Chapter 11. Motor Control and Plasticity
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|By Tara Haelle The first step to treating or preventing a disease is often finding out what drives it. In the case of neurodegenerative disorders, the discovery two decades ago of what drives them changed the field: all of them—including Alzheimer's, Parkinson's, Huntington's and amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease)—involve the accumulation of misfolded proteins in brain cells. Typically when a protein misfolds, the cell destroys it, but as a person ages, this quality-control mechanism starts to fail and the rogue proteins build up. In Huntington's, for example, huntingtin protein—used for many cell functions—misfolds and accumulates. Symptoms such as muscular difficulties, irritability, declining memory, poor impulse control and cognitive deterioration accompany the buildup. Mounting evidence suggests that not only does the accumulation of misfolded proteins mark neurodegenerative disease but that the spread of the proteins from one cell to another causes the disease to progress. Researchers have seen misfolded proteins travel between cells in Alzheimer's and Parkinson's. A series of experiments reported in Nature Neuroscience in August suggests the same is true in Huntington's. In their tests, researchers in Switzerland showed that mutated huntingtin protein in diseased brain tissue could invade healthy brain tissue when the two were placed together. And when the team injected the mutated protein into a live mouse's brain, it spread through the neurons within a month—similar to the way prions spread, says Francesco Paolo Di Giorgio of the Novartis Institutes for BioMedical Research in Basel, who led the research. Prions are misfolded proteins that travel through the body and confer their disease-causing characteristics onto other proteins, as seen in mad cow disease. But it is not known if misfolded proteins involved in Huntington's convert other proteins as true prions do, according to Di Giorgio. © 2014 Scientific American
Link ID: 20181 - Posted: 10.08.2014
|By Tori Rodriguez Imagining your tennis serve or mentally running through an upcoming speech might help you perform better, studies have shown, but the reasons why have been unclear. A common theory is that mental imagery activates some of the same neural pathways involved in the actual experience, and a recent study in Psychological Science lends support to that idea. Scientists at the University of Oslo conducted five experiments investigating whether eye pupils adjust to imagined light as they do to real light, in an attempt to see whether mental imagery can trigger automatic neural processes such as pupil dilation. Using infrared eye-tracking technology, they measured the diameter of participants' pupils as they viewed shapes of varying brightness and as they imagined the shapes they viewed or visualized a sunny sky or a dark room. In response to imagined light, pupils constricted 87 percent as much as they did during actual viewing, on average; in response to imagined darkness, pupils dilated to 56 percent of their size during real perception. Two other experiments ruled out the possibility that participants were able to adjust their pupil size at will or that pupils were changing in response to mental effort, which can cause dilation. The finding helps to explain why imagined rehearsals can improve your game. The mental picture activates and strengthens the very neural circuits—even subconscious ones that control automated processes like pupil dilation—that you will need to recruit when it is time to perform. © 2014 Scientific American
Keyword: Learning & Memory
Link ID: 20176 - Posted: 10.08.2014
By Julie Rehmeyer Eight years ago, collapsed on a neurologist’s examining table, I asked a naive question that turned out to be at the center of a long-running controversy: “So what is chronic fatigue syndrome?” I had just been diagnosed with the illness, which for six years had been gradually overtaking me. A week earlier, I had woken up barely able to walk. Fatigue hardly described what I felt. Paralysis was more like it. My legs seemed to have been amputated and replaced with tubes of liquid concrete, and just shifting them on the table made me grunt like an Olympic weightlifter. My bones hurt; my brain felt like a swollen mass. Speaking required tracking down and spearing each word individually as it scampered away from me. I felt as capable of writing an article about science — my job — as of killing a rhino with my teeth. “We don’t understand it very well,” my neurologist said, his face blank. He could recommend no tests, no treatments, no other doctors. I came to understand that, for him, the term chronic fatigue syndrome meant “I can’t help you.” My neurologist’s understanding of the illness mirrored that of many doctors, who believe two things about CFS: that it’s probably psychosomatic and that there’s nothing doctors can do for it. One survey found that nearly half of doctors thought that CFS was or might be psychosomatic, and 58 percent said there wasn’t enough information available to help them diagnose it. An examination of medical textbooks found that CFS was underrepresented, even compared with less-prevalent illnesses.
