Chapter 5. The Sensorimotor System
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If you were stung by a bark scorpion, the most venomous scorpion in North America, you’d feel something like the intense, painful jolt of being electrocuted. Moments after the creature flips its tail and injects venom into your skin, the intense pain would be joined by a numbness or tingling in the body part that was stung, and you might experience a shortness of breath. The effect of this venom on some people—small children, the elderly or adults with compromised immune systems—can even trigger frothing at the mouth, seizure-like symptoms, paralysis and potentially death. Based solely on its body size, the four-inch-long furry grasshopper mouse should die within minutes of being stung—thanks to the scorpion’s venom, which causes temporary paralysis, the muscles that allow the mouse to breathe should shut down, leading to asphyxiation—so you’d think the rodent would avoid the scorpions at all costs. But if you put a mouse and a scorpion in the same place, the rodent’s reaction is strikingly brazen. If stung, the four-inch-long rodent might jump back for a moment in surprise. Then, after a brief pause, it’ll go in for the kill and devour the scorpion piece by piece: This predatory behavior isn’t the result of remarkable toughness. As scientists recently discovered, the mouse has evolved a particularly useful adaptation: It’s immune to both the pain and paralytic effects that make the scorpion’s venom so toxic. Although scientists long knew that the mouse, native to the deserts of the American Southwest, preys upon a range of non-toxic scorpions, “no one had ever really asked whether they attack and kill really toxic scorpions,” says Ashlee Rowe of Michigan State University, who led the new study published today in Science.
Who would win in a fight: a bark scorpion or a grasshopper mouse? It seems like an easy call. The bark scorpion (Centruroides sculpturatus) delivers one of the most painful stings in the animal kingdom—human victims have compared the experience to being branded. The 25-gram grasshopper mouse (Onychomys torridus) is, well, a mouse. But as you can see in the video above, grasshopper mice routinely kill and eat bark scorpions, blissfully munching away even as their prey sting them repeatedly (and sometimes right in the face). Now, scientists have discovered why the grasshopper mice don’t react to bark scorpion stings: They simply don’t feel them. Evolutionary neurobiologist Ashlee Rowe at the University of Texas, Austin, has been studying the grasshopper mice’s apparent superpower since she was in graduate school. For the new study, she milked venom from nearly 500 bark scorpions and started experimenting. When she injected the venom into the hind paws of regular laboratory mice, the mice furiously licked the site for several minutes. But when she injected the same venom into grasshopper mice, they licked their paws for just a few seconds and then went about their business, apparently unfazed. In fact, the grasshopper mice appeared to be more irritated by injections of the saline solution Rowe used as a control. Rowe knew that grasshopper mice weren’t entirely impervious to pain—they reacted to injections of other painful chemicals such as formalin, just not the bark scorpion venom. To find out what was going on, she and her team decided to determine how the venom affects the grasshopper mouse’s nervous system, in particular the parts responsible for sensing pain. © 2013 American Association for the Advancement of Science
By JAMES GORMAN Worldwide, 100,000 people have electrical implants in their brains to treat the involuntary movements associated with Parkinson’s disease, and scientists are experimenting with the technique for depression and other disorders. But today’s so-called deep brain stimulation only treats — it does not monitor its own effectiveness, partly because complex ailments like depression do not have defined biological signatures. The federal Defense Advanced Research Projects Agency, known as Darpa, announced Thursday that it intended to spend more than $70 million over five years to jump to the next level of brain implants, either by improving deep brain stimulation or by developing new technology. Justin Sanchez, Darpa program manager, said that for scientists now, “there is no technology that can acquire signals that can tell them precisely what is going on with the brain.” And so, he said, Darpa is “trying to change the game on how we approach these kinds of problems.” The new program, called Systems-Based Neurotechnology and Understanding for the Treatment of Neuropsychological Illnesses, is part of an Obama administration brain initiative, announced earlier this year, intended to promote innovative basic neuroscience. Participants in the initiative include Darpa, as well as the National Institutes of Health and the National Science Foundation. The announcement of Darpa’s goal is the first indication of how that research agency will participate in the initiative. The money is expected to be divided among different teams, and research proposals are now being sought. Darpa’s project is partly inspired by the needs of combat veterans who suffer from mental and physical conditions, and is the first to invest directly in researching human illness as part of the brain initiative. © 2013 The New York Times Company
