Chapter 11. Motor Control and Plasticity
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by Emily Underwood Globs of protein clustered in the neurons that control muscles have long been the hallmark of amyotrophic lateral sclerosis (ALS), the fatal neurodegenerative disease also commonly known as Lou Gehrig's disease. Now, a study of the most commonly found mutant gene in people with ALS reveals an unexpected origin of some of those sticky masses, a finding that may offer drug developers a new target for treatments. Located on the ninth chromosome, which explains part of its unwieldy name, the C9orf72 gene has a bit of a stutter. A typical version in healthy people contains a stretch of DNA where a string of six genetic letters—GGGGCC—repeats up to 25 times. Scientists have recently found that in a sizable share of people with ALS and frontotemporal dementia (FTD), a less common neurological disease characterized by language, memory, and emotional problems, this repeat occurs many more times; some people have thousands of copies. Since these C9orf72 mutations were discovered in 2011, some researchers have speculated that the repeats interrupt production of the gene's normal protein, which serves some as-yet unknown, but vital function in motor neurons or other brain cells. Others have hypothesized that the mutation spawns a large, misshapen strand of RNA that grabs on to proteins such as TDP-43, which normally help process RNA, creating protein tangles that starve the cell of the machinery it needs to function. © 2010 American Association for the Advancement of Science
Keyword: ALS-Lou Gehrig's Disease
Link ID: 17776 - Posted: 02.09.2013
Voluntary movements involve the coordinated activation of two brain pathways that connect parts of deep brain structures called the basal ganglia, according to a study in mice by researchers at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health. The findings, which challenge the classical view of basal ganglia function, were published online in Nature on Jan. 23. “By improving our understanding of how the basal ganglia control movements, these findings could aid in the development of treatments for disorders in which these circuits are disrupted, such as Parkinson’s disease, Huntington’s disease and addiction,” says NIAAA Acting Director Kenneth R. Warren, Ph.D. The predominant model of basal ganglia function proposes that direct and indirect pathways originating in a brain region called the striatum have opposing effects on movement. Activity of neurons in the direct pathway is thought to promote movement, while activity in the indirect pathway is thought to inhibit movement. Newer models, however, suggest that co-activation of these pathways is necessary to synchronize basal ganglia circuits during movement. “Testing these models has been difficult due to the lack of methods to measure specific neurons in the direct and indirect pathways in freely moving animals,” explains first author Guohong Cui, Ph.D., of the NIAAA Laboratory for Integrated Neuroscience (LIN). To overcome these difficulties, Dr. Cui and colleagues devised a new approach for measuring the activity of neurons deep within the brain during complex behaviors. Their technique uses fiber optic probes implanted in the mouse brain striatum to measure light emissions from neurons engineered to glow when activated.
Keyword: Movement Disorders
Link ID: 17729 - Posted: 01.29.2013
by Gretchen Cuda Kroen A day in the life of a male dung beetle goes something like this: Fly to a heap of dung, sculpt a clump of it into a large ball, then roll the ball away from the pile as fast as possible. However, it turns out that the beetles, who work at night, need some sort of compass to prevent them from rolling around in circles. New research in Current Biology suggests that the insects use starlight to guide their way. Birds, seals, and humans also use starlight to navigate, but this is the first time it's been shown in an insect. The whole point of rolling dung is to impress the female beetle with provisions—i.e., excrement—for her future progeny and entice her to mate. She then lays an egg in the ball and buries it in a network of tunnels more than a meter deep, where it serves as food for the developing larvae inside. But rolling dung balls in a straight line is also key to the male dung beetle's reproductive success. Rival males have been known to overtake a slower moving insect and claim the hard-earned treasure as their own. Competition is fiercest near the dung heap, so making a quick and efficient getaway is crucial for mating success. The discovery that dung beetles use starlight "was an accident more than anything," explains study author Eric Warrant, professor of zoology at the Lund University in Sweden. His research group was studying how the beetles used the polarized light patterns of the moon to stay on their paths, when one moonless night they made a surprising observation—the beetles maintained straight trajectories. "Even without the moon—just with the stars—they were still able to navigate," Warrant says. "We were just flabbergasted." © 2010 American Association for the Advancement of Science