By Gretchen Reynolds Encourage young boys and girls to run, jump, squeal, hop and chase after each other or after erratically kicked balls, and you substantially improve their ability to think, according to the most ambitious study ever conducted of physical activity and cognitive performance in children. The results underscore, yet again, the importance of physical activity for children’s brain health and development, especially in terms of the particular thinking skills that most affect academic performance. The news that children think better if they move is hardly new. Recent studies have shown that children’s scores on math and reading tests rise if they go for a walk beforehand, even if the children are overweight and unfit. Other studies have found correlations between children’s aerobic fitness and their brain structure, with areas of the brain devoted to thinking and learning being generally larger among youngsters who are more fit. But these studies were short-term or associational, meaning that they could not tease out whether fitness had actually changed the children’s’ brains or if children with well-developed brains just liked exercise. So for the new study, which was published in September in Pediatrics, researchers at the University of Illinois at Urbana-Champaign approached school administrators at public elementary schools in the surrounding communities and asked if they could recruit the school’s 8- and 9-year-old students for an after-school exercise program. This group was of particular interest to the researchers because previous studies had determined that at that age, children typically experience a leap in their brain’s so-called executive functioning, which is the ability to impose order on your thinking. Executive functions help to control mental multitasking, maintain concentration, and inhibit inappropriate responses to mental stimuli. © 2014 The New York Times Company
By Lisa Sanders, M.D. On Thursday, we challenged Well readers to solve the mystery of a 62-year-old man with severe neck pain that spread down his arm, a facial droop, and numbness on his torso. Nearly 200 of you wrote in, and 20 of you correctly diagnosed the patient. The correct diagnosis is… Lyme disease. And more precisely, the early disseminated form of Lyme disease with neurological involvement The first person with the correct answer was Dr. Arielle Hay, a pediatric rheumatologist in Miami, who nailed it just half an hour after the case was posted. Dr. Hay said that the biggest clue was the UConn letterhead. When combined with the odd neurological symptoms, this reminder of where the case took place brought Lyme disease to mind. Lyme disease is one of those diseases that hardly needs an explanation. It was first described in 1977, in a case series of 51 children and parents who had mysterious episodes of joint pain and swelling. The children were initially diagnosed with juvenile rheumatoid arthritis, but the clustering of cases eventually led the investigators, Dr. Allen Steere and Dr. Stephen Malawista, to consider an infectious disease. The illness was named after the Connecticut town where most of the initial cases were located. The disease is caused by a spirochete, a spiral shaped bacterium carried by the Ixodes tick, and usually presents first with a distinctive, expanding red rash (called erythema migrans) that appears at the site of the bite in the early, localized stage of the disease. It is thought that the rash appears in up to 80 percent of Lyme infections. © 2014 The New York Times Company
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. The improvements in this case came in executive control, which consists of inhibition (resisting distraction, maintaining focus), working memory, and cognitive flexibility (switching between tasks). The images above show the brain activity in the group of kids who did the program as opposed to the group that didn't. It's the kind of difference that's so dramatic it's a little unsettling. The study only lasted nine months, but when you're only seven years old, nine months is a long time to be sitting in class with a blue head. © 2014 by The Atlantic Monthly Group.