By NELSON GRAVES Six years ago I suffered a stroke that forced me to relearn how to walk. The other day I ran a half-marathon. Strokes strike with stealth, but for me it was not entirely a surprise. During a physical in Milan in 2007, the doctor listened to my heart, then ordered an electrocardiogram. “Fair enough,” I reassured myself. “I’m 52 years old, and it’s no use taking anything for granted.” The nurse furrowed her brow as she studied the first read-out, then conducted a second, longer EKG. I put my shirt back on and returned to the doctor’s office. “I have some news for you,” he said. “You have atrial fibrillation. AF for short.” He wrote down the two words and explained they meant an irregular beating of the heart’s upper chambers. “It’s not life threatening. But it increases the risk of stroke six-fold.” I was too young to have a stroke. “I work 12-hour days, play squash three times a week and haven’t missed a day of work in 24 years,” I said. My attention piqued, I could now hear my heart’s irregular beat as I lay my head on my pillow. That must explain the dizziness when I get up at night to go to the bathroom. Or the fatigue at the end of a squash match. So when, on a September afternoon in Tokyo, my head began to spin wildly and I could hardly speak, I knew what was happening. After an ambulance ride to the hospital and an M.R.I., I heard the doctor say, “You’ve had a cerebral embolism.” That would be a stroke. Copyright 2013 The New York Times Company
Link ID: 18833 - Posted: 10.26.2013
People with Parkinson's disease are dancing at the National Ballet School as part of a study into how learning dance moves can change the brain. Anecdotally, learning to dance seems to improve motor skills in the short-term among people with Parkinson's disease, a neurological disorder that interferes with gait and balance. As part of a 12-week program, 20 people with Parkinson's disease are taking weekly dance classes at the National Ballet School in Toronto. The classes began in September. The research team is led by neuroscientist Prof. Joseph DeSouza of York University's Faculty of Health and National Ballet School instructor Rachel Bar. The volunteers are also getting a series of functional MRI scans to help researchers understand how the brain reacts and learns. "We know that balance can improve and gait can improve and even there's social benefits but we want to see why that's happening, how is it happening? To do that, we're looking inside the brain," Bar said. People aren't able to dance in scanner but they are asked to visualize the dance while listening to the accompanying music. "If you visualize a dance, theoretically you're using almost all the same neural circuitry as if you were doing it," DeDouza said. The hypothesis is that the brain of someone with Parkinson's may develop new paths around damaged areas if stimulated by the movement of dance. © CBC 2013
Link ID: 18826 - Posted: 10.23.2013
by NPR Staff Soon you'll be able to direct the path of a cockroach with a smartphone and the swipe of your finger. Greg Gage and his colleagues at Backyard Brains have developed a device called the that lets you control the path of an insect. It may make you squirm, but Gage says the device could inspire a new generation of neuroscientists. "The sharpest kids amongst us are probably going into other fields right now. And so we're kind of in the dark ages when it comes to neuroscience," he tells NPR's Arun Rath. He wants to get kids interested in neuroscience early enough to guide them toward that career path. And a cyborg cockroach might be the inspiration. "The neurons in the insects are very, very similar to the neurons inside the human brain," Gage says. "It's a beautiful way to just really understand what's happening inside your brain by looking at these little insects." The idea was spawned by a device the Backyard Brain-iacs developed called , which is capable of amplifying real living neurons. Insert a small wire into a cockroach's antennae, and you can hear the sound of actual neurons. "Lining the inside of the cockroach are these neurons that are picking up touch or vibration sensing, chemical sensing," Gage says. "They use it like a nose or a large tongue, their antennas, and they use it to sort of navigate the world. "So when you put a small wire inside of there, you can actually pick up the information as it's being encoded and being sent to the brain." With the RoboRoach device and smartphone app, you can interact with the antennae to influence the insect's behavior. ©2013 NPR
