Chapter 11. Motor Control and Plasticity

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By Amy Ellis Nutt Surgeons snaked the electrodes under the 65-year-old woman’s scalp. Thirty years of Parkinson’s disease had almost frozen her limbs. The wires, connected to a kind of pacemaker under the skin, were aimed at decreasing the woman’s rigidity and allowing for more fluid movement. But five seconds after the first electrical pulse was fired into her brain, something else happened. Although awake and fully alert, she seemed to plunge into sadness, bowing her head and sobbing. One of the doctors asked what was wrong. “I no longer wish to live, to see anything, to hear anything, feel anything,” she said. Was she in some kind of pain? “No, I’m fed up with life. I’ve had enough,” she replied. “Everything is useless.” The operating team turned off the current. Less than 90 seconds later, the woman was smiling and joking, even acting slightly manic. Another five minutes more, and her normal mood returned. The patient had no history of depression. Yet in those few minutes after the electrical pulse was fired, the despair she expressed met nine of the 11 criteria for severe major depressive disorder in the Diagnostic and Statistical Manual of Mental Disorders. Fascinated by the anomaly, the French physicians wrote up the episode for the New England Journal of Medicine. The year was 1999, and hers was one of the first documented cases of an electrically induced, instantaneous, yet reversible depression. © 1996-2016 The Washington Post

Keyword: Parkinsons; Emotions
Link ID: 21955 - Posted: 03.05.2016

Laura Sanders For some adults, Zika virus is a rashy, flulike nuisance. But in a handful of people, the virus may trigger a severe neurological disease. About one in 4,000 people infected by Zika in French Polynesia in 2013 and 2014 got a rare autoimmune disease called Guillain-Barré syndrome, researchers estimate in a study published online February 29 in the Lancet. Of 42 people diagnosed with Guillain-Barré in that outbreak, all had antibodies that signaled a Zika infection. Most also had recent symptoms of the infection. In a control group of hospital patients who did not have Guillain-Barré, researchers saw signs of Zika less frequently: Just 54 out of 98 patients tested showed signs of the virus. The message from this earlier Zika outbreak is that countries in the throes of Zika today “need to be prepared to have adequate intensive care beds capacity to manage patients with Guillain-Barré syndrome,” writes study coauthor Arnaud Fontanet of the Pasteur Institute in Paris and colleagues, some of whom are from French Polynesia. The study, says public health researcher Ernesto Marques of the University of Pittsburgh, “tells us what I think a lot of people already thought: that Zika can cause Guillain-Barré syndrome.” As with Zika and the birth defect microcephaly (SN: 2/20/16, p. 16), though, more work needs to be done to definitively prove the link. Several countries currently hard-hit by Zika have reported upticks in Guillain-Barré syndrome. Colombia, for instance, usually sees about 220 cases of the syndrome a year. But in just five weeks between mid-December 2015 to late January 2016, doctors diagnosed 86 cases, the World Health Organization reports. Other Zika-affected countries, including Brazil, El Salvador and Venezuela, have also reported unusually high numbers of cases. © Society for Science & the Public 2000 - 2016. All rights reserved.

Keyword: Movement Disorders; Neuroimmunology
Link ID: 21939 - Posted: 03.01.2016

Mo Costandi People who are prone to falling and injuring and injuring themselves in middle age are at significantly increased risk of developing Parkinson’s Disease decades later, according to a new study by researchers in Sweden. The findings, published earlier this month in the open access journal PLoS Medicine, suggest that frailty – and especially an increased risk of falling and fracturing one’s hip – could be a marker for degenerative brain changes, which may occur decades before disease symptoms appear, and possibly aid in early diagnosis. Parkinson’s Disease is a progressive neurodegenerative disease characterised by the death of dopamine-producing neurons in a region of the midbrain called the substantia nigra. This causes the three main symptoms of tremor, muscle rigidity, and slow movements, which typically appear at around 60 years of age, and progress at varying rates. Although widely considered to be a movement disorder, Parkinson’s is also associated with cognitive impairments, which in severe cases can develop into full-blown dementia. Last year, Peter Nordström of Umeå University and his colleagues published the results of a large population study, in which they examined the medical records of all the approximately 1.35 million Swedish men conscripted at age 18 for compulsory military service between the years of 1969 and 1996. Looking specifically at measures of muscle strength, they found that those who scored lowest on handgrip and elbow flexion strength at the time of conscription were significantly more likely to develop Parkinson’s 30 years later. © 2016 Guardian News and Media Limited