Link ID: 20152 - Posted: 10.02.2014
By CATHERINE SAINT LOUIS Driven by a handful of reports of poliolike symptoms in children, federal health officials have asked the nation’s physicians to report cases of children with limb weakness or paralysis along with specific spinal-cord abnormalities on a magnetic resonance imaging test. As a respiratory illness known as enterovirus 68 is sickening thousands of children from coast to coast, officials are trying to figure out if the weakness could be linked to the virus. The emergence of several cases of limb weakness among children in Colorado put doctors on alert in recent months. The Centers for Disease Control and Prevention issued an advisory on Friday, and this week, other cases of unexplained muscle weakness or paralysis came to light in Michigan, Missouri and Massachusetts. The C.D.C. is investigating the cases of 10 children hospitalized at Children’s Hospital Colorado with unexplained arm or leg weakness since Aug. 9. Some of the children, who range in age from 1 to 18, also developed symptoms like facial drooping, double vision, or difficulty swallowing or talking. Four of them tested positive for enterovirus 68, also known as enterovirus D68, which has recently caused severe respiratory illness in children in 41 states and the District of Columbia. One tested positive for rhinovirus, which can cause the common cold. Two tested negative. Two patients’ specimens are still being processed; another was never tested. It is unclear whether the muscle weakness is connected to the viral outbreak. “It’s one possibility we are looking at, but certainly not the only possibility,” said Mark Pallansch, director of the C.D.C.’s division of viral diseases. © 2014 The New York Times Company
Keyword: Movement Disorders
Link ID: 20150 - Posted: 10.02.2014
By Gretchen Reynolds Exercise may help to safeguard the mind against depression through previously unknown effects on working muscles, according to a new study involving mice. The findings may have broad implications for anyone whose stress levels threaten to become emotionally overwhelming. Mental health experts have long been aware that even mild, repeated stress can contribute to the development of depression and other mood disorders in animals and people. Scientists have also known that exercise seems to cushion against depression. Working out somehow makes people and animals emotionally resilient, studies have shown. But precisely how exercise, a physical activity, can lessen someone’s risk for depression, a mood state, has been mysterious. So for the new study, which was published last week in Cell, researchers at the Karolinska Institute in Stockholm delved into the brains and behavior of mice in an intricate and novel fashion. Mouse emotions are, of course, opaque to us. We can’t ask mice if they are feeling cheerful or full of woe. Instead, researchers have delineated certain behaviors that indicate depression in mice. If animals lose weight, stop seeking out a sugar solution when it’s available — because, presumably, they no longer experience normal pleasures — or give up trying to escape from a cold-water maze and just freeze in place, they are categorized as depressed. And in the new experiment, after five weeks of frequent but intermittent, low-level stress, such as being restrained or lightly shocked, mice displayed exactly those behaviors. They became depressed. The scientists could then have tested whether exercise blunts the risk of developing depression after stress by having mice run first. But, frankly, from earlier research, they knew it would. They wanted to parse how. So they bred pre-exercised mice. © 2014 The New York Times Company
Link ID: 20145 - Posted: 10.01.2014
By Bec Crew Mike meet everyone, everyone meet Mike. No, no, don’t wave. He can’t see, you’re just making this awkward. Also known as Miracle Mike, Mike the Headless Chicken was a plump, five-year-old cockerel when he was unceremoniously beheaded on 10 September 1945. Farmer Lloyd Olsen of Fruita in Colorado did the deed because his wife Clara was having her mother over for dinner that night, and Olsen knew she’d always enjoyed a bit of roast chicken neck. With that in mind, Olsen tried to save most of Mike’s neck as he lopped his head off, but in doing so, he accidentally made his axe miss Mike’s jugular vein, plus one ear and most of his brain stem, and to his surprise, Mike didn’t die. In fact, Mike stuck around for a good 18 months without his head. Immediately after it happened, Mike reeled around like any headless chicken would, but soon settled down. He even started pecking at the ground for food with his newly minted stump, and made preening motions. His crows had become throaty gurglings. Olsen, bewildered, left him to it. The next morning, when Olsen found Mike asleep in the barn, having attempted to tuck his head under his wing as he always had, the farmer took it upon himself to figure out how to feed this unwitting monstrosity. Mike had earned that much. All Olsen had to do was deposit food and water into Mike’s exposed oesophagus via a little eyedropper. He even got small grains of corn sometimes as a treat. © 2014 Scientific American