By Christine Gorman In the January 2013 issue of Scientific American, D. Kacy Cullen and Douglas H. Smith of the University of Pennsylvania reported on their work using stretch-grown axons (the long thin "arm" of a nerve cell) to some day connect prosthetic devices to the peripheral nervous systems of people who had to have part of their arm amputated. There wasn't enough room to talk about it in the article, but there is another way that these "living bridges" could be used to help people with devastating injuries. The stretch-grown axons could also be used to treat people with major nerve damage that does not necessarily require amputation. The biohybrid bridge provides a conduit for the undamaged part of the peripheral nervous system to bypass the injured nerve and regrow its own axons all the way to the end of the affected limb. If such bridges could be implanted within a few days to weeks of the injury, they would benefit from the fact that neural support cells are still active throughout the length of the limb (these cells usually take a few months to disappear after nerve death) and could guide the regrowing nerve fiber to its final destination. Cullen and Smith hope to begin testing their stretch-grown axons soon in a few U.S. soldiers who were injured while fighting overseas. Cullen described their efforts in a recent email: Peripheral nerve injury (PNI) is a major source of warfighter morbidity. Indeed, only 50% of patients achieve good to normal restoration of function following surgical repair, regardless of the strategy. Moreover, failure of nerve regeneration may necessitate amputation of an otherwise salvaged limb. This stems from the inadequacy of current PNI repair strategies, where even the “gold-standard“ treatment – the nerve autograft – is largely ineffective for major nerve trauma. © 2013 Scientific American
Link ID: 17682 - Posted: 01.15.2013
Fran Lowry Salivary gland biopsy appears to be a diagnostic test for Parkinson's disease, a new study suggests. A biopsy of the submandibular gland that shows the presence of the abnormal protein alpha-synuclein is highly indicative of Parkinson's, as distinct from other neurodegenerative disorders that can mimic the disease, said lead study author, Charles Adler, MD, PhD, from the Mayo Clinic Arizona, Scottsdale, Arizona. "There is currently no diagnostic test for Parkinson's disease in living patients. The only way to make the diagnosis is at autopsy, when you can see an abnormal protein, alpha-synuclein, in certain brain regions," Dr. Adler, a fellow of the American Academy of Neurology, told Medscape Medical News. Their preliminary findings were released January 10; full results will be presented at the American Academy of Neurology's 65th Annual Meeting in San Diego. Dr. Adler and his team have been working on determining whether there is evidence of alpha-synuclein in other organs of the body so that they could develop a diagnostic test in living patients. "We previously published the fact that the submandibular gland has one of the densest concentrations of alpha-synuclein in an organ outside the brain. When we tested this in an autopsy study of 28 Parkinson's disease patients, we found that all 28 of them had alpha-synuclein in the submandibular gland," he said. The discovery led the researchers to biopsy the submandibular gland in living patients with Parkinson's disease to see whether this protein was present. If it was, then the biopsy could potentially be used as a diagnostic test, they reasoned. © 1994-2013 by WebMD LLC
Link ID: 17671 - Posted: 01.12.2013
By Alexandra Witze Quietly, on the top floor of a nondescript commercial building overlooking Boston Harbor, the future is being born. Rows of young scientists tap intently in front of computer monitors, their concentration unbroken even as the occasional plane from Logan Airport buzzes by. State-of-the-art lab equipment hums away in the background. This office, in Boston’s Marine Industrial Park, is what California’s Silicon Valley was four decades ago — the vanguard of an industry that will change your life. Just as researchers from Stanford provided the brains behind the semiconductor revolution, so are MIT and Harvard fueling the next big transformation. Students and faculty cross the Charles River not to build computer chips, but to re-engineer life itself. Take Reshma Shetty, one of the young minds at work in the eighth-floor biological production facility. After receiving her doctorate at MIT in 2008, she, like many new graduates, decided she wanted to make her mark on the world. She got together with four colleagues, including her Ph.D. adviser Tom Knight, to establish a company that aims “to make biology easy to engineer.” Place an order with Ginkgo BioWorks and its researchers will make an organism to do whatever you want. Need to suck carbon dioxide out of the atmosphere? They can engineer the insides of a bacterium to do just that. Want clean, biologically based fuels to replace petroleum taken from the ground? Company scientists will design a microbe to poop those out. © Society for Science & the Public 2000 - 2013