Link ID: 18819 - Posted: 10.22.2013
Henry Astley In the Mark Twain story The Celebrated Jumping Frog of Calaveras County, a frog named Daniel Webster "could get over more ground at one straddle than any animal of his breed you ever see." Now, scientists have visited the real Calaveras County in hopes of learning more about these hopping amphibians. They’ve found that what they see in the lab doesn’t always match the goings-on in the real world. If you wanted to know how far the bullfrog Rana catesbeiana could jump, the scientific literature would give you one answer: 1.295 meters, published in Smithsonian Contributions to Zoology in 1978. If you looked at the Guinness Book of World Records, though, you'd find a different answer. In 1986, a bullfrog called Rosie the Ribeter covered 6.55 meters in three hops. If you divide by three, at least one of those hops had to be no shorter than 2.18 meters—about four bullfrog body lengths more than the number in the scientific paper. The disparity matters. If bullfrogs can hop only 1.3 meters, they have enough power in their muscles to pull off the jump without any other anatomical help. But if they can jump farther, they must also be using a stretchy tendon to power their hops—an ability that other frogs have but that researchers thought bullfrogs had lost. These particular amphibians, scientists speculated, might have made some kind of evolutionary tradeoff that shortened their jumps but enabled them to swim better in the water, where they spend much of their lives. © 2013 American Association for the Advancement of Science
Link ID: 18800 - Posted: 10.17.2013
By Lary C. Walker Clumps of proteins twisted into aberrant shapes cause the prion diseases that have perplexed biologists for decades. The surprises just keep coming with a new report that the simple clusters of proteins responsible for Mad Cow and other prions diseases may, without help from DNA or RNA, be capable of changing form to escape the predations of drugs that target their eradication. Prion drug resistance could be eerily similar to that found in cancer and HIV—and may have implications for drug development for Alzheimer’s and Parkinson’s, neurodegenerative diseases also characterized by misfolded proteins. Prion diseases include scrapie, chronic wasting disease and bovine spongiform encephalopathy (mad cow disease) in nonhuman species, and Creutzfeldt-Jakob disease and fatal insomnia in humans. They are unusual in that they can arise spontaneously, as a result of genetic mutations, or, in some instances, through infection. Remarkably, the infectious agent is not a microbe or virus, but rather the prion itself, a clump of proteins without genetic material. The noxious agents originate when a normally generated protein – called the prion protein – mistakenly folds into a stable, sticky, and potentially toxic shape. When the misfolded protein contacts other prion protein molecules, they too are corrupted and begin to bind to one another. In the ensuing chain reaction, the prions grow, break apart, and spread; within the nervous system, they relentlessly destroy neurons, ultimately, and invariably, leading to death. © 2013 Scientific American
by Alyssa Botelho A sense of touch lets you connect with loved ones, makes your limbs feel your own, and helps you to interact with your surroundings. But people who are paraplegics or have lost limbs have to navigate the world without this most fundamental of sensory inputs. Sliman Bensmaia at the University of Chicago, Illinois, is working to change that with a new model for transmitting a sense of touch to the brain that bypasses regular routes. He hopes it will be a blueprint for constructing prosthetics that convey touch in the same way that natural limbs do. To start, Bensmaia and his colleagues trained rhesus macaques to focus their gaze in different directions depending on whether their index finger or fourth finger were being prodded. Microelectrodes were then placed in an area of the brain called the primary somatosensory cortex. This area represents an entire map of the body, with each neuron responsible for sensing when a different part of the skin is touched. Microelectrodes record the activity pattern of neurons. They can also be used in reverse – to deliver electrical stimulation to make neurons fire. Fourth finger exercise Next, the team recorded what activity occurred and where it registered in the somatosensory cortex when a monkey had its index or fourth finger poked. Then they stimulated the brain using the same pattern of activity. The monkeys reacted as if they had been touched – fixing their gaze in the direction they been taught in response to a poke. © Copyright Reed Business Information Ltd.