Link ID: 20126 - Posted: 09.29.2014
By Rachel Feltman With the help of electrical stimulation, a paralyzed rat is "walking" again. It's actually being controlled by a computer that monitors its gait and adjusts it to keep the rat balanced. When a spinal cord is severed, the electrical pulses sent out by the brain to control limb movement are interrupted. With this method of treatment, the rat's leg movements are driven by electrical pulses shot directly into the spinal cord (which has unfortunately been severed in the name of science). Scientists have been working on this method in humans for awhile, but have only had moderate success — some subjects have regained sensation and movement in their legs, but haven't walked on their own. In the experiment described in the video above, published Wednesday in Science Translational Medicine, researchers tweaked this use of electrical stimulation: They primed the rats with a drug to boost their ability to respond to the electrical signal. Then, while the rats were placed in treadmill harnesses to support their weight, the researchers trained a camera on their subjects. The camera tracked the rats as they took electrically stimulated steps, and corrected their movement in real time. This instant feedback made the system precise enough to get the rats up tiny sets of stairs. MIT Technology Review reports that the team hopes to use a human volunteer within the next year. If the system works on humans, doctors can prescribe its use in rehabilitation therapy. You can watch the actual experiment in the video below:
By Roni Caryn Rabin When I was in college, my father David started walking with an odd, barely perceptible limp. He was in his mid-40s, a gregarious physician, teacher and researcher who was always upbeat. He told his four kids that he had a “back problem” — a deliberately vague cover story that I, for one, was willing to believe. I had never heard of the real culprit — amyotrophic lateral sclerosis, or A.L.S. In fact, no one had. A.L.S. was a disease in the shadows. During my father’s life, it didn’t even have its own advocacy organization. This was the early ’80s, long before support groups and the Internet and a colored ribbon for every cause. And it was way before ice bucket challenges. My parents continued to use their code — “back problem” — to talk about the disease. They used it to protect my younger sisters, who were about to start high school, but I think they were also protecting themselves. My mother was also a physician, and they both knew exactly what lay ahead. Saying “A.L.S.” out loud was too threatening. But soon there was no getting around it. My father’s legs were getting weaker, his muscles were wasting, and he started relying on a cane to get around. I was 19, and my mother and I were out running errands one afternoon when she pulled the car over to the curb and stopped. She told me the truth. This was no slipped disc. She laid it all out for me in black and white: A.L.S. is a progressive, degenerative neurological disease that causes paralysis in the entire body. It’s fatal. There is no cure. It sounded like something from a horror movie. Over the next five years, as my father’s health deteriorated, he remained remarkably determined. He ate a high-protein diet and swam laps every day in an attempt to maintain his muscle and fend off the atrophy caused by the disease. He kept on swimming laps in our next-door neighbor’s pool, even when he had to use a walker — and later a wheelchair — to get there. © 2014 The New York Times Company
Keyword: ALS-Lou Gehrig's Disease
Link ID: 20120 - Posted: 09.27.2014
By Sarah C. P. Williams Press the backs of your hands against the inside of a door frame for 30 seconds—as if you’re trying to widen the frame—and then let your arms down; you’ll feel something odd. Your arms will float up from your sides, as if lifted by an external force. Scientists call this Kohnstamm phenomenon, but you may know it as the floating arm trick. Now, researchers have studied what happens in a person’s brain and nerve cells when they repress this involuntary movement, holding their arms tightly by their sides instead of letting them float up. Two theories existed as to how this repression worked: The brain could send a positive “push down” signal to the arm muscles at the same time as the involuntary “lift up” signal was being transmitted to cancel it out; or the brain could entirely block the involuntary signal at the root of the nerves. The new study, which analyzed brain scans and muscle activity recordings from 39 volunteers, found that the latter was true—when a person stifles Kohnstamm phenomenon, the involuntary “lift” signal is blocked before it reaches the muscle. The difference between the repression mechanisms may seem subtle, but understanding it could help people repress other involuntary movements—including the tremors associated with Parkinson’s disease and the tics associated with Tourette syndrome, the team reports online today in the Proceedings of the Royal Society B. © 2014 American Association for the Advancement of Science
