Chapter 5. The Sensorimotor System
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It can start with flashing lights, a tingling sensation and a feeling of unease, followed by excruciating pain. Migraines can be triggered by lack of food or too much stress but their underlying cause has remained a mystery. Now researchers have found that a migraine may be triggered by a protein deep in the brain that stimulates the neurons controlling facial sensations. The discovery creates a potential new target for safer migraine medicines and adds weight to the theory that neurons, not blood vessels, are responsible for migraine attacks. “Where a migraine starts is a key question,” says Debbie Hay at the University of Auckland in New Zealand. “There has been a great deal of debate around the mechanisms of migraine. If we can pin this down, we may have better chances of preventing it.” To investigate, Simon Akerman at New York University and Peter Goadsby at Kings College London, UK, studied two neuropeptides released by neurons thought to play a role in the pain associated with migraine. These protein-like molecules, called VIP and PACAP, first raised suspicion after they were found to be elevated in blood drained from the brains of people having a migraine attack. When researchers administered these peptides to volunteers, they found that they could cause a headache or migraine about two hours later. Both peptides widen blood vessels, which was thought to be significant in migraine. In fact, the only drugs specifically developed for migraine that are in use today – triptans – were designed to shrink blood vessels in the brain. As a result, they cannot be used by people with cardiovascular disorders. © Copyright Reed Business Information Ltd.
Keyword: Pain & Touch
Link ID: 21489 - Posted: 10.08.2015
Jo Marchant Most new painkiller drugs fail in clinical trials — but a growing placebo response may be to blame. Drug companies have a problem: they are finding it ever harder to get painkillers through clinical trials. But this isn't necessarily because the drugs are getting worse. An extensive analysis of trial data1 has found that responses to sham treatments have become stronger over time, making it harder to prove a drug’s advantage over placebo. The change in reponse to placebo treatments for pain, discovered by researchers in Canada, holds true only for US clinical trials. “We were absolutely floored when we found out,” says Jeffrey Mogil, who directs the pain-genetics lab at McGill University in Montreal and led the analysis. Simply being in a US trial and receiving sham treatment now seems to relieve pain almost as effectively as many promising new drugs. Mogil thinks that as US trials get longer, larger and more expensive, they may be enhancing participants’ expectations of their effectiveness. Stronger placebo responses have already been reported for trials of antidepressants and antipsychotics2, 3, triggering debate over whether growing placebo effects are seen in pain trials too. To find out, Mogil and his colleagues examined 84 clinical trials of drugs for the treatment of chronic neuropathic pain (pain which affects the nervous system) published between 1990 and 2013. © 2015 Nature Publishing Group,
Keyword: Pain & Touch
Link ID: 21484 - Posted: 10.07.2015
Laura Sanders Scribes usually have pretty good handwriting. That’s not the case for one prolific 13th century writer known to scholars only as the Tremulous Hand of Worcester. Now scientists suggest the writer suffered from a neurological condition called essential tremor. Neurologist Jane Alty and historical handwriting researcher Deborah Thorpe, both of the University of York in England, made the retrospective diagnosis August 31 in Brain after studying the spidery wiggles that pervade the scribe’s writing. Essential tremor can cause shaking of the hands, head and voice and is distinct from other tremor-causing conditions such as Parkinson’s disease. Here, the anonymous writer’s peculiar script is evident (lighter portion of text) in an early Middle English version of the Nicene Creed, a summary of the Christian faith. Buried in the manuscript are clues that helped the researchers conclude that essential tremor plagued the Tremulous Hand. The Tremulous Hand of Worcester’s writing appeared in more than 20 books, including the Nicene Creed, a summary of the Christian faith. The writer’s distinctive script is the lighter portion of the text, about a third of the way down the page. Several clues led researchers to diagnose the scribe with essential tremor (see following images). © Society for Science & the Public 2000 - 2015.
