Chapter 11. Motor Control and Plasticity
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Jon Hamilton Researchers have identified a substance in muscles that helps explain the connection between a fit body and a sharp mind. When muscles work, they release a protein that appears to generate new cells and connections in a part of the brain that is critical to memory, a team reports Thursday in the journal Cell Metabolism. The finding "provides another piece to the puzzle," says Henriette van Praag, an author of the study and an investigator in brain science at the National Institute on Aging. Previous research, she says, had revealed factors in the brain itself that responded to exercise. The discovery came after van Praag and a team of researchers decided to "cast a wide net" in searching for factors that could explain the well-known link between fitness and memory. They began by looking for substances produced by muscle cells in response to exercise. That search turned up cathepsin B, a protein best known for its association with cell death and some diseases. Experiments showed that blood levels of cathepsin B rose in mice that spent a lot of time on their exercise wheels. What's more, as levels of the protein rose, the mice did better on a memory test in which they had to swim to a platform hidden just beneath the surface of a small pool. The team also found evidence that, in mice, cathepsin B was causing the growth of new cells and connections in the hippocampus, an area of the brain that is central to memory. But the researchers needed to know whether the substance worked the same way in other species. So they tested monkeys, and found that exercise did, indeed, raise circulating levels of cathepsin in the blood. © 2016 npr
Megan Scudellari Shinya Yamanaka looked up in surprise at the postdoc who had spoken. “We have colonies,” Kazutoshi Takahashi said again. Yamanaka jumped from his desk and followed Takahashi