Link ID: 17650 - Posted: 01.05.2013
By GRETCHEN REYNOLDS Anyone whose resolve to exercise in 2013 is a bit shaky might want to consider an emerging scientific view of human evolution. It suggests that we are clever today in part because a million years ago, we could outrun and outwalk most other mammals over long distances. Our brains were shaped and sharpened by movement, the idea goes, and we continue to require regular physical activity in order for our brains to function optimally. The role of physical endurance in shaping humankind has intrigued anthropologists and gripped the popular imagination for some time. In 2004, the evolutionary biologists Daniel E. Lieberman of Harvard and Dennis M. Bramble of the University of Utah published a seminal article in the journal Nature titled “Endurance Running and the Evolution of Homo,” in which they posited that our bipedal ancestors survived by becoming endurance athletes, able to bring down swifter prey through sheer doggedness, jogging and plodding along behind them until the animals dropped. Endurance produced meals, which provided energy for mating, which meant that adept early joggers passed along their genes. In this way, natural selection drove early humans to become even more athletic, Dr. Lieberman and other scientists have written, their bodies developing longer legs, shorter toes, less hair and complicated inner-ear mechanisms to maintain balance and stability during upright ambulation. Movement shaped the human body. But simultaneously, in a development that until recently many scientists viewed as unrelated, humans were becoming smarter. Their brains were increasing rapidly in size. Copyright 2012 The New York Times Company
By Rachel Ehrenberg Outfitted with a bionic eye, arm, legs and fantastic ’70s hair, Steve Austin was a cyborg whose implants allowed him to recover stolen atomic weapons, fight aliens and protect cryptographers in distress. Finally, real life is starting to catch up with the Six Million Dollar Man. In one of this year’s bionic breakthroughs, a paralyzed woman carried out her own superhuman feat: Using an implanted brain chip, she controlled a robotic arm with her mind (SN: 6/16/12, p. 5). She used the arm to grasp a cuppa joe and take a long, satisfying sip of coffee through a straw, an act she hadn’t done on her own for nearly 15 years. “We’re entering a really exciting area where we can develop all sorts of very complicated technologies that can actually have biomedical applications and improve the quality of life for people,” says bioengineer Grégoire Courtine of the Swiss Federal Institute of Technology in Lausanne. “It’s a revolution.” After her groundbreaking sip, Cathy Hutchinson, who had been paralyzed years earlier by a stroke, smiled and then laughed. A roomful of scientists burst into applause. This was a big year for prosthetic parts, both in and out of the lab. Athletes in London for the Paralympics and the Olympics sprinted on high-tech carbon blades and hurled javelins while balancing on the microprocessor-controlled C-Leg. People in wheelchairs used battery-powered robotic suits to keep their lower limbs in shape. A young man who lost his right leg in a motorcycle accident climbed the 103 flights of stairs in Chicago’s Willis Tower with a thought-controlled limb. That technology is still in development. But some bionic add-ons are starting to come out of the lab and into the clinic for the first time, though costs remain prohibitive for many potential users. © Society for Science & the Public 2000 - 2012
Link ID: 17634 - Posted: 12.27.2012
By Sandra G. Boodman, For the first decade of his life, every doctor who saw Jack DeWitt inevitably zeroed in on the harrowing circumstances of his premature birth. Delivered by emergency Caesarean section in December 1999, doctors universally ascribed his developmental problems to his being born six weeks early, said his mother, Ruth DeWitt. “It always came back to that.” When Jack’s walking became odd at age 5, doctors chalked it up to a mild form of cerebral palsy that can occur in children born too soon. “We were okay with it,” his mother said, because mild cerebral palsy would not “affect the length of his life or his enjoyment of it.” Jack’s parents were also reassured by his ability to catch up; with help, he mastered various skills: jumping, walking and writing in cursive. But by age 10, when his ability to walk badly deteriorated, a reevaluation by his doctors resulted in a very different diagnosis and prognosis. “We had all those years of feeling that he was a normal, healthy kid with some challenges,” his mother recalled. Discovering what was really wrong has been a heavy blow, magnified by Jack’s perceptive awareness of its implications. Ruth DeWitt, who lives with her family in Howell, Mich., outside Ann Arbor, was in the hospital undergoing a test for preeclampsia, or pregnancy-induced hypertension, when she began hemorrhaging, a sign of placental abruption. The life-threatening condition occurs when the placenta prematurely detaches from a woman’s uterus. Rushed into surgery, Jack was born weighing 3 pounds, 9 ounces, and was transferred to the neonatal intensive care unit at the University of Michigan Medical Center. Small but strong, he needed oxygen but no ventilator, and he came home 15 days later. © 1996-2012 The Washington Post