Keyword: Movement Disorders
Link ID: 21482 - Posted: 10.07.2015
By Jon Cohen A virus that long ago spliced itself into the human genome may play a role in amyotrophic lateral sclerosis (ALS), the deadly muscle degenerative disease that crippled baseball great Lou Gehrig and ultimately took his life. That’s the controversial conclusion of a new study, which finds elevated levels of human endogenous retrovirus K (HERV-K) in the brains of 11 people who died from the disease. “This certainly is interesting and provocative work,” says Raymond Roos, a neurologist at the University of Chicago in Illinois who treats and studies ALS but who was not involved with the finding. Still, even the scientists behind the work caution that more research is needed to confirm the link. “I’m very careful to say HERV-K doesn’t cause the disease but may play a role in the pathophysiology,” says study leader Avindra Nath, a neuroimmunologist at the National Institute of Neurological Disorders and Stroke in Bethesda, Maryland. “The darn thing is in the chromosomes to begin with. It’s going to be very hard to prove causation.” It was another retrovirus, HIV, that led Nath to first suspect a connection between viruses and ALS. In 2006, he was helping a patient control his HIV infection with antiretroviral drugs when he noticed that the man’s ALS also improved. “That intrigued me, and I looked in the ALS literature and saw that people had reported they could see reverse transcriptase in the blood.” Reverse transcriptase, an enzyme that converts RNA to DNA, is a hallmark of retroviruses, which use it to insert copies of their genes into chromosomes of their hosts. © 2015 American Association for the Advancement of Science
James Hamblin Mental exercises to build (or rebuild) attention span have shown promise recently as adjuncts or alternatives to amphetamines in addressing symptoms common to Attention Deficit Hyperactivity Disorder (ADHD). Building cognitive control, to be better able to focus on just one thing, or single-task, might involve regular practice with a specialized video game that reinforces "top-down" cognitive modulation, as was the case in a popular paper in Nature last year. Cool but still notional. More insipid but also more clearly critical to addressing what's being called the ADHD epidemic is plain old physical activity. This morning the medical journal Pediatrics published research that found kids who took part in a regular physical activity program showed important enhancement of cognitive performance and brain function. The findings, according to University of Illinois professor Charles Hillman and colleagues, "demonstrate a causal effect of a physical program on executive control, and provide support for physical activity for improving childhood cognition and brain health." If it seems odd that this is something that still needs support, that's because it is odd, yes. Physical activity is clearly a high, high-yield investment for all kids, but especially those attentive or hyperactive. This brand of research is still published and written about as though it were a novel finding, in part because exercise programs for kids remain underfunded and underprioritized in many school curricula, even though exercise is clearly integral to maximizing the utility of time spent in class.
By Sarah C. P. Williams Looking at photos of starving refugees or earthquake victims can trigger a visceral sense of empathy. But how, exactly, do we feel others’ agony as our own? A new study suggests that seeing others in pain engages some of the same neural pathways as when we ourselves are in pain. Moreover, both pain and empathy can be reduced by a placebo effect that acts on the same pathways as opioid painkillers, the researchers found. “This study provides one of the most direct demonstrations to date that first-hand pain and pain empathy are functionally related,” says neurobiologist Bernadette Fitzgibbon of Monash University in Melbourne, Australia, who was not involved in the new research. “It’s very exciting.” Previous studies have used functional magnetic resonance imaging (fMRI) scans to show that similar areas of the brain are activated when someone is in pain and when they see another person in pain. But overlaps on a brain scan don’t necessarily mean the two function through identical pathways—the shared brain areas could relate to attention or emotional arousal, among other things, rather than pain itself. Social neuroscientist Claus Lamm and colleagues at the University of Vienna took a different approach to test whether pain and empathy are driven by the same pathways. The researchers first divided about 100 people into control or placebo groups. They gave the placebo group a pill they claimed to be an expensive, over-the-counter painkiller, when in fact it was inactive. This well-established placebo protocol is known to function similarly to opioid painkillers, while avoiding the drugs’ side effects. © 2015 American Association for the Advancement of Science.
