagues, have trained rats with nearly severed spinal cords to walk again. One week after being injured, the rats could not move their hind limbs at all. Six weeks later they could walk, run, climb stairs and even sprint—but only with the support of the robotic arm accompanied by electrical and chemical stimulation of the spinal cord. Rats that trained on a moving treadmill instead of on a stationary runway moved their feet reflexively but never learned to walk voluntarily. Only conscious participation in walking encouraged new connections between the rodents' brains, spinal cords and limbs, which they needed to take those first deliberate steps. "It's kind of like how a toddler learns to walk," Courtine says. "Their spinal cord is full of activity and the brain needs to learn to take control of the spinal cord. As long as the brain has something to control it can learn progressively to communicate again with these cells." © 2012 Scientific American,

Keyword: Regeneration
Link ID: 16864 - Posted: 06.02.2012

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.

Keyword: Parkinsons; Aggression
Link ID: 16833 - Posted: 05.23.2012

By Meghan Holohan You're drifting off to sleep, when suddenly you feel like you're plunging off a cliff -- and you jerk awake. The jolt is disorienting, and you must try again to fall asleep. As many as 70 percent of people experience sleep starts or hypnic jerks while falling asleep, says Dr. William Kohler, medical director of the Florida Sleep Institute and director of the pediatric sleep services at Florida Hospital, Tampa. “A hypnic jerk or sleep starts are a perfectly normal occurrence that is almost universal,” explains James K. Walsh, executive director and senior scientist at St. Luke’s Sleep Medicine and Research Center in St. Louis. “It involves a total body experience where your muscle contracts therefore your limbs jerk or your body twitches. They generally occur during the transition between wakefulness and sleep. All of these things are very, very brief, lasting a half second or less.” Hypnic jerks are myoclonus twitches, or involuntary muscle spasms, but sleep starts occur during hypnagogia, the stage when the body is falling asleep. While most people have felt hypnic jerks, a small number of people experience the frightfully-named exploding head syndrome, the sensation that there is an explosion, crashing cymbals, or thunder near (or in) one’s head. Exploding head syndrome is so rare that it is mostly reported by individual case studies. While exploding head syndrome distresses people with it, both Walsh and Kohler stress that this, too, is normal and not a sign of any problem, physical or mental. © 2012 msnbc.com

Keyword: Sleep
Link ID: 16830 - Posted: 05.23.2012

By Rachel Ehrenberg Directing a robotic arm with her thoughts, a paralyzed woman named Cathy can pick up a bottle of coffee and sip it through a straw, a simple task that she hasn’t done on her own for nearly 15 years. The technology that brought about the feat is a brain-computer interface system: A computer decodes signals from a tiny chip implanted in the woman’s brain, translating her thoughts into actions that are carried out by the robot arm. The seemingly mundane task of bringing a drink to one’s mouth is the first published demonstration that severely paralyzed people can conduct directed movements in three-dimensional space using a brain-controlled robotic device. This latest application of the system, called BrainGate, is described in the May 17 Nature. “Much has been demonstrated in terms of laboratory work and monkeys, but this is the first time showing something that’s going to be useful for patients,” says neuroscientist Andrew Jackson, of Newcastle University in England. A commentary by Jackson on the new developments appears in the same issue of Nature. There’s still a lot of work to do before BrainGate can be used outside a lab. In the current design, the tiny sensor that sits in the patient’s brain is attached to a mini fridge–sized computer via ungainly wires. So making the system wireless is one goal. The researchers hope that within a decade the BrainGate system will be available and affordable for people who are paralyzed or have prosthetic limbs. Eventually, similar technology might restore function to a natural limb that no longer works. © Society for Science & the Public 2000 - 2012