By James Gallagher Health and science reporter, BBC News Unrivalled control of a robotic arm has been achieved using a paralysed woman's thoughts, a US study says. Jan Scheuermann, who is 53 and paralysed from the neck down, was able to deftly grasp and move a variety of objects just like a normal arm. Brain implants were used to control the robotic arm, in the study reported in the Lancet medical journal. Experts in the field said it was an "unprecedented performance" and a "remarkable achievement". Jan was diagnosed with spinocerebellar degeneration 13 years ago and progressively lost control of her body. She is now unable to move her arms or legs. She was implanted with two sensors - each four millimetres by four millimetres - in the motor cortex of her brain. A hundred tiny needles on each sensor pick up the electrical activity from about 200 individual brain cells. "The way that neurons communicate with each other is by how fast they fire pulses, it's a little bit akin to listening to a Geiger counter click, and it's that property that we lock onto," said Professor Andrew Schwartz from the University of Pittsburgh. The pulses of electricity in the brain are then translated into commands to move the arm, which bends at the elbow, wrist and could grab an object. BBC © 2012
Link ID: 17611 - Posted: 12.17.2012
by Christian Jarrett, Ph.D in Brain Myths Back in the 1990s neuroscientists at the University of Parma identified cells in the premotor cortex of monkeys that had an unusual response pattern. They were activated when the monkeys performed a given action and, mirror-like, when they saw another individual perform that same movement. Since then, the precise function and influence of these neurons has become perhaps the most hyped topic in neuroscience. In 2000, Vilayanur Ramachandran, the charismatic neuroscientist, made a bold prediction: “mirror neurons will do for psychology what DNA did for biology.” He's at the forefront of a frenzy of excitement that has followed these cells ever since their discovery. For many, they have came to represent all that makes us human. Perhaps, in those early heady years, Ramachandran was just getting a little carried away? Not at all. For his 2011 book, The Tell-Tale Brain, Ramachandran took his claims further. In the chapter “The neurons that shaped civilisation”, he argues that mirror neurons underlie empathy, allow us to imitate other people, that they accelerated the evolution of the brain, that they help explain the origin of language, and most impressively of all, that they prompted the great leap forward in human culture that happened about 60,000 years ago. “We could say mirror neurons served the same role in early hominin evolution as the Internet, Wikipedia, and blogging do today,” he concludes. “Once the cascade was set in motion, there was no turning back from the path to humanity.” © Copyright 2002-2012 Sussex Directories, Inc
by Jessica Hamzelou A single session of nerve stimulation has improved the movement of people with spinal cord injuries. Mimicking the passage of nerve signals by stimulating a muscle as well as the brain has boosted recovery and helped people to regain better control of their movements. Voluntary movement requires a signal from the brain, which is passed down the spinal cord and then to neurons in muscles. Damage to the spinal cord can interrupt this pathway, resulting in paralysis. To improve the control of movement in people with these injuries, Monica Perez and Karen Bunday at the University of Pittsburgh in Pennsylvania used electrical and magnetic stimulation to strengthen the connection between two nerves involved in voluntary movement of the index finger. The pair used transcranial magnetic stimulation (TMS), a non-invasive technique in which a magnetic field alters brain activity, to target the corticospinal tract. This bundle of nerves connects movement-associated parts of the brain with the spinal cord. "The corticospinal tract plays a major role in the recovery of motor function in spinal cord injury," says Perez. Just 1 to 2 milliseconds after stimulating the brain, they used an electrode to stimulate a nerve that innervates an index-finger muscle – mimicking normal brain-to-muscle nerve signalling. © Copyright Reed Business Information Ltd.