Keyword: Parkinsons
Link ID: 21919 - Posted: 02.20.2016

By Gretchen Reynolds Some forms of exercise may be much more effective than others at bulking up the brain, according to a remarkable new study in rats. For the first time, scientists compared head-to-head the neurological impacts of different types of exercise: running, weight training and high-intensity interval training. The surprising results suggest that going hard may not be the best option for long-term brain health. As I have often written, exercise changes the structure and function of the brain. Studies in animals and people have shown that physical activity generally increases brain volume and can reduce the number and size of age-related holes in the brain’s white and gray matter. Exercise also, and perhaps most resonantly, augments adult neurogenesis, which is the creation of new brain cells in an already mature brain. In studies with animals, exercise, in the form of running wheels or treadmills, has been found to double or even triple the number of new neurons that appear afterward in the animals’ hippocampus, a key area of the brain for learning and memory, compared to the brains of animals that remain sedentary. Scientists believe that exercise has similar impacts on the human hippocampus. These past studies of exercise and neurogenesis understandably have focused on distance running. Lab rodents know how to run. But whether other forms of exercise likewise prompt increases in neurogenesis has been unknown and is an issue of increasing interest, given the growing popularity of workouts such as weight training and high-intensity intervals. So for the new study, which was published this month in the Journal of Physiology, researchers at the University of Jyvaskyla in Finland and other institutions gathered a large group of adult male rats. The researchers injected the rats with a substance that marks new brain cells and then set groups of them to an array of different workouts, with one group remaining sedentary to serve as controls. © 2016 The New York Times Company

Keyword: Neurogenesis
Link ID: 21902 - Posted: 02.17.2016

By Sheena Goodyear, A brain implant the size of a paper-clip might one day help paralyzed people regain the ability to use their arms and legs via a wireless connection that will transmit their thoughts to an exoskeleton. It's not the first technology to allow paralyzed people to operate mechanical limbs with signals from their brain, but it has the potential to revolutionize the field because it's minimally invasive and totally wireless. It's made possible because of a matchstick-sized implant called a stentrode, crafted from nitinol, an alloy that is commonly used in brassiere underwires and eyeglass frames, according to a study published in the journal Nature Biotechnology. ​"It's really a new method for getting brain data out of the brain without performing brain surgery," Thomas Oxley, a neurologist at the University of Melbourne who designed the device, told CBC News. "Part of the reason that brain-machine interfaces have not been successful to this point is because they get rejected by the body, and the reason they get rejected is because they all require direct implantation into the brain. And to do that you have to take off the skull — you have to perform a craniotomy." ©2016 CBC/Radio-Canada.

Keyword: Robotics
Link ID: 21886 - Posted: 02.11.2016

Jo Marchant The brain cells of people with Parkinson’s disease can be trained to reliably respond to placebo drugs, Italian neuroscientists report. The training wears off after 24 hours but the effect shows it may be possible to reduce the medication needed to treat Parkinson’s by interspersing real drugs with inert injections or pills, says placebo researcher Fabrizio Benedetti at the University of Turin, Italy, who led the work. A few people with Parkinson’s disease do respond dramatically to placebos, but most do not1. People with the condition suffer characteristic tremors and stiff muscles because their dopamine-producing brain cells are gradually dying off. They alleviate their symptoms by taking drugs such as apomorphine, which activate receptors for dopamine. For some conditions — such as pain and immune disorders — trials have shown2 that it is possible to train people to respond to placebos, although this practice hasn’t made its way into clinical care. Benedetti and his colleagues wondered whether the same effect might be possible for neurological disorders. They studied 42 people with advanced Parkinson’s disease who were having electrodes implanted into their brains for a therapy called deep brain stimulation, which eases symptoms by stimulating affected brain areas directly. That surgery gave Benedetti’s team a rare opportunity to measure the activity of individual neurons in the thalamus, a brain region known to be inhibited by lack of dopamine in people with Parkinson's. © 2016 Nature Publishing Grou