Keyword: Robotics
Link ID: 16807 - Posted: 05.17.2012

By James Gallagher Health and science reporter, BBC News The tantalising prospect of treating a range of brain diseases, such as Alzheimer's and Parkinson's, all with the same drug, has been raised by UK researchers. In a study, published in Nature, they prevented brain cells dying in mice with prion disease. It is hoped the same method for preventing brain cell death could apply in other diseases. The findings are at an early stage, but have been heralded as "fascinating". Many neuro-degenerative diseases result in the build-up of proteins which are not put together correctly - known as misfolded proteins. This happens in Alzheimer's, Parkinson's and Huntington's as well as in prion diseases, such as the human form of mad cow disease. Turn off Researchers at the University of Leicester uncovered how the build-up of proteins in mice with prion disease resulted in brain cells dying. They showed that as misfolded protein levels rise in the brain, cells respond by trying to shut down the production of all new proteins. It is the same trick cells use when infected with a virus. Stopping production of proteins stops the virus spreading. However, shutting down the factory for a long period of time ends up killing the brain cells as they do not produce the proteins they actually need to function. BBC © 2012

Keyword: Prions; Aggression
Link ID: 16759 - Posted: 05.07.2012

By GRETCHEN REYNOLDS ONE lesson I’ve learned while writing about fitness is that few things impinge on an active life as much as writing about fitness — all that time spent hunched before a computer or puzzling over scientific journals, the countless hours of feckless, seated procrastination. While writing about the benefits of exercise, my muscles slackened. Fat seeped insidiously into my blood, liver and ventricles. Stupor infiltrated my brain. We all know by now that being inactive is unhealthy. But far too many of us think that being inactive is something that happens to other people. Studies of daily movement patterns, though, show that your typical modern exerciser, even someone who runs, subsequently sits for hours afterward, often moving less over all than on days when he or she does not work out. The health consequences are swift, pervasive and punishing. In a noteworthy recent experiment conducted by scientists at the University of Massachusetts and other institutions, a group of healthy young men donned a clunky platform shoe with a 4-inch heel on their right foot, leaving the left leg to dangle above the ground. For two days, the men hopped about using crutches (and presumably gained some respect for those people who regularly toddle about in platform heels). Each man’s left leg never touched the ground. Its muscles didn’t contract. It was fully sedentary. © 2012 The New York Times Company

Keyword: Alzheimers
Link ID: 16717 - Posted: 04.28.2012

By GRETCHEN REYNOLDS Ferrets don’t often figure in studies of exercise, perhaps because they don’t exercise much. They slink like fog through tunnels, sprint briefly over open ground and spend much of their time sleeping. They are, in biological terms, what’s called a noncursorial species, meaning that they are reluctant and lousy distance runners. Which is why they were ideal subjects for a new experiment conducted at the University of Arizona in Tucson looking at whether humans and other species evolved to like running. Many anthropologists and distance runners believe that running guided the evolution of early humans. We ran in search of dinner and away from predators. But running is costly, metabolically. It incinerates energy. It can also cause injury. A twisted ankle would have removed your typical early human from the gene pool. So why did our ancestors continue to run over the millennia “and not evolve other strategies for survival?” asks David A. Raichlen, a professor of anthropology at the University of Arizona, who led the study, which was published in The Journal of Experimental Biology. “We wondered if natural selection might have used neurobiological mechanisms to encourage exercise activity,” he continues. Specifically, he and his colleagues became interested in the evolutionary role of the endocannabinoid system. As the name suggests, endocannabinoids are chemicals that, like cannabis in marijuana, alter and lighten moods. But the body produces endocannabinoids naturally. In other studies, endocannabinoid levels have been shown to increase after prolonged running and cycling, leading many scientists to conclude that endocannabinoids help to create runner’s high. Copyright 2012 The New York Times Company