Link ID: 17554 - Posted: 12.01.2012
By JAMES GORMAN For the first time, researchers at the Massachusetts Institute of Technology report, brain imaging has been able to show in living patients the progressive damage Parkinson’s disease causes to two small structures deep in the brain. The new technique confirms some ideas about the overall progress of the disease in the brain. But the effects of Parkinson’s vary in patients, the researchers said, and in the future, the refinement in imaging may help doctors monitor how the disease is affecting different people and adjust treatment accordingly. The outward symptoms and progress of Parkinson’s disease — tremors, stiffness, weakness — have been well known since James Parkinson first described them in 1817. But its progress in the brain has been harder to document. Some of the structures affected by the disease have been buried too deep to see clearly even with advances in brain imaging. An important recent hypothesis about how the disease progresses was based on the examinations of brains of patients who had died. Now, a group of scientists at M.I.T. and Massachusetts General Hospital report that they have worked out a way to combine four different sorts of M.R.I. to get clear pictures of damage to two brain structures in people living with Parkinson’s. In doing so, they have added support to one part of the recent hypothesis, which is that the disease first strikes an area involved in movement and later progresses to a higher part of the brain more involved in memory and attention. Suzanne Corkin, a professor emerita of behavioral neuroscience at M.I.T. and the senior author on the paper published online Monday in The Archives of Neurology, said that this progression was part of the hypothesis put forward in 2003 by Heiko Braak, a German neuroscientist, based on autopsies. © 2012 The New York Times Company
Link ID: 17544 - Posted: 11.27.2012
By Maggie Fox, NBC News Seniors who fit in the most daily physical activity – from raking leaves to dancing – can have more gray matter in important brain regions, researchers reported on Monday. The scientists have images that show people who were the most active had 5 percent more gray matter than people who were the least active. Having more little gray brain cells translates into a lower risk of Alzheimer’s disease, other studies have shown. “People really want to know what they can do to reduce their risk of Alzheimer’s disease,” said Dr. Cyrus Raji of the University of California in Los Angeles, who presented his team’s findings to a meeting of the Radiological Society of North America. Raji’s team looked at the records of 876 adults, who were recruited into a larger study on heart health starting in 1989. They all got magnetic resonance imaging (MRI) brain scans in 1998 and 1999, when they were on average 78 years old, and filled out detailed questionnaires on exercise and other types of activity. Most of them were a little overweight – with a body mass index or BMI of 27. People with BMIs above 25 are considered overweight and at 30 they are considered clinically obese. The researchers found a huge difference in the amount of activity people reported. They were asked about everything from cycling to yard work, dancing and bicycle riding. © 2012 NBCNews.com
Link ID: 17543 - Posted: 11.27.2012
David Perlman With an ultimate goal to help paralyzed patients achieve a degree of independence, Stanford brain researchers report they have taken a promising step forward in efforts to link nerve centers in the human brain with computers controlled by only a person's thought. In their latest development, the Stanford scientists have successfully enabled a pair of rhesus monkeys to move a virtual cursor across a computer screen merely by thinking about their response to human commands. The monkeys' ability to manipulate a cursor without using a mouse is based on a powerful new algorithm, a mathematical computing program devised by Vikash Gilja, a Stanford electrical engineer and computer scientist. Four years ago, neurosurgeons at Brown University and Massachusetts General Hospital had demonstrated a simpler version of an algorithm that enabled completely paralyzed humans with implanted sensors in their brains to command a cursor to move erratically toward targets on a computer screen. But with Gilja's algorithm, called ReFit, the monkeys showed they could aim their virtual cursor, a moving dot of light, at another bright light on a computer screen, and hold it steadily there for 15 seconds - far more precisely than the humans four years ago. With the new algorithm, they were able to perform their thinking tasks faster and more accurately as they sat comfortably in a chair facing the computer. The development is "a big step toward clinically useful brain-machine technology that has faster, smoother, and more natural movements" than anything before it, said James Gnadt of the National Institute of Neurological Disorders and Stroke. © 2012 Hearst Communications Inc.
Link ID: 17537 - Posted: 11.26.2012
By David Pogue Okay, great: we can control Our phones with speech recognition and our television sets with gesture recognition. But those technologies don't work in all situations for all people. So I say, forget about those crude beginnings; what we really want is thought recognition. As I found out during research for a recent NOVA episode, it mostly appears that brain-computer interface (BCI) technology has not advanced very far just yet. For example, I tried to make a toy helicopter fly by thinking “up” as I wore a $300 commercial EEG headset. It barely worked. Such “mind-reading” caps are quick to put on and noninvasive. They listen, through your scalp, for the incredibly weak remnants of electrical signals from your brain activity. But they're lousy at figuring out where in your brain they originated. Furthermore, the headset software didn't even know that I was thinking “up.” I could just as easily have thought “goofy” or “shoelace” or “pickle”—whatever I had thought about during the 15-second training session. There are other noninvasive brain scanners—magnetoencephalography, positron-emission tomography and near-infrared spectroscopy, and so on—but each also has its trade-offs. Of course, you can implant sensors inside someone's skull for the best readings of all; immobilized patients have successfully manipulated computer cursors and robotic arms using this approach. Still, when it comes to controlling everyday electronics, brain surgery might be a tough sell. © 2012 Scientific American,