Keyword: Parkinsons
Link ID: 21884 - Posted: 02.10.2016

Colombia says three people have died after contracting the Zika virus and developing a rare nerve disorder. Health Minister Alejandro Gaviria said there was a "causal connection" between Zika, the Guillain-Barre disorder and the three deaths. Earlier, Brazilian scientists said they had detected for the first time active samples of Zika in urine and saliva. However, it is not clear whether the virus can be transmitted through bodily fluids. Zika, a mosquito-borne disease, has been linked to cases of babies born in Brazil with microcephaly - underdeveloped brains. "We have confirmed and attributed three deaths to Zika," said the head of Colombia's National Health Institute, Martha Lucia Ospina. "In this case, the three deaths were preceded by Guillain-Barre syndrome." Guillain-Barre is a rare disorder in which the body's immune system attacks part of the nervous system. It isn't normally fatal. Ms Ospina said another six deaths were being investigated for possible links to Zika. "Other cases (of deaths linked to Zika) are going to emerge," she said. "The world is realising that Zika can be deadly. The mortality rate is not very high, but it can be deadly." Mr Gaviria said one of the fatalities took place in San Andres and the other two in Turbo, in Antioquia department. UK virologist Prof Jonathan Ball, of the University of Nottingham, told the BBC: "We have been saying Zika has been associated with Guillain-Barre. One of the complications of that could be respiratory failure. But it is still probably a very rare event." Although Zika usually causes mild, flu-like symptoms, it has been linked to thousands of suspected birth defects. However, it has not yet been proved that Zika causes either microcephaly or Guillain-Barre. © 2016 BBC

Keyword: Movement Disorders; Neuroimmunology
Link ID: 21865 - Posted: 02.06.2016

By Anne Pycha Future doctors may ask us to say more than “Ahhh.” Several groups of neuroscientists, psychiatrists and computer scientists are now investigating the extent to which patients' language use can provide diagnostic clues—before a single laboratory test is run. Increased computing power and new methods to measure the relation between behavior and brain activity have advanced such efforts. And although tests based on the spoken word may not be as accurate as gene sequencing or MRI scans, for diseases lacking clear biological indicators, language mining could help fill the gap. Psychiatrists at Columbia University interviewed 34 young adults at risk for psychosis, a common sign of schizophrenia that includes delusions and hallucinations. Two and a half years later five of the subjects had developed psychosis, and the remaining 29 remained free of the disorder. A specially designed algorithm combed the initial interviews collectively to look for language features that distinguished the two groups and found that psychosis correlated with shorter sentences, loss of flow in meaning from one sentence to the next and less frequent use of the words “that,” “what” and “which.” When later tested on each individual interview, the computer program predicted who did and who did not develop psychosis with 100 percent accuracy. The results were recently published in Schizophrenia, and a second round of testing with another group of at-risk subjects is now under way. Parkinson's Disease Twenty-seven subjects in a study at Favaloro University in Argentina listened to recorded sentences containing verbs associated with specific hand shapes (such as “applaud” or “punch”). As soon as they understood the sentence, participants pressed a button while keeping both hands in either a flat or clenched-fist position. © 2016 Scientific American