By Jane E. Brody Mark Hammel’s hearing was damaged in his 20s by machine gun fire when he served in the Israeli Army. But not until decades later, at 57, did he receive his first hearing aids. “It was very joyful, but also very sad, when I contemplated how much I had missed all those years,” Dr. Hammel, a psychologist in Kingston, N.Y., said in an interview. “I could hear well enough sitting face to face with someone in a quiet room, but in public, with background noise, I knew people were talking, but I had no idea what they were saying. I just stood there nodding my head and smiling. “Eventually, I stopped going to social gatherings. Even driving, I couldn’t hear what my daughter was saying in the back seat. I live in the country, and I couldn’t hear the birds singing. “People with hearing loss often don’t realize what they’re missing,” he said. “So much of what makes us human is social contact, interaction with other human beings. When that’s cut off, it comes with a very high cost.” And the price people pay is much more than social. As Dr. Hammel now realizes, “the capacity to hear is so essential to overall health.” Hearing loss is one of the most common conditions affecting adults, and the most common among older adults. An estimated 30 million to 48 million Americans have hearing loss that significantly diminishes the quality of their lives — academically, professionally and medically as well as socially. One person in three older than 60 has life-diminishing hearing loss, but most older adults wait five to 15 years before they seek help, according to a 2012 report in Healthy Hearing magazine. And the longer the delay, the more one misses of life and the harder it can be to adjust to hearing aids. © 2015 The New York Times Company
By Simon Makin Most people associate the term “subliminal conditioning” with dystopian sci-fi tales, but a recent study has used the technique to alter responses to pain. The findings suggest that information that does not register consciously teaches our brain more than scientists previously suspected. The results also offer a novel way to think about the placebo effect. Our perception of pain can depend on expectations, which explains placebo pain relief—and placebo's evil twin, the nocebo effect (if we think something will really hurt, it can hurt more than it should). Researchers have studied these expectation effects using conditioning techniques: they train people to associate specific stimuli, such as certain images, with different levels of pain. The subjects' perception of pain can then be reduced or increased by seeing the images during something painful. Most researchers assumed these pain-modifying effects required conscious expectations, but the new study, from a team at Harvard Medical School and the Karolinska Institute in Stockholm, led by Karin Jensen, shows that even subliminal input can modify pain—a more cognitively complex process than most that have previously been discovered to be susceptible to subliminal effects (timeline below). The scientists conditioned 47 people to associate two faces with either high or low pain levels from heat applied to their forearm. Some participants saw the faces normally, whereas others were exposed subliminally—the images were flashed so briefly, the participants were not aware of seeing them, as verified by recognition tests. © 2015 Scientific American
A 26-year-old man who is paralysed in both legs has walked for the first time in five years – just by thinking about it. He is the first person to have his brain activity recorded and used to control a muscle-stimulating device in his legs. Every year, 250,000 to 500,000 people worldwide suffer spinal cord injuries, which can leave them partially or completely paralysed below the site of damage. Many rehabilitation clinics already offer functional electric stimulation (FES) devices, which activate the nerves that innervate leg muscles at the push of a button. But people with upper-body paralysis are not always able to operate the FES in this way. The new system bypasses the button and returns control to the brain. “We want to re-establish the connection between the brain and the leg muscles, to bring back the function that was once present,” says Zoran Nenadic at the University of California Irvine. To do that, Nenadic and his colleagues combined an FES system with a brain-computer interface. The team developed an electrode cap that picks up the brainwaves created when a person thinks specifically about walking or standing still. They tailored the device to pick up brain signals from their volunteer – a man who has had little sensation below his shoulder blades for five years. © Copyright Reed Business Information Ltd.
Link ID: 21437 - Posted: 09.24.2015
By Kristin Ozelli Four years ago writer and producer Jon Palfreman was diagnosed with Parkinson’s disease. He has chronicled his experience and that of many other “Parkies,” as patients sometimes call themselves, in two books, the latest of which is Brain Storms: The Race to Unlock the Mysteries of Parkinson’s Disease, published this year by Scientific American / Farrar, Straus and Giroux, which traces some of the recent progress of medical researchers in treating this disease. He shared with Scientific American MIND senior editor Kristin Ozelli some of the insights he gleaned while working on this book. You wrote an earlier book about Parkinson’s and produced a prize-winning documentary, The Case of the Frozen Addicts, and have experienced the disease personally. While you were researching Brain Storms, was there anything new you learned about the disease that really surprised you? What is truly surprising is just how long biomedical research takes to deliver life-changing therapies. The promising therapies around when I wrote my first book 20 years ago, like neural grafting and growth factors—therapies designed to replace, revive or protect dopamine neurons—well they haven’t panned out. On the other hand, since my first involvement with Parkinson’s, there have been some extraordinary advances in basic science. In a sense, the disease has been rebranded from a movement disorder (resulting from damage to a very small part of the brain) to a systemic condition involving not only tremor and rigidity but also a whole host of symptoms—from depression to sleep disorders, from constipation to dementia. Indeed, there’s an entirely new theory of the disease that sees it as being driven by a protein alpha-synuclein that goes rogue and, prionlike, jumps from neuron to neuron creating havoc. © 2015 Scientific American