Keyword: Drug Abuse
Link ID: 16712 - Posted: 04.26.2012

By Sandra G. Boodman, Liisa Ecola lay on the sofa in the living room of her Capitol Hill home counting the hours until she could see a specialist who, she fervently hoped, would tell her why she could no longer keep her eyes open. For several months, the 42-year-old transportation policy researcher for Rand had been squinting, even in the dark. Her puzzled optometrist had suggested she consult a neuro-ophthalmologist, a doctor who specializes in diseases of the eye originating in the central nervous system. Ecola had waited weeks to get an appointment, which was scheduled for Dec. 15, 2010. But the day before, Ecola recalled, “I opened my laptop and my eyes snapped shut.” To her horror, she discovered that her eyes would stay open only for a few minutes at a time. Panicked, she called the specialist to confirm the appointment, only to discover that she wouldn’t be seeing him at all. The office had no record of her. “I was really scared,” said Ecola, who called it the lowest moment in her quest for a diagnosis. “I was convinced I had a brain tumor.” Her problem turned out to be far less serious and far more easily treated. The following day she lucked into an appointment with another specialist, who explained the odd constellation of symptoms that had left her unable to leave her house. For several years, Ecola had suffered an unexplained, intermittent facial tic, in which she scrunched up her face as if she were tasting something awful. Because it seemed linked to stress, Ecola consulted a behavioral therapist in an effort to banish it through habit reversal training — using relaxation exercises and making a conscious effort to stop the tic. Until early 2010, the treatment usually worked, and Ecola seemed able to control it. © 1996-2012 The Washington Post

Keyword: Movement Disorders; Aggression
Link ID: 16696 - Posted: 04.24.2012

By GRETCHEN REYNOLDS The value of mental-training games may be speculative, as Dan Hurley writes in his article on the quest to make ourselves smarter, but there is another, easy-to-achieve, scientifically proven way to make yourself smarter. Go for a walk or a swim. For more than a decade, neuroscientists and physiologists have been gathering evidence of the beneficial relationship between exercise and brainpower. But the newest findings make it clear that this isn’t just a relationship; it is the relationship. Using sophisticated technologies to examine the workings of individual neurons — and the makeup of brain matter itself — scientists in just the past few months have discovered that exercise appears to build a brain that resists physical shrinkage and enhance cognitive flexibility. Exercise, the latest neuroscience suggests, does more to bolster thinking than thinking does. The most persuasive evidence comes from several new studies of lab animals living in busy, exciting cages. It has long been known that so-called “enriched” environments — homes filled with toys and engaging, novel tasks — lead to improvements in the brainpower of lab animals. In most instances, such environmental enrichment also includes a running wheel, because mice and rats generally enjoy running. Until recently, there was little research done to tease out the particular effects of running versus those of playing with new toys or engaging the mind in other ways that don’t increase the heart rate. So, last year a team of researchers led by Justin S. Rhodes, a psychology professor at the Beckman Institute for Advanced Science and Technology at the University of Illinois, gathered four groups of mice and set them into four distinct living arrangements. © 2012 The New York Times Company

Keyword: Learning & Memory; Aggression
Link ID: 16691 - Posted: 04.23.2012

by Greg Miller Spinal cord injuries cause paralysis because they sever crucial communication links between the brain and the muscles that move limbs. A new study with monkeys demonstrates a way to re-establish those connections. By implanting electrodes in a movement control center in the brain and wiring them up to electrodes attached to muscles in the arm, researchers restored movement to monkeys with a temporarily paralyzed hand. The work is the latest promising development in the burgeoning field of neuroprosthetics. In recent years, scientists have taken many steps toward creating prosthetics to help paralyzed people interact more with the world around them. They've developed methods to decode signals from electrodes implanted in the brain so that a paralyzed person can control a cursor on a computer screen or manipulate a robotic arm with their thoughts alone. Such brain implants are still experimental, and only a handful of people have received them. Several hundred patients have received a different kind of neural prosthetic that uses residual shoulder movement or nerve activity to stimulate arm muscles, allowing them to grasp objects with their hands. The new study combines these two approaches. Neuroscientist Lee Miller of the Northwestern University Feinberg School of Medicine in Chicago, Illinois, and colleagues implanted electrode grids into the primary motor cortex of two monkeys. This brain region issues commands that move muscles throughout the body, and the researchers positioned the electrodes in the part of the primary motor cortex that controls the hand, enabling them to record the electrical activity of about 100 neurons there. © 2010 American Association for the Advancement of Science.