Keyword: Parkinsons; Schizophrenia
Link ID: 21818 - Posted: 01.25.2016

Videos just discovered show the first people ever to be treated for the symptoms of Parkinson’s disease. The footage, hidden for half a century, shows Chilean miners with severe movement problems improving on daily doses of L-dopa. The videos were filmed by George Cotzias at Brookhaven National Laboratory in Upton, New York. In 1963, while studying the toxic effects of manganese in human tissues, Cotzias learned of four workers in the Corral del Quemado mine in Andacollo, Chile, who had developed a syndrome called manganism – which resembled Parkinson’s – through inhaling manganese dust. Cotzias travelled to Chile to include the miners in a trial of leva-dopa, a chemical building block that the body converts into dopamine, low levels of which cause uncontrolled movements in people with Parkinson’s. L-dopa was being tested in Parkinson’s patients around the same time but with little success – even small amounts caused adverse side-effects that prevented a high enough dose reaching the brain. The footage clearly shows the severe problems with walking and turning miners had before treatment. After several months of receiving a daily dose of L-dopa, they were able to feed themselves, shave, tie their shoelaces, and run. “It’s a very important part of the history of neurology,” says Marcelo Miranda, a researcher at Clinica Las Condes in Santiago, Chile, who found the footage, some of which was shown at a conference in the 1960s, but hasn’t been seen since. “It’s the only available document of that period that shows the first patients with Parkinson’s symptoms treated with L-dopa and their extraordinary response.” © Copyright Reed Business Information Ltd.

Keyword: Parkinsons
Link ID: 21811 - Posted: 01.23.2016

The Chamorro people of the Pacific island of Guam know it as lytigo-bodig. For decades, they have been struck down by a mysterious illness that resembles the muscle-wasting disease amyotrophic lateral sclerosis (ALS), Parkinson’s disease and Alzheimer’s-like dementia. It now looks like we have a clue that could point to a way of slowing its development. Lytigo-bodig is a progressive disease. ALS symptoms arrive when people are in their mid-40s and early 50s. By the time they reach their 60s, they also have the shaking and lack of coordination that characterises Parkinson’s, before the cognitive problems associated with dementia also set in. “Initially they stumble a bit, but as their muscles wither, they need help with eating and going to the toilet, as well as having difficulty swallowing and breathing,” says Paul Cox of the Institute for Ethnomedicine in Wyoming. For a long time, a chemical called BMAA, found in the cycad seeds that the Chamorro grind up to make flour, has been suspected as the cause of the disease. The toxin builds up in the cyanobacteria that grow in the roots of cycad plants. It also accumulates in the tissue of seed-eating flying foxes, which the Chamorro hunt and eat. To see if they could confirm BMAA as the culprit, Cox fed fruit spiked with the toxin to vervet monkeys for 140 days. They estimated this was equivalent to the dose a typical islander might get over a lifetime. Although they didn’t show cognitive problems, the animals did develop brain abnormalities called tau tangles and deposits of amyloid plaque. The density and placement of these abnormalities were similar to those seen in the islanders. “The structure of the pathology is almost identical,” says Cox. “We were stunned.” © Copyright Reed Business Information Ltd.

Keyword: ALS-Lou Gehrig's Disease ; Parkinsons
Link ID: 21802 - Posted: 01.20.2016

By Ralph G. Neas In mid-February of 1979, I started experiencing tingling sensations in my feet and fingers. I told myself I was only feeling some residual effects from a bout with the flu several weeks before, and I caught the afternoon plane to Minneapolis to join my new boss, U.S. Sen. David Durenberger (R-Minn.), for several days of political meetings. That was on Sunday. On Tuesday, midway through a presentation, I began slurring my words and I found it hard to swallow. A local doctor, on hearing I’d had the flu, told me to go to my hotel room, take a couple of aspirin and call him in the morning. I spent the night moving from the bed to the couch to the chair to the floor, seeking relief from pain that was affecting more and more of my body. Just before dawn, I noticed that the right side of my face was paralyzed. On my way to the ER, the left side became paralyzed. I wasn’t having a recurrence of the flu. A spinal tap confirmed doctors’ suspicions that I’d come down with Guillain-Barré syndrome, or GBS, a rare neurological disorder that can cause total paralysis. Within 10 days I was so weakened by the spreading paralysis in my legs and arms that I could not get out of my bed at St. Mary’s, the Minneapolis hospital where I was being treated. Within three weeks, doctors performed a tracheostomy — connecting a mechanical respirator to my windpipe — because my ability to breathe was getting so poor.