Link ID: 21435 - Posted: 09.23.2015
David Cyranoski A dispute has broken out at two of China’s most prestigious universities over a potentially groundbreaking discovery: the identification of a protein that may allow organisms to sense magnetic fields. On 14 September, Zhang Sheng-jia, a neuroscientist at Tsinghua University in Beijing, and his colleagues published a paper1 in Science Bulletin claiming to use magnetic fields to remotely control neurons and muscle cells in worms, by employing a particular magnetism-sensing protein. But Xie Can, a biophysicist at neighbouring Peking University, says that Zhang’s publication draws on a discovery made in his laboratory, currently under review for publication, and violates a collaboration agreement the two had reached. Administrators at Tsinghua and Peking universities, siding with Xie, have jointly requested that the journal retract Zhang’s paper, and Tsinghua has launched an investigation into Zhang’s actions. The dispute revolves around an answer to the mystery of how organisms as diverse as worms, butterflies, sea turtles and wolves are capable of sensing Earth’s magnetic field to help them navigate. Researchers have postulated that structures in biological cells must be responsible, and dubbed these structures magnetoreceptors. But they have never been found. In research starting in 2009, Xie says that he used a painstaking whole-genome screen to identify a protein containing iron and sulfur that seems, according to his experiments, to have the properties of a magnetoreceptor. He called it MagR, to note its purported properties, and has since been examining its function and structure to determine how it senses magnetic fields. © 2015 Nature Publishing Group,
Keyword: Animal Migration
Link ID: 21431 - Posted: 09.22.2015
Nathan Seppa For a historically mistrusted drink, coffee is proving to be a healthy addiction. Scientific findings in support of coffee’s nutritional attributes have been arriving at a steady drip since the 1980s, when Norwegian researchers reported that coffee seemed to fend off liver disease. Since then, the dark brown beverage has shown value against liver cancer, too, as well as type 2 diabetes, heart disease and stroke. Coffee even appears to protect against depression, Parkinson’s and Alzheimer’s diseases. Taken as a whole, these results might explain the most astonishing finding of all. People who drink two or more cups of coffee a day live longer than those who don’t, after accounting for behavioral differences, U.S. researchers reported in 2012. Studies in Japan, Scotland and Finland agree. Talk about a twofer. Coffee not only picks you up, it might put off the day they lower you down. Yet coffee has had trouble shaking its bad-for-you reputation. It may be one of the most widely consumed drinks in the world, but people have long assumed that, at least in its energizing caffeinated version, coffee comes with a catch. “People notice the caffeine,” says cardiologist Arthur Klatsky, who has researched coffee for decades at the Kaiser Permanente Northern California Division of Research in Oakland. “And there is this general feeling that anything that has some effect on the nervous system has to have something bad about it.” It doesn’t help that caffeine is mildly addictive.
By Larry Greenemeier Advanced prosthetics have for the past few years begun tapping into brain signals to provide amputees with impressive new levels of control. Patients think, and a limb moves. But getting a robotic arm or hand to sense what it’s touching, and send that feeling back to the brain, has been a harder task. The U.S. Defense Department’s research division last week claimed a breakthrough in this area, issuing a press release touting a 28-year-old paralyzed person’s ability to “feel” physical sensations through a prosthetic hand. Researchers have directly connected the artificial appendage to his brain, giving him the ability to even identify which mechanical finger is being gently touched, according to the Defense Advanced Research Projects Agency (DARPA). In 2013, other scientists at Case Western Reserve University also gave touch to amputees, giving patients precise-enough feeling of pressure in their fingertips to allow them to twist the stems off cherries. The government isn’t providing much detail at this time about its achievement other than to say that researchers ran wires from arrays connected to the volunteer’s sensory and motor cortices—which identify tactile sensations and control body movements, respectively—to a mechanical hand developed by the Applied Physics Laboratory (APL) at Johns Hopkins University. The APL hand’s torque sensors can convert pressure applied to any of its fingers into electrical signals routed back to the volunteer’s brain. © 2015 Scientific American
A choir of Canadians with Parkinson's disease is helping researchers test how well the performers regain facial movement to express emotions. Tremors and difficulty walking are often the most noticeable symptoms of Parkinson's disease, which affects about one in 500 people in Canada. Those with the disease may also have limited facial movement, which hampers the ability to express themselves. For people with Parkinson's who have "masked face syndrome," it can be difficult for others to decipher how they're feeling. That's because we unknowingly mimic or mirror each other during interaction to connect. "Within a hundred milliseconds of seeing someone else smile or frown, we are smiling or frowning," said Frank Russo, a psychology professor at Ryerson University in Toronto. "We're mirroring what the other person is doing. And that's one of the things that is absent in Parkinson's. It's the absence of mirroring that is leading to some of the deficit in understanding other people's emotions." Having a static face can leave people with Parkinson's seem cold and aloof as they also show deficits in understanding other people's emotions. The patient can then become emotionally disconnected from others. Studying the 28 members of the Parkinson's choir has bolstered Russo's thinking that singing, facial expressions and social communications are interconnected. So far Russo has found that mirroring effect or mimicry was restored among choir participants who sang for 13 weeks. ©2015 CBC/Radio-Canada.