Kashmira Gander A team in Bristol have created an implant that encourages cells damaged by the disease to grow again. It does this through a system of tubes and catheters that pump proteins into patients’ brain once a month, potentially stopping the disease from progressing by encouraging the damaged cells to grow again. The port located behind a patient’s ear releases a protein called glial cell line-derived neurotrophic factor (GDNF). Six patients at Frenchay Hospital, Bristol, have trialled the system, and doctors are now looking for another 36 to help them continue their research. Dr Kieran Breen, director of research and innovation at Parkinson's UK, said: “For years, the potential of GDNF as a treatment for Parkinson's has remained one of the great unanswered research questions. ”This new study will take us one step closer to finally answering this question once and for all. “We believe GDNF could have the potential to unlock a new approach for treating Parkinson's that may be able to slow down and ultimately stop the progression of the condition all together. ”Currently there are very few treatments available for people with Parkinson's and none capable of stopping the condition from advancing.“ More than 127,000 people in the UK currently have the disease, which is caused when nerve cells in the brain die due to a lack of the chemical dopamine. Symptoms include slowness of movement, stiffness and tremors. © independent.co.uk
Mind over matter. New research explains how abstract benefits of exercise—from reversing depression to fighting cognitive decline—might arise from a group of key molecules. While our muscles pump iron, our cells pump out something else: molecules that help maintain a healthy brain. But scientists have struggled to account for the well-known mental benefits of exercise, from counteracting depression and aging to fighting Alzheimer’s and Parkinson’s disease. Now, a research team may have finally found a molecular link between a workout and a healthy brain. Much exercise research focuses on the parts of our body that do the heavy lifting. Muscle cells ramp up production of a protein called FNDC5 during a workout. A fragment of this protein, known as irisin, gets lopped off and released into the bloodstream, where it drives the formation of brown fat cells, thought to protect against diseases such as diabetes and obesity. (White fat cells are traditionally the villains.) While studying the effects of FNDC5 in muscles, cellular biologist Bruce Spiegelman of Harvard Medical School in Boston happened upon some startling results: Mice that did not produce a so-called co-activator of FNDC5 production, known as PGC-1α, were hyperactive and had tiny holes in certain parts of their brains. Other studies showed that FNDC5 and PGC-1α are present in the brain, not just the muscles, and that both might play a role in the development of neurons. © 2013 American Association for the Advancement of Science.
Link ID: 18781 - Posted: 10.12.2013
By Stephen L. Macknik and Susana Martinez-Conde Dennis Rogers is an unassuming guy. He's on the short side. And though muscular, he doesn't come across as the kind of towering Venice Beach, muscle-bound Arnold that you might expect from someone billed as the World's Strongest Man. Rather he has the kind of avuncular intensity you find in a great automobile mechanic—a mechanic who happens to be able to lift an engine with one hand while using the fingertips of the other hand to wrench the spark plugs out. Like it's nothing. Rogers, who has been known to keep two U.S. Air Force fighter planes from blasting away in opposite directions by holding them back with his bare hands, performed at the most recent Gathering for Gardner—a conference that celebrates the interests of one of Scientific American's greatest columnists, the late mathemagician Martin Gardner. We asked Rogers about the source of his incredible powers after the show, and we were surprised to learn that he did not know. Bill Amonette of the University of Houston–Clear Lake found that Rogers could recruit an abnormally high number of muscle fibers. But was this ability because of a freak genetic mutation? Another possibility, which Rogers thinks is more likely, is the way he processes pain when he strains those muscles. What if, instead of superpowered muscles, Rogers has a normal—though extremely well exercised—body, and his abilities arise because he can withstand more pain than most mere mortals? He claims that he does feel pain and is actually scared of dentists. In fact, during one stunt in which he held back four souped-up Harley motorbikes with straps, he bit down so hard he split a tooth from top to bottom. Rather than taking his chances at the dentist, he reached into his mouth, clamped his viselike fingertips onto the broken tooth, and extracted it, root and all. Rogers reasons that, unlike in the dentist's office—where he has no control over the pain that is inflicted on him—he has direct executive control over pain that he inflicts on himself. “I know it's coming, I have an idea of what to expect and I can decide to ignore it,” he says. © 2013 Scientific American