Keyword: Movement Disorders; Neuroimmunology
Link ID: 21777 - Posted: 01.12.2016

By NICHOLAS WADE After decades of disappointingly slow progress, researchers have taken a substantial step toward a possible treatment for Duchenne muscular dystrophy with the help of a powerful new gene-editing technique. Duchenne muscular dystrophy is a progressive muscle-wasting disease that affects boys, putting them in wheelchairs by age 10, followed by an early death from heart failure or breathing difficulties. The disease is caused by defects in a gene that encodes a protein called dystrophin, which is essential for proper muscle function. Because the disease is devastating and incurable, and common for a hereditary illness, it has long been a target for gene therapy, though without success. An alternative treatment, drugs based on chemicals known as antisense oligonucleotides, is in clinical trials. But gene therapy — the idea of curing a genetic disease by inserting the correct gene into damaged cells — is making a comeback. A new technique, known as Crispr-Cas9, lets researchers cut the DNA of chromosomes at selected sites to remove or insert segments. Three research groups, working independently of one another, reported in the journal Science on Thursday that they had used the Crispr-Cas9 technique to treat mice with a defective dystrophin gene. Each group loaded the DNA-cutting system onto a virus that infected the mice’s muscle cells, and excised from the gene a defective stretch of DNA known as an exon. Without the defective exon, the muscle cells made a shortened dystrophin protein that was nonetheless functional, giving all of the mice more strength. The teams were led by Charles A. Gersbach of Duke University, Eric N. Olson of the University of Texas Southwestern Medical Center and Amy J. Wagers of Harvard University. © 2016 The New York Times Company

Keyword: Movement Disorders; Muscles
Link ID: 21745 - Posted: 01.02.2016

Tina Hesman Saey SAN DIEGO — Friendly ghosts help muscles heal after injury. Connective tissue sheaths that bundle muscle cells together leave behind hollow fibers when muscles are injured, Micah Webster of the Carnegie Institution for Science in Baltimore and colleagues discovered. Muscle-repairing stem cells build new tissue from inside those empty tunnels, known as ghost fibers, Webster reported December 13 at the annual meeting of the American Society for Cell Biology. Researchers previously knew that stem cells can heal muscle, but how stem cells integrate new cells into muscle fibers has been a mystery. Webster and colleagues used a special microscopy technique to watch stem cells in live mice as the cells fixed muscles damaged by snake venom. Stem cells from undamaged parts of the muscle fiber crawled back and forth through the ghostly part of the fibers and spaced themselves out evenly. Stem cells replicated themselves to reconstruct each muscle fiber inside its ghostly shell the researchers found. Stem cells didn’t move from one ghost fiber to another. The finding suggests that researchers will need to create artificial ghost fibers to repair injuries in which chunks of muscles are lost, such as in soldiers hit by explosives, Webster said. The researchers also reported the results online December 10 in Cell Stem Cell. M.T. Webster et al. Intravital imaging reveals ghost fibers as architectural units guiding muscle progenitors. Annual meeting of the American Society for Cell Biology, San Diego, December 13, 2015. M.T. Webster et al. Intravital imaging reveals ghost fibers as architectural units guiding myogenic progenitors during regeneration. Cell Stem Cell. Published online December 10, 2015. doi: 10.1016/j.stem.2015.11.005 © Society for Science & the Public 2000 - 2015

Keyword: Muscles
Link ID: 21704 - Posted: 12.16.2015

The clock is ticking for Ronald Cohn. He wants to use CRISPR gene editing to correct the genes of his friend’s 13-year-old son. The boy, Gavriel, has Duchenne muscular dystrophy, a genetic disease in which muscles degenerate. Breathing and heart problems often start by the time people with the condition are in their early twenties. Life expectancy is about 25 years. By the standards of science, the field of CRISPR gene editing is moving at a lightning fast pace. Although the technique was only invented a few years ago, it is already being used for research by thousands of labs worldwide to make extremely precise changes to DNA. A handful of people have already been treated using therapies enabled by the technology, and last week an international summit effectively endorsed the idea of gene editing embryos. It is too soon to try the technique out, but the summit concluded that basic research on embryos should be permitted, alongside a debate on how we should use the technology. But for people like Cohn, progress can’t come fast enough. Gavriel was diagnosed at age 4. He has already lost the use of his legs but still has some movement in his upper body, and uses a manual wheelchair. Cohn, a clinician at the Hospital for Sick Children in Toronto, estimates that he has three years to develop and test a CRISPR-based treatment if he is to help Gavriel. Muscular dystrophy is caused by a faulty gene for the protein dystrophin, which holds our muscles together. Gavriel has a duplicated version of the gene. This week, Cohn’s team published a paper describing how they grew Gavriel’s cells in a dish and used CRISPR gene-editing techniques to snip out the duplication. With the duplication removed, his cells produced normal dystrophin protein. © Copyright Reed Business Information Ltd.

