Chapter 11. Motor Control and Plasticity
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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
By Lenny Bernstein Comedian Robin Williams was grappling with severe depression when he committed suicide Monday, and on Thursday we learned that he also was in the early stages of Parkinson's disease. Sadly, the two conditions are often found together. In a 2012 study conducted by the National Parkinson Foundation, 61 percent of 5,557 Parkinson's patients surveyed reported that they also suffered from depression, with symptoms that ranged from mild to severe. Both conditions are associated with a shortage of dopamine, a neurotransmitter that helps regulate movement and control the brain's pleasure center. "Dopamine is a feel-good chemical. If you are low in dopamine, you are not going to feel so good," said Joyce Oberdorf, president and CEO of the National Parkinson Foundation. "There are [also] other neurotransmitters that can be low." A separate study published Friday found that newly-diagnosed Parkinson's patients have higher rates of depression, anxiety, fatigue, and apathy than a control group of people without Parkinson's. Researchers from the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania found that 13.9 percent of patients had symptoms of depression when they were diagnosed with Parkinson's, a proportion that rose to 18.7 percent after 24 months. Just 6.6 percent of people without the disease had depression, and that dropped to just 2.4 percent after 24 months. Despite their depressive symptoms, most of the Parkinson's patients who also had that condition were not treated with anti-depressants at any point in the two-year study. The findings were published in the journal Neurology.
by Catherine Brahic Think crayfish and you probably think supper, perhaps with mayo on the side. You probably don't think of their brains. Admittedly, crayfish aren't known for their grey matter, but that might be about to change: they can grow new brain cells from blood. Humans can make new neurons, but only from specialised stem cells. Crayfish, meanwhile, can convert blood to neurons that resupply their eyestalks and smell circuits. Although it's a long way from crayfish to humans, the discovery may one day help us to regenerate our own brain cells. Olfactory nerves are continuously exposed to damage and so naturally regenerate in many animals, from flies to humans, and crustaceans too. It makes sense that crayfish have a way to replenish these nerves. To do so, they utilise what amounts to a "nursery" for baby neurons, a little clump at the base of the brain called the niche. In crayfish, blood cells are attracted to the niche. On any given day, there are a hundred or so cells in this area. Each cell will split into two daughter cells, precursors to full neurons, both of which migrate out of the niche. Those that are destined to be part of the olfactory system head to two clumps of nerves in the brain called clusters 9 and 10. It's there that the final stage of producing new smell neurons is completed. © Copyright Reed Business Information Ltd.
By ZACH SCHONBRUN EAST RUTHERFORD, N.J. — Victor Cruz dumped a bucket of ice water on his head at home on Sunday and then stepped out on thin ice himself — challenging the Giants’ co-owners to do the same. Taking part in the Ice Bucket Challenge — a social media craze that raises awareness for Lou Gehrig’s disease (amyotrophic lateral sclerosis) — Cruz, a wide receiver, posted the video on his Twitter feed. “That water was cold, man,” Cruz said Monday. The Ice Bucket Challenge was started by friends and family members of Pete Frates, a 29-year-old from Beverly, Mass., who played baseball at Boston College and was found to have A.L.S., a neurodegenerative condition, in 2012. As a reward for withstanding the icy punishment, the participant gets to nominate another person, who has 24 hours to complete the task. Cruz aimed high, calling out the co-owners John Mara and Steve Tisch to step under the bucket themselves. Just before practice on Monday, the 59-year-old Mara, wearing a white Giants T-shirt and black shorts, allowed Cruz to dump a Gatorade tub filled with ice water over his head. Before doing so, Mara nominated the Jets’ owner, Woody Johnson; the Patriots’ owner, Robert K. Kraft; and Patriots Coach Bill Belichick to do the same. “Feels good,” a smiling Mara said in a video posted on the Giants’ team website. It is unclear if Tisch will follow suit. Those who fail to complete the task within 24 hours are asked to donate to A.L.S. research. © 2014 The New York Times Company
Keyword: ALS-Lou Gehrig's Disease
Link ID: 19937 - Posted: 08.12.2014
By Fredrick Kunkle The way older people walk may provide a reliable clue about how well their brain is aging and could eventually allow doctors to determine whether they are at risk of Alzheimer’s, researchers have found. The study, involving thousands of older people in several countries, suggests that those whose walking pace begins to slow and who also have cognitive complaints are more than twice as likely to develop dementia within 12 years. The findings are among the latest attempts to find and develop affordable, inexpensive diagnostic tools to determine whether a person is at risk for dementia. Last month, researchers attending the Alzheimer’s Association International Conference in Copenhagen presented several studies focused on locating biomarkers of dementia in its earliest stages. Among other things, scientists reported a connection between dementia and sense of smell that suggested a common scratch-and-sniff test could be used to help identify onset of dementia, while other researchers suggested that eye scans could also be useful someday be able to detect Alzheimer’s. Different studies found a new abnormal protein linked to Alzheimer’s and a possible link between sleep disorders and the onset of dementia. Now, researchers at the Albert Einstein College of Medicine of Yeshiva University and Montefiore Medical Center say that a simple test to measure a patient’s cognitive abilities and walking speed could provide a new diagnostic tool to identify people at risk for dementia. It could be especially important tool in low- and middle-income countries with less access to sophisticated and costly technology, the scientists said.
Link ID: 19910 - Posted: 08.02.2014
Using data from over 18,000 patients, scientists have identified more than two dozen genetic risk factors involved in Parkinson’s disease, including six that had not been previously reported. The study, published in Nature Genetics, was partially funded by the National Institutes of Health (NIH) and led by scientists working in NIH laboratories. A gene chip. Scientists used gene chips to help discover new genes that may be involved with Parkinson's disease “Unraveling the genetic underpinnings of Parkinson’s is vital to understanding the multiple mechanisms involved in this complex disease, and hopefully, may one day lead to effective therapies,” said Andrew Singleton, Ph.D., a scientist at the NIH’s National Institute on Aging (NIA) and senior author of the study. Dr. Singleton and his colleagues collected and combined data from existing genome-wide association studies (GWAS), which allow scientists to find common variants, or subtle differences, in the genetic codes of large groups of individuals. The combined data included approximately 13,708 Parkinson’s disease cases and 95,282 controls, all of European ancestry. The investigators identified potential genetic risk variants, which increase the chances that a person may develop Parkinson’s disease. Their results suggested that the more variants a person has, the greater the risk, up to three times higher, for developing the disorder in some cases.