By Jocelyn Kaiser A virus that shuttles a therapeutic gene into cells has strengthened the muscles, improved the motor skills, and lengthened the lifespan of mice afflicted with two neuromuscular diseases. The approach could one day help people with a range of similar disorders, from muscular dystrophy to amyotrophic lateral sclerosis, or ALS. Many of these diseases involve defective neuromuscular junctions—the interface between neurons and muscle cells where brain signals tell muscles to contract. In one such disease, a form of familial limb-girdle myasthenia, people carry two defective copies of the gene called DOK7, which codes for a protein that’s needed to form such junctions. Their hip and shoulder muscles atrophy over many years, and some eventually have trouble breathing or end up in a wheelchair. Mice similarly missing a properly working Dok7 gene are severely underweight and die within a few weeks. In the new study, researchers led by molecular biologist Yuji Yamanashi of the University of Tokyo first injected young mice engineered to have defective Dok7 with a harmless virus carrying a good copy of the Dok7 gene, which is expressed only in muscle. Within about 7 weeks, the rodents recovered. Their muscle cells cranked out the DOK7 protein, and under a microscope their muscles had larger neuromuscular junctions than those of untreated mice with defective Dok7. What’s more, the mice grew to a healthy body weight and had essentially normal scores on tests of motor skills and muscle strength. © 2014 American Association for the Advancement of Science.
by Helen Thomson DON'T mind the gap. A woman has reached the age of 24 without anyone realising she was missing a large part of her brain. The case highlights just how adaptable the organ is. The discovery was made when the woman was admitted to the Chinese PLA General Hospital of Jinan Military Area Command in Shandong Province complaining of dizziness and nausea. She told doctors she'd had problems walking steadily for most of her life, and her mother reported that she hadn't walked until she was 7 and that her speech only became intelligible at the age of 6. Doctors did a CAT scan and immediately identified the source of the problem – her entire cerebellum was missing (see scan, below left). The space where it should be was empty of tissue. Instead it was filled with cerebrospinal fluid, which cushions the brain and provides defence against disease. The cerebellum – sometimes known as the "little brain" – is located underneath the two hemispheres. It looks different from the rest of the brain because it consists of much smaller and more compact folds of tissue. It represents about 10 per cent of the brain's total volume but contains 50 per cent of its neurons. Although it is not unheard of to have part of your brain missing, either congenitally or from surgery, the woman joins an elite club of just nine people who are known to have lived without their entire cerebellum. A detailed description of how the disorder affects a living adult is almost non-existent, say doctors from the Chinese hospital, because most people with the condition die at a young age and the problem is only discovered on autopsy (Brain, doi.org/vh7). © Copyright Reed Business Information Ltd.
By Tanya Lewis, In an experiment that sounds more like science fiction than reality, two humans were able to send greetings to each other using only a digital connection linking their brains. Using noninvasive means, researchers made brain recordings of a person in India thinking the words "hola" and "ciao," and then decoded and emailed the messages to France, where a machine converted the words into brain stimulation in another person, who perceived the signals as flashes of light. From the sequence of flashes, the French recipient was able to successfully interpret the greetings, according to a new study published today (Sept. 5) in the journal PLOS ONE. The researchers wanted to know if it is possible for two people to communicate by reading out the brain activity of one person and injecting that activity into a second person. "Could we develop an experiment that would bypass the talking or typing part of [the] Internet and establish direct brain-to-brain communication between subjects located far away from each other, in India and France?" co-author Dr. Alvaro Pascual-Leone said in a statement. Pascual-Leone is a neurologist at Beth Israel Deaconess Medical Center in Boston, and a professor at Harvard Medical School, in Cambridge, Massachusetts. To answer that question, Pascual-Leone and his colleagues at Starlab Barcelona, in Spain, and Axilum Robotics, in Strasbourg, France, turned to several widely used brain technologies. Electroencephalogram, or EEG, recordings are taken by placing a cap of electrodes on a person's scalp, and recording the electrical activity of large regions of the brain's cortex. Previous studies have recorded EEG from a person thinking about an action, such as moving his or her arm, while a computer translates the signal into an output used to move a robotic exoskeleton or drive a wheelchair.