Ever waited for a bus rather than take the short walk to work? Headed for the escalator instead of the stairs? Humans clearly harbour a deep love of lethargy – and now we know how far people will go to expend less energy. We will change our walking style on the fly when our normal gait becomes even a little more difficult. The finding could have implications for the rehabilitation offered to people with spinal injuries. Jessica Selinger and her colleagues at Simon Fraser University in Burnaby, British Columbia, Canada, strapped volunteers into a lightweight robotic exoskeleton and put them on a treadmill. Initially, the team let the volunteers find their preferred walking rhythm – which turned out to be 1.8 steps per second, on average. Then the researchers switched on the exoskeleton, programming it to make it more difficult for the volunteers to walk at their preferred pace by preventing the knee from bending – and leg swinging – as freely. The exoskeleton didn’t interfere with the human guinea pigs’ ability to walk faster or slower than they preferred. Within minutes the volunteers had found a walking style that the exoskeleton would allow without offering resistance. Remarkably, though, they did so despite the fact that the exoskeleton only ever offered minimal resistance. By using breathing masks to analyse the volunteers’ metabolic activity, Selinger’s team found that subjects would shift to an awkward new gait even if the energy saving was only 5 per cent. “People are able to adapt and fine-tune in order to move in the most energetically optimal way,” says Selinger. “People will change really fundamental characteristics of their gait.” © Copyright Reed Business Information Ltd.
Keyword: Movement Disorders
Link ID: 21398 - Posted: 09.11.2015
By Olivia Campbell Leave it to childbirth to cause a woman who’s never felt pain in her life to now experience persistent discomfort. When a 37-year-old woman with a condition known as congenital insensitivity to pain gave birth, her labor was as painless as expected. But during the delivery, she sustained pelvic fractures and an epidural hematoma that impinged on a nerve in her lower spine. Since then, she has added an unfortunate variety of words to her vocabulary: Her hips “hurt” and “ache;” she feels a “continuous buzzing in both legs and a vice-like squeezing in the pelvis.” When resting, she is left with “tingling” and “electric shocks.” She now has headaches, backaches, period pains, and stomach cramps; and even describes “the sting” of a graze and “the sharpness” of an exposed gum. According to doctors who treated her, the woman's sensitivity to pain -- tested on the tops of her feet -- is 10 times higher than it was before she gave birth. Congenital insensitivity to pain is an incredibly rare genetic disorder — there are only 20 recorded cases — that causes individuals to be totally unaware of pain. Co-author of the paper Michael Lee explained how pain pathways start with specialized nerves, called nociceptors, that sense damaging temperatures or pressure and then fire off signals to the brain. Those signals make us feel pain to prevent further damage. In people with CIP, a defective gene prevents these signals from going through. But pain can also arise when nociceptors or nerves are damaged, as was the case when this woman’s lumbar nerve was pinched during childbirth.
Keyword: Pain & Touch
Link ID: 21379 - Posted: 09.03.2015
By Jennifer Couzin-Frankel Some rare diseases pull researchers in and don’t let them go, and the unusual bone condition called fibrodysplasia ossificans progressiva (FOP) has long had its hooks in Aris Economides. “The minute you experience it it’s impossible to step back and forget it,” says the functional geneticist who runs the skeletal disease program at Regeneron Pharmaceuticals in Tarrytown, New York. “It’s devastating in the most profound way.” The few thousand or so people with FOP worldwide live with grueling uncertainty: Some of their muscles or other soft tissues periodically, and abruptly, transform into new bone that permanently immobilizes parts of their bodies. Joints such as elbows or ankles may become frozen in place; jaw motion can be impeded and the rib cage fixed, making eating or even breathing difficult. Twenty years after he first stumbled on FOP, Economides and his colleagues report today that the gene mutation shared by 97% of people with the disease can trigger its symptoms in a manner different than had been assumed—through a single molecule not previously eyed as a suspect. And by sheer chance, Regeneron had a treatment for this particular target in its freezers. The company tested that potential therapy, a type of protein known as a monoclonal antibody, on mice with their own form of FOP and lo and behold, they stopped growing unwelcome new bone. © 2015 American Association for the Advancement of Science.