By JAMES GORMAN SEATTLE — To hear Michael Dickinson tell it, there is nothing in the world quite as wonderful as a fruit fly. And it’s not because the fly is one of the most important laboratory animals in the history of biology, often used as a simple model for human genetics or neuroscience. “I don’t think they’re a simple model of anything,” he says. “If flies are a great model, they’re a great model for flies. “These animals, you know, they’re not like us,” he says, warming to his subject. “We don’t fly. We don’t have a compound eye. I don’t think we process sensory information the same way. The muscles that they use are just incredibly much more sophisticated and interesting than the muscles we use. “They can taste with their wings,” he adds, as his enthusiasm builds. “No one knows any reason why they have taste cells on their wing. Their bodies are just covered with sensors. This is one of the most studied organisms in the history of science, and we’re still fundamentally ignorant about many features of its basic biology. It’s like having an alien in your lab. “And,” he says, pausing, seeming puzzled that the world has not joined him in open-mouthed wonder for his favorite creature, “they can fly!” If he had to define his specialty, Dr. Dickinson, 50, who counts a MacArthur “genius” award among his honors, would call himself a neuroethologist. As such, he studies the basis of behavior in the brain at the University of Washington, in Seattle. In practice he is a polymath of sorts who has targeted the fruit fly, Drosophila melanogaster, and its flying behavior for studies that involve physics, mathematics, neurobiology, computer vision, muscle physiology and other disciplines. © 2013 The New York Times Company
Keyword: Movement Disorders
Link ID: 18762 - Posted: 10.08.2013
by Colin Barras It's like pulling a rabbit out of a hat. Researchers have reached inside the brain of a rat and pulled out neural stem cells – without harming the animal. Since the technique uses nanoparticles already approved for use in humans, it is hoped that it could be used to extract neural stem cells (NSCs) from people to treat conditions like Parkinson's, Huntington's and multiple sclerosis. Extracting NSCs from the person who needs them would avoid immune rejection – but they are difficult to remove safely. So Edman Tsang at the University of Oxford and his colleagues have developed a technique to safely fish out NSCs that originate in cavities in the brain called ventricles. Tsang's team coated magnetic nanoparticles with antibodies that bond tightly to a protein found on the surface of NSCs. They then injected the nanoparticles into the lateral ventricles of rats' brains. Six hours later, after the nanoparticles had bonded to the NSCs, the researchers used a magnetic field around the rats' heads to pull the stem cells together. They could then be sucked out of the brain with a syringe. After freeing the stem cells from the nanoparticles, the team found they could grow them in a dish, suggesting they were undamaged by the process. The rats, meanwhile, were back on their feet within hours of the surgery, showing no ill effects. © Copyright Reed Business Information Ltd.
By NICHOLAS BAKALAR Depression may be an independent risk factor for Parkinson’s disease, a new study has found. In a retrospective analysis, researchers followed 4,634 patients with depression and 18,544 matched controls for 10 years. To rule out the possibility that depression is an early symptom of Parkinson’s disease, their analysis excluded patients who received a diagnosis of depression within five years of their Parkinson’s diagnosis. The average age of people with depression was 41, while it was 64 for those with both depression and Parkinson’s. The study, published online in Neurology, found that 66 patients with depression, or 1.42 percent, developed Parkinson’s disease, compared with 97, or 0.52 percent, among those who were not depressed. After controlling for age, sex, diabetes, hypertension and other factors, the researchers found clinical depression was associated with more than three times the risk for Parkinson’s disease. “Our paper does not convey the message that all depression leads to Parkinson’s disease,” said the senior author, Dr. Albert C. Yang, a professor of psychiatry at the National Yang-Ming University in Taiwan. “But particularly the depressed elderly and those with difficult-to-treat depression should be alert to the possibility of neurological disease and Parkinson’s.” Copyright 2013 The New York Times Company
By NICHOLAS BAKALAR Black and Hispanic children who go to an emergency room with stomach pain are less likely than white children to receive pain medication, a new study reports, and more likely to spend long hours in the emergency room. The analysis, published in the October issue of Pediatrics, examined the records of 2,298 emergency room visits by people under 21, a nationally representative sample from a large survey conducted by the Centers for Disease Control and Prevention. About 53 percent were white, 24 percent non-Hispanic black, 21 percent Hispanic, and the rest from other ethnic or racial groups. Over all, 27.1 percent of white children with severe pain received analgesics, but only 15.8 percent of blacks, 18.9 percent of Hispanics and 7.1 percent of children of other races did. Black children were about 68 percent more likely than white children to spend longer than six hours in the emergency room, although there were no statistically significant differences among races in results for any diagnostic test. “This data set will not answer the question of why,” said the lead author, Dr. Tiffani J. Johnson, an instructor at the University of Pennsylvania School of Medicine. “It could be that white parents are more likely to ask for pain meds, or that minority patients are likely to get care in E.R.’s that have longer wait times. And it could be racial bias.” Copyright 2013 The New York Times Company