By GRETCHEN REYNOLDS Amyotrophic lateral sclerosis has been all over the news lately because of the ubiquitous A.L.S. ice bucket challenge. That attention has also reinvigorated a long-simmering scientific debate about whether participating in contact sports or even vigorous exercise might somehow contribute to the development of the fatal neurodegenerative disease, an issue that two important new studies attempt to answer. Ever since the great Yankees first baseman Lou Gehrig died of A.L.S. in 1941 at age 37, many Americans have vaguely connected A.L.S. with athletes and sports. In Europe, the possible linkage has been more overtly discussed. In the past decade, several widely publicized studies indicated that professional Italian soccer players were disproportionately prone to A.L.S., with about a sixfold higher incidence than would have been expected numerically. Players were often diagnosed while in their 30s; the normal onset is after 60. These findings prompted some small, follow-up epidemiological studies of A.L.S. patients in Europe. To the surprise and likely consternation of the researchers, they found weak but measurable associations between playing contact sports and a heightened risk for A.L.S. The data even showed links between being physically active — meaning exercising regularly — and contracting the disease, raising concerns among scientists that exercise might somehow be inducing A.L.S. in susceptible people, perhaps by affecting brain neurons or increasing bodily stress. But these studies were extremely small and had methodological problems. So to better determine what role sports and exercise might play in the risk for A.L.S., researchers from across Europe recently combined their efforts into two major new studies. The results should reassure those of us who exercise. The numbers showed that physical activity — whether at work, in sports or during exercise — did not increase people’s risk of developing A.L.S. © 2014 The New York Times Company
Keyword: ALS-Lou Gehrig's Disease
Link ID: 20031 - Posted: 09.03.2014
By JOHN MARKOFF STANFORD, Calif. — In factories and warehouses, robots routinely outdo humans in strength and precision. Artificial intelligence software can drive cars, beat grandmasters at chess and leave “Jeopardy!” champions in the dust. But machines still lack a critical element that will keep them from eclipsing most human capabilities anytime soon: a well-developed sense of touch. Consider Dr. Nikolas Blevins, a head and neck surgeon at Stanford Health Care who routinely performs ear operations requiring that he shave away bone deftly enough to leave an inner surface as thin as the membrane in an eggshell. Dr. Blevins is collaborating with the roboticists J. Kenneth Salisbury and Sonny Chan on designing software that will make it possible to rehearse these operations before performing them. The program blends X-ray and magnetic resonance imaging data to create a vivid three-dimensional model of the inner ear, allowing the surgeon to practice drilling away bone, to take a visual tour of the patient’s skull and to virtually “feel” subtle differences in cartilage, bone and soft tissue. Yet no matter how thorough or refined, the software provides only the roughest approximation of Dr. Blevins’s sensitive touch. “Being able to do virtual surgery, you really need to have haptics,” he said, referring to the technology that makes it possible to mimic the sensations of touch in a computer simulation. The software’s limitations typify those of robotics, in which researchers lag in designing machines to perform tasks that humans routinely do instinctively. Since the first robotic arm was designed at the Stanford Artificial Intelligence Laboratory in the 1960s, robots have learned to perform repetitive factory work, but they can barely open a door, pick themselves up if they fall, pull a coin out of a pocket or twirl a pencil. © 2014 The New York Times Company
Learning is easier when it only requires nerve cells to rearrange existing patterns of activity than when the nerve cells have to generate new patterns, a study of monkeys has found. The scientists explored the brain’s capacity to learn through recordings of electrical activity of brain cell networks. The study was partly funded by the National Institutes of Health. “We looked into the brain and may have seen why it’s so hard to think outside the box,” said Aaron Batista, Ph.D., an assistant professor at the University of Pittsburgh and a senior author of the study published in Nature, with Byron Yu, Ph.D., assistant professor at Carnegie Mellon University, Pittsburgh. The human brain contains nearly 86 billion neurons, which communicate through intricate networks of connections. Understanding how they work together during learning can be challenging. Dr. Batista and his colleagues combined two innovative technologies, brain-computer interfaces and machine learning, to study patterns of activity among neurons in monkey brains as the animals learned to use their thoughts to move a computer cursor. “This is a fundamental advance in understanding the neurobiological patterns that underlie the learning process,” said Theresa Cruz, Ph.D., a program official at the National Center for Medical Rehabilitations Research at NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD). “The findings may eventually lead to new treatments for stroke as well as other neurological disorders.”