Keyword: Movement Disorders; Muscles
Link ID: 21698 - Posted: 12.14.2015

By Gretchen Reynolds Physical fitness may be critical for maintaining a relatively youthful and nimble brain as we age, according to a new study of brain activation patterns in older people. For most of us, our bodies begin to lose flexibility and efficiency as we enter our 40s. Running and other movements slow down and become more awkward, and something similar seems to occur within our heads. As middle age encroaches, our thinking becomes less efficient. We don’t toggle between mental tasks as nimbly as we once did or process new information with the same aplomb and clarity. Recently, neuroscientists have begun to quantify how those cognitive changes play out in our brains, to disquieting effect. In studies comparing brain activation in young people with that of people past 40, they have found notable differences, especially during mental tasks that require attention, problem solving, decision-making and other types of high-level thinking. Such thinking primarily involves activation of the brain’s prefrontal cortex. In young people, activation in the cortex during these cognitive tasks tends to be highly localized. Depending on the type of thinking, young people’s brains light up almost exclusively in either the right or left portion of the prefrontal cortex. But in older people, studies show, brain activity during the same mental tasks requires far more brainpower. They typically display activity in both hemispheres of their prefrontal cortex. In effect, they require more of their brains’ resources to complete the same tasks that young people do with less cognitive effort. Neuroscientists coined an acronym for this phenomenon: Harold, for hemispheric asymmetry reduction in older adults. Most agree that it represents a general reorganization and weakening of the brain’s function with age. © 2015 The New York Times Company

Keyword: Alzheimers; Development of the Brain
Link ID: 21688 - Posted: 12.10.2015

by Chris Samoray Every fall, blackpoll warblers fly from North America to South America in what’s the longest migration route of any warbler in the Western Hemisphere. But some of the tiny songbirds take a detour before making their epic transoceanic leap. Over 40 years of data from 22,295 birds show that blackpoll warblers (Setophaga striata) living in western North America head east for a pit stop to put on weight, giving the birds the energy stores they need to cross the Atlantic Ocean, researchers report December 9 in the Auk: Ornithological Advances. For birds that breed farther west in places like Alaska, the eastern stopover means a migration distance that’s nearly twice that of their eastern U.S. counterparts, the scientists find. © Society for Science & the Public 2000 - 2015.

Keyword: Animal Migration
Link ID: 21687 - Posted: 12.10.2015

By SINDYA N. BHANOO Moderate levels of exercise may increase the brain’s flexibility and improve learning, a new study suggests. The visual cortex, the part of the brain that processes visual information, loses the ability to “rewire” itself with age, making it more difficult for adults to recover from injuries and illness, said Claudia Lunghi, a neuroscientist at the University of Pisa and one of the study’s authors. In a study in the journal Current Biology, she and her colleagues asked 20 adults to watch a movie with one eye patched while relaxing in a chair. Later, the participants exercised on a stationary bike for 10-minute intervals while watching a movie. When one eye is patched, the visual cortex compensates for the limited input by increasing its activity level. Dr. Lunghi and her colleagues tested the imbalance in strength between the participants’ eyes after the movie — a measure of changeability in the visual cortex. © 2015 The New York Times Company