By Simon Makin Scientists claim to have discovered the first new human prion in almost 50 years. Prions are misfolded proteins that make copies of themselves by inducing others to misfold. By so doing, they multiply and cause disease. The resulting illness in this case is multiple system atrophy (MSA), a neurodegenerative disease similar to Parkinson's. The study, published August 31 in Proceedings of the National Academy of Sciences, adds weight to the idea that many neurodegenerative diseases are caused by prions. In the 1960s researchers led by Carleton Gajdusek at the National Institutes of Health transmitted kuru, a rare neurodegenerative disease found in Papua New Guinea, and Creutzfeldt–Jakob disease (CJD), a rare human dementia, to chimpanzees by injecting samples from victims' brains directly into those of chimps. It wasn't until 1982, however, that Stanley Prusiner coined the term prion (for “proteinaceous infectious particle”) to describe the self-propagating protein responsible. Prusiner and colleagues at the University of California, San Francisco, showed this process caused a whole class of diseases, called spongiform encephalopathies (for the spongelike appearance of affected brains), including the bovine form known as “mad cow” disease. The same protein, PrP, is also responsible for kuru, which was spread by cannibalism; variant-CJD, which over 200 people developed after eating beef infected with the bovine variety; and others. The idea that a protein could transmit disease was radical at the time but the work eventually earned Prusiner the 1997 Nobel Prize in Physiology or Medicine. He has long argued prions may underlie other neurodegenerative diseases but the idea has been slow to gain acceptance. © 2015 Scientific American
Boer Deng Palaeontologist Stephen Gatesy wants to bring extinct creatures to life — virtually speaking. When he pores over the fossilized skeletons of dinosaurs and other long-dead beasts, he tries to imagine how they walked, ran or flew, and how those movements evolved into the gaits of their modern descendents. “I'm a very visual guy,” he says. But fossils are lifeless and static, and can only tell Gatesy so much. So instead, he relies on XROMM, a software package that he developed with his colleagues at Brown University in Providence, Rhode Island. XROMM (X-ray Reconstruction of Moving Morphology) borrows from the technology of motion capture, in which multiple cameras film a moving object from different angles, and markers on the object are rendered into 3D by a computer program. The difference is that XROMM uses not cameras, but X-ray machines that make videos of bones and joints moving inside live creatures such as pigs, ducks and fish. Understanding how the movements relate to the animals' bone structure can help palaeontologists to determine what movements would have been possible for fossilized creatures. “It's a completely different approach” to studying evolution, says Gatesy. XROMM, released to the public in 2008 as an open-source package, is one of a number of software tools that are expanding what researchers know about how animals and humans walk, crawl and, in some cases, fly (see ‘Movement from inside and out’). That has given the centuries-old science of animal motion relevance to a wide range of fields, from studying biodiversity to designing leg braces, prostheses and other assistive medical devices.“We're in an intense period of using camera-based and computer-based approaches to expand the questions we can ask about motion,” says Michael Dickinson, a neuroscientist at the California Institute of Technology in Pasadena. © 2015 Nature Publishing Group
Keyword: Movement Disorders
Link ID: 21370 - Posted: 09.01.2015
By Diana Kwon Each year doctors diagnose approximately 60,000 Americans with Parkinson’s disease, an incurable neurodegenerative condition for which the number-one risk factor is age. Worldwide an estimated seven to 10 million people currently live with the malady. As U.S. and global populations grow older, it is becoming increasingly urgent to understand its causes. So far, researchers know that Parkinson’s involves cell death in a few restricted areas of the brain including the substantia nigra (SNc), one of two big cell clusters in the midbrain that house a large population of dopamine neurons. These cells release dopamine and are involved in a variety of functions including reward processing and voluntary movement. Their death leads to the motor control and balance issues that are core symptoms of the disease. New research shows that these brain cells, most at risk in Parkinson’s disease, require unusually high amounts of energy to carry out their tasks because of their highly branched structures. Like a massive car with an overheating engine, these neurons are susceptible to burnout and early death. This discovery emerged from a comparison of energy use in nigral dopamine neurons and in similar neurons found in the nearby ventral tegmental area (VTA), also in the midbrain. “We were trying to understand why dopamine neurons of the substantia nigra die in Parkinson’s disease patients while there are so many other brain cells that have no problem at all,” says Louis-Eric Trudeau, a neuroscientist at the University of Montreal and senior author of the study published in the August 27 Current Biology. © 2015 Scientific American,
Link ID: 21353 - Posted: 08.28.2015