by Tom Siegfried René Descartes was a very clever thinker. He proved his own existence, declaring that because he thought, he must exist: “I think, therefore I am.” But the 17th century philosopher-mathematician-scientist committed a serious mental blunder when he decided that the mind doing the thinking was somehow separate from the brain it lived in. Descartes believed that thought was insubstantial, transmitted from the ether to the pineal gland, which played the role of something like a Wi-Fi receiver embedded deep in the brain. Thereafter mind-brain dualism became the prevailing prejudice. Nowadays, though, everybody with a properly working brain realizes that the mind and brain are coexistent. Thought processes and associated cognitive mental activity all reflect the physics and chemistry of cells and molecules inhabiting the brain’s biological tissue. Many people today do not realize, though, that there’s a modern version of Descartes’ mistaken dichotomy. Just as he erroneously believed the mind was distinct from the brain, some scientists have mistakenly conceived of the brain as distinct from the body. Much of the early research in artificial intelligence, for instance, modeled the brain as a computer, seeking to replicate mental life as information processing, converting inputs to outputs by logical rules. But even if such a machine could duplicate the circuitry of the brain, it would be missing essential peripheral input from an attached body. Actual intelligence requires both body and brain, as the neurologist Antonio Damasio pointed out in his 1994 book, Descartes’ Error. “Mental activity, from its simplest aspects to its most sublime, requires both brain and body proper,” Damasio wrote. © Society for Science & the Public 2000 - 2013.
Link ID: 20002 - Posted: 08.27.2014
Ian Sample, science editor Scientists have prevented muscle wastage in mice with a form of muscular dystrophy by editing the faulty gene that causes the disease. The radical procedure could not be performed in humans, but researchers believe the work raises hopes for future gene-editing therapies to stop the disease from progressing in people. Duchenne muscular dystrophy is caused by mutations in a gene on the X chromosome and affects around one in 3,500 boys. Because girls have two X chromosomes they tend not to be affected, but can be carriers of the disease. The pivotal gene is used to make a protein called dystrophin which is crucial for muscle fibre strength. Without the protein, muscles in the body, including the heart and skeletal muscles, weaken and waste away. Most patients die by the age of 25 from breathing or heart problems. Researchers in the US used a powerful new gene-editing procedure called CRISPR to correct mutations in the dystrophin gene in mice that were destined to develop the disease. They extracted mouse embryos from their mothers and injected them with the CRISPR biological machinery, which found and corrected the faulty gene. After the injections, the mouse embryos were reimplanted in females and carried to term. Tests on the mice found that the therapy helped to restore levels of dystrophin, and that their skeletal muscle performed normally, even when only 17% of their cells contained corrected genes. The procedure could not be done in humans, but the proof-of-principle experiment demonstrates that correcting only a small proportion of cells could lead to a dramatic improvement for patients. © 2014 Guardian News and Media Limited