Erika Check Hayden The power of thought alone is not enough to move inanimate objects — unless the object is a robotic leg wired to your brain, that is. A 32-year-old man whose knee and lower leg were amputated in 2009 after a motorcycle accident is apparently the first person with a missing lower limb to control a robotic leg with his mind. A team led by biomedical engineer Levi Hargrove at the Rehabilitation Institute of Chicago in Illinois reported the breakthrough last week in the New England Journal of Medicine1, including a video that shows the man using the bionic leg to walk up stairs and down a ramp, and to kick a football. The major advance is that the man does not have to use a remote-control switch or exaggerated muscle movements to tell the robotic leg to switch between types of movements, and he does not have to reposition the leg with his hands when seated, Hargrove says. “To our knowledge, this is the first time that neural signals have been used to control both a motorized knee and ankle prosthesis,” he says. Scientists had previously shown that paralysed people could move robotic arms using their thoughts and that able-bodied people can walk using robotic legs controlled by their brains (see, for example, go.nature.com/dgtykw). The latest work goes a step further by using muscle signals to amplify messages sent by the brain when the person intends to move. © 2013 Nature Publishing Group
Link ID: 18725 - Posted: 10.01.2013
The Conservative government is launching a $1.3-billion free market in medical marijuana on Tuesday, eventually providing an expected 450,000 Canadians with quality weed. Health Canada is phasing out an older system on Monday that mostly relied on small-scale, homegrown medical marijuana of varying quality, often diverted illegally to the black market. In its place, large indoor marijuana farms certified by the RCMP and health inspectors will produce, package and distribute a range of standardized weed, all of it sold for whatever price the market will bear. The first sales are expected in the next few weeks, delivered directly by secure courier. "We're fairly confident that we'll have a healthy commercial industry in time," Sophie Galarneau, a senior official with the department, said in an interview. "It's a whole other ball game." The sanctioned birth of large-scale, free-market marijuana production comes as the Conservatives pillory Liberal Leader Justin Trudeau's campaign to legalize recreational marijuana. Health Canada is placing no limits on the number of these new capital-intensive facilities, which will have mandatory vaults and security systems. Private-dwelling production will be banned. Imports from places such as the Netherlands will be allowed. Already 156 firms have applied for lucrative producer and distributor status since June, with the first two receiving licences just last week. © CBC 2013
Ballet dancers develop differences in their brain structures to allow them to perform pirouettes without feeling dizzy, a study has found. A team from Imperial College London said dancers appear to suppress signals from the inner ear to the brain. Dancers traditionally use a technique called "spotting", which minimises head movement. The researchers say their findings may help patients who experience chronic dizziness. Dizziness is the feeling of movement when, in reality, you are still. For most it is an occasional, temporary sensation. But around one person in four experiences chronic dizziness at some point in their life. When someone turns or spins around rapidly, fluid in the vestibular organs of the inner ear can be felt moving through tiny hairs. Once they stop, the fluid continues to move, which can make a person feel like they are still spinning. Ballet dancers train hard to be able to spin, or pirouette, rapidly and repeatedly. They use a technique called spotting, focusing on a spot on the floor - as they spin, their head should be the last bit to move and the first to come back. In the study, published in the journal Cerebral Cortex, the team recruited 29 female ballet dancers and 20 female rowers of similar age and fitness levels. BBC © 2013
Link ID: 18709 - Posted: 09.28.2013
By Todd Sherer Parkinson’s disease is coming to prime time. Tomorrow night Michael J. Fox returns to television as the star of his own sitcom nearly 15 years after retiring from Spin City to focus on finding a cure for his disease. Michael has been careful to emphasize that the show isn’t really about Parkinson’s. Based loosely on his real life, The Michael J. Fox Show mines laughs from the everyday trials and tribulations of family man Mike Henry as he resumes his TV news job following a Parkinson’s diagnosis. Yet simply by featuring a main character living with the disease, the show puts Parkinson’s into the national conversation. This is a good moment to consider how much work remains to be done in the realm of neurodegeneration research. The question we’ve heard most often at The Michael J. Fox Foundation is: After more than 20 years with Parkinson’s, how is Michael doing well enough to go back to work? There’s no simple answer. He acknowledges the good fortune he has in a loving, supportive family and financial independence, which have provided advantages in dealing with his disease. He says, “Everybody gets their own version of Parkinson’s. Different meds work for different people, and you’re always trying to find the perfect combination. I think I found what works for me right now. And I’m so lucky.” But the reality is that for the estimated five million Parkinson’s patients worldwide, the status quo is still not good enough. They are living with Parkinson’s movement difficulties and nonmotor symptoms such as mood and sleep disorders as well as cognitive impairment. Medication and therapies alleviate some symptoms, but create their own problems and fail to address all the effects of Parkinson’s. We have some disease-modifying treatments in clinical trials, but nothing on the market yet. The grim truth is that those diagnosed with Parkinson’s will get worse. And for every patient, a community is affected, as the impact of the disease ripples to loved ones and caregivers. This is a global problem, but one that we can solve. © 2013 Scientific American
Link ID: 18708 - Posted: 09.26.2013