Keyword: Robotics
Link ID: 16675 - Posted: 04.19.2012

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

Keyword: Parkinsons
Link ID: 16657 - Posted: 04.16.2012

By Erica Westly Nerve cells in our limbs can regenerate after injury, but neurons in the central nervous system, which includes the brain and spinal cord, cannot. Figuring out why this is the case is critical to helping brain and spinal cord injuries heal. A study published in the January 26 issue of Neuron may offer a promising solution. Not only did the researchers, Rachid El Bejjani and Marc Hammarlund of Yale University, identify what appears to be a key chemical regulator of neuron repair, but drugs that target this regulator already exist, making the path to clinical treatments easier. The molecule they identified, called Notch, is a receptor that influences many biochemical pathways inside cells. Scientists used to think that Notch was active only during fetal and childhood development, but increasing evidence suggests that Notch is also involved in neurodegenerative conditions such as Alzheimer’s disease and stroke. Using C. elegans, a microscopic worm, El Bejjani and Hammarlund showed that Notch impeded neurons from healing themselves. When they blocked Notch’s activity with a drug, the neurons’ growth improved. The drug used in the study is already being tested in rodents and humans for potential use in Alz­hei­mer’s and other disorders, although whether it can help damaged neurons regenerate in mammals is unclear. “We know that the Notch pathway is con­served in vertebrates, but we don’t know if the re­generation mechanism is conserved,” Hammarlund says. If Notch stops neurons from growing back in humans as it does in C. elegans, it could be a major breakthrough in spinal cord medicine. © 2012 Scientific American

Keyword: Regeneration; Aggression
Link ID: 16650 - Posted: 04.14.2012

By James Gallagher Health and science reporter, BBC News People with Huntington's disease, a debilitating brain condition, appear have a "protection" from cancer, according to a study in Sweden. Nearly 40 years of medical records showed patients with Huntington's had half the normal expected risk of developing tumours. Researchers, writing in The Lancet Oncology, said the reason was unclear. Cancer Research UK said the findings presented another avenue to explore in tackling cancer. Academics at Lund University analysed Swedish hospital data from 1969 to 2008. They found 1,510 patients with Huntington's disease. During the study period, 91 of those patients subsequently developed cancer. The authors said that was 53% lower than the levels expected for the general population. Huntington's is one of a group of illnesses called "polyglutamine diseases". Data from other polyglutamine diseases also showed lower levels of cancer. The authors said: "We found that the incidence of cancer was significantly lower among patients with polyglutamine diseases than in the general population. "The mechanisms behind the protective effects against cancer are unclear and further research is warranted." BBC © 2012

Keyword: Huntingtons
Link ID: 16644 - Posted: 04.12.2012

By GRETCHEN REYNOLDS, Columnist Statistically, people who exercise are much less likely than inactive people to abuse drugs or alcohol. But can exercise help curb addictions? Some research shows that exercise may stimulate reward centers in the brain, helping to ease cravings for drugs or other substances. But according to an eye-opening new study of cocaine-addicted mice, dedicated exercise may in some cases make it even harder to break an addiction. The study, conducted by researchers at the Beckman Institute for Advanced Science and Technology at the University of Illinois in Urbana-Champaign, began by dividing male mice into those that had or did not have running wheels in their cages. All of the mice were injected with a chemical that marks newly created brain cells. The animals then sat in their cages or ran at will for 30 days. Afterward, the mice were placed in small multiroom chambers in the lab and introduced to liquid cocaine. They liked it. Researchers frequently use a model known as “conditioned place preference” to study addiction in animals. If a rodent returns to and stubbornly plants itself in a particular place where it has received a drug or other pleasurable experience, then the researchers conclude that the animal has become habituated. It badly wants to repeat the experience that it associates with that place. All of the mice displayed a decided place preference for the spot within their chamber where they received cocaine. They had learned to associate that location with the pleasures of the drug. All of the mice had, essentially, become addicts. © 2012 The New York Times Company