Link ID: 17518 - Posted: 11.21.2012
Scientists have reversed paralysis in dogs after injecting them with cells grown from the lining of their nose. The pets had all suffered spinal injuries which prevented them from using their back legs. The Cambridge University team is cautiously optimistic the technique could eventually have a role in the treatment of human patients. The study is the first to test the transplant in "real-life" injuries rather than laboratory animals. The only part of the body where nerve fibres continue to grow in adults is the olfactory system. Found in the at the back of the nasal cavity, olfactory ensheathing cells (OEC) surround the receptor neurons that both enable us to smell and convey these signals to the brain. The nerve cells need constant replacement which is promoted by the OECs. For decades scientists have thought OECs might be useful in spinal cord repair. Initial trials using OECs in humans have suggested the procedure is safe. In the study, funded by the Medical Research Council and published in the neurology journal Brain, the dogs had olfactory ensheathing cells from the lining of their nose removed. These were grown and expanded for several weeks in the laboratory. BBC © 2012
By Laura Sanders The insidious spread of an abnormal protein may be behind Parkinson’s disease, a study in mice suggests. A harmful version of the protein crawls through the brains of healthy mice, killing brain cells and damaging the animals’ balance and coordination, researchers report in the Nov. 16 Science. If a similar process happens in humans, the results could eventually point to ways to stop Parkinson’s destruction in the brain. “I really think that this model will increase our ability to come up with Parkinson’s disease therapies,” says study coauthor Virginia Lee of the University of Pennsylvania Perelman School of Medicine in Philadelphia. The new study targets a hallmark of Parkinson’s disease — clumps of a protein called alpha-synuclein. The clumps, called Lewy bodies, pile up inside nerve cells in the brain and cause trouble, particularly in cells that make dopamine, a chemical messenger that helps control movement. Death of these dopamine-producing cells leads to the characteristic tremors and muscle rigidity seen in people with Parkinson’s. Lee and her team injected alpha-synuclein into the brains of healthy mice. After 30 days, the protein had spread to connected brain regions, suggesting that rouge alpha-synuclein moves from cell to cell, the scientists found. Months later, the spreading was even more extensive. © Society for Science & the Public 2000 - 2012
Link ID: 17499 - Posted: 11.17.2012
By Ben Thomas In the early 1990s, a team of neuroscientists at the University of Parma made a surprising discovery: Certain groups of neurons in the brains of macaque monkeys fired not only when a monkey performed an action – grabbing an apple out of a box, for instance – but also when the monkey watched someone else performing that action; and even when the monkey heard someone performing the action in another room. In short, even though these “mirror neurons” were part of the brain’s motor system, they seemed to be correlated not with specific movements, but with specific goals. Over the next few decades, this “action understanding” theory of mirror neurons blossomed into a wide range of promising speculations. Since most of us think of goals as more abstract than movements, mirror neurons confront us with the distinct possibility that those everyday categories may be missing crucial pieces of the puzzle – thus, some scientists propose that mirror neurons might be involved in feelings of empathy, while others think these cells may play central roles in human abilities like speech. Some doctors even say they’ve discovered new treatments for mental disorders by reexamining diseases through the mirror neuron lens. For instance, UCLA’s Marco Iacoboni and others have put forth what Iacoboni called the “broken mirror hypothesis” of autism – the idea that malfunctioning mirror neurons are likely responsible for the lack of empathy and theory of mind found in severely autistic people. © 2012 Scientific American,
Danish researchers Krogh and colleagues randomly 115 assigned depressed people to one of two exercise programs. One was a strenuous aerobic workout - cycling for 30 minutes, 3 times per week, for 3 months. The other was various stretching exercises. The idea was that stretching was a kind of placebo control group on the grounds that, while it is an intervention, it's not the kind of exercise that gets you fit. It doesn't burn many calories, it doesn't improve your cardiovascular system, etc. Aerobic exercise is the kind that's most commonly been proposed as having an antidepressant effect. So what happened? Not much. Both groups got less depressed but there was zero difference between the two conditions. The cyclists did get physically fitter than the stretchers, losing more weight and improving on other measures. But they didn't feel any better. If this is true, it might mean that the antidepressant effects of aerobic exercise are psychological rather than physical - it's about the idea of 'exercising', not the process of becoming fitter. While many trials have found modest beneficial effects of exercise vs a "control condition", the control condition was often just doing nothing much - such as being put on a waiting-list. So the placebo effect or the motivational benefits of 'doing something', rather than the effects of exercise per se, could be behind it. In the current study though the stretching avoided that problem.
Link ID: 17463 - Posted: 11.07.2012