Keyword: Regeneration
Link ID: 21681 - Posted: 12.08.2015

By Karen Weintraub Essential tremor is involuntary shaking – usually of the hands, but sometimes also of the neck, jaw, voice or legs. “Any fine tasks with the hands can be very difficult when the tremor is pronounced,” said Dr. Albert Hung, center director of the Massachusetts General Hospital National Parkinson Foundation Center of Excellence. Essential tremor can affect balance, walking, hearing and cognition, and can get worse over time, said Dr. Elan Louis, chief of the division of movement disorders at Yale School of Medicine. People with essential tremor run almost twice the risk of developing Alzheimer’s as the general population. Essential tremor appears with movement; if people let their hands sit still, they don’t tremble. That is the big difference between an essential tremor and the tremor of Parkinson’s disease, which can occur while at rest, Dr. Louis said. Essential tremor also tends to strike both hands while Parkinson’s is more one-sided at first, said Dr. Hung. The cause of essential tremor remains a mystery, though it seems to run in families. People of any age or sex can have the condition, though it is more common as people grow older. Roughly 4 percent of 40-year-olds have essential tremor, compared with about 20 percent of 90-year-olds, Dr. Louis said. Available treatments “aren’t great,” Dr. Louis said. Two medications – the beta blocker propranolol and the epilepsy drug primidone, sold under the brand name Mysoline – can reduce tremors by 10 to 30 percent, he said, but they work only in about half of patients. Deep brain stimulation – implanting electrodes into the brain to override faulty electrical signals – has been shown to markedly reduce hand tremor severity, he said. But the treatment can worsen cognitive and balance problems and “doesn’t cure the underlying disease. It merely and temporarily lessons a single symptom, which is the tremor.” © 2015 The New York Times Company

Keyword: Movement Disorders
Link ID: 21653 - Posted: 11.24.2015

By Gretchen Reynolds Sturdy legs could mean healthy brains, according to a new study of British twins. As I frequently have written in this column, exercise may cause robust improvements in brain health and slow age-related declines in memory and thinking. Study after study has shown correlations between physical activity, muscular health and mental acuity, even among people who are quite old. But these studies have limitations and one of them is that some people may be luckier than others. They may have been born to have a more robust brain than someone else. Their genes and early home environment might have influenced their brain health as much as or more than their exercise habits. Their genes and early home environment also might have influenced those exercise habits, as well as how their bodies and brains responded to exercise. In other words, genes and environment can seriously confound experimental results. That problem makes twins so valuable for scientific purposes. (Full disclosure, I am a twin, although not an identical one.) Twins typically share the same early home environment and many of the same genes, and if they are identical, all their genes are the same. So if one twin’s body, brain and thinking abilities begin to differ substantially over the years from their twin’s, the cause is less likely to be solely genetic or the early environment, and more likely to be attributable to lifestyle, including exercise habits. It was that possibility that recently prompted Claire Steves, a senior lecturer in twin research at King’s College London, to consider twins and their thighs. © 2015 The New York Times Company

Keyword: Alzheimers
Link ID: 21641 - Posted: 11.18.2015

Ewen Callaway Ringo, a golden retriever born in 2003 in a Brazilian kennel, was never expected to live long. Researchers bred him and his littermates to inherit a gene mutation that causes severe muscular dystrophy. They hoped that the puppies would provide insight into Duchenne muscular dystrophy (DMD), an untreatable and ultimately fatal human disease caused by inactivation of the same gene. But Ringo’s muscles didn't waste away like his littermates', and researchers have now determined why: he was born with another mutation that seems to have protected him from the disease, according to a paper published in Cell1. Scientists hope that by studying Ringo’s mutation — which has never before been linked to muscular dystrophy — they can find new treatments for the disease. As many as 1 in 3,500 boys inherit mutations that produce a broken version of a protein called dystrophin, causing DMD. (The disease appears in boys because the dystrophin gene sits on the X chromosome, so girls must inherit two copies of the mutated gene to develop DMD.) The protein helps to hold muscle fibres together, and its absence disrupts the regenerative cycle that rebuilds muscle tissue. Eventually, fat and connective tissue replace muscle, and people with DMD often become reliant on a wheelchair before their teens. Few survive past their thirties. Some golden retriever females carry dystrophin mutations that cause a similar disease when passed onto male puppies. Dog breeders can prevent this through genetic screening. But Mayana Zatz, a geneticist at the University of São Paulo in Brazil, and her colleagues set out to breed puppies with the mutation to model the human disease. © 2015 Nature Publishing Group,

Keyword: Movement Disorders; Muscles
Link ID: 21632 - Posted: 11.14.2015