Keyword: Drug Abuse
Link ID: 16642 - Posted: 04.12.2012

By LISA SANDERS, M.D., Columnist On Thursday, we challenged Well readers to figure out the diagnosis for a 27-year-old woman with an odd walk and slowly progressive weakness of her hips and thighs. The correct diagnosis is… Adult-onset Tay-Sachs disease The first person to get it right was Jason Maley, a third-year medical student at Tulane University. His answer came in just after 1 a.m., an hour after the case was posted. He says that all the clues were there; he just had to put it all together. He’s planning to go into internal medicine. (I certainly hope that he will!) Tay-Sachs is an inherited disease in which the inability to get rid of discarded parts of the cell membrane causes the death of certain nerve cells. There are several forms of the disease. The most common affects infants. Babies born with this version of the disease usually die by age 4. Another form of the disease affects children who usually die before reaching adulthood. Late-onset Tay-Sachs, the form of the disease this patient has, doesn’t manifest itself until adolescence or young adulthood and causes a slow loss of strength and coordination. While the form seen in children was first described over a century ago, this version wasn’t recognized until the 1970s. Patients with this form of the disease can get rid of some but not all of the fatty components of the cell wall and so have a much slower rate of cell death and disability. The degree of disability varies widely in this group, and there are patients who have the disease but appear to be completely asymptomatic. For many with this disease, life expectancy is normal, but most eventually require a wheelchair. © 2012 The New York Times Company

Keyword: Movement Disorders; Aggression
Link ID: 16621 - Posted: 04.07.2012

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

Keyword: Parkinsons
Link ID: 16616 - Posted: 04.05.2012

By DAVID EWING DUNCAN SAN DIEGO — Already surrounded by machines that allow him, painstakingly, to communicate, the physicist Stephen Hawking last summer donned what looked like a rakish black headband that held a feather-light device the size of a small matchbox. Called the iBrain, this simple-looking contraption is part of an experiment that aims to allow Dr. Hawking — long paralyzed by amyotrophic lateral sclerosis, or Lou Gehrig’s disease — to communicate by merely thinking. The iBrain is part of a new generation of portable neural devices and algorithms intended to monitor and diagnose conditions like sleep apnea, depression and autism. Invented by a team led by Philip Low, a 32-year-old neuroscientist who is chief executive of NeuroVigil, a company based in San Diego, the iBrain is gaining attention as a possible alternative to expensive sleep labs that use rubber and plastic caps riddled with dozens of electrodes and usually require a patient to stay overnight. “The iBrain can collect data in real time in a person’s own bed, or when they’re watching TV, or doing just about anything,” Dr. Low said. The device uses a single channel to pick up waves of electrical brain signals, which change with different activities and thoughts, or with the pathologies that accompany brain disorders. © 2012 The New York Times Company

Keyword: Robotics; Aggression
Link ID: 16600 - Posted: 04.04.2012

By Bruce Bower An ancient member of the human evolutionary family has put what’s left of a weird, gorillalike foot forward to show that upright walking evolved along different paths in East Africa. A 3.4 million-year-old partial fossil foot unearthed in Ethiopia comes from a previously unknown hominid species that deftly climbed trees but walked clumsily, say anthropologist Yohannes Haile-Selassie of the Cleveland Museum of Natural History and his colleagues. Their report appears in the March 29 Nature. To the scientists’ surprise, this creature lived at the same time and in the same region as Australopithecus afarensis, a hominid species best known for a partial skeleton dubbed Lucy. Another recent fossil discovery in Ethiopia suggests that Lucy’s kind walked much as people do today (SN: 7/17/10, p. 5). “For the first time, we have evidence of another hominid lineage that lived at the same time as Lucy,” says anthropologist and study coauthor Bruce Latimer of Case Western Reserve University in Cleveland. “This new find has a grasping big toe and no arch, suggesting [the species] couldn’t walk great distances and spent a lot of time in the trees.” Lucy’s flat-footed compatriot adds to limited evidence that some hominids retained feet designed for adept tree climbing several million years after the origin of an upright gait, writes Harvard University anthropologist Daniel Lieberman in a comment published in the same issue of Nature. © Society for Science & the Public 2000 - 2012

Keyword: Evolution
Link ID: 16583 - Posted: 03.29.2012

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.

Keyword: Parkinsons; Aggression
Link ID: 16538 - Posted: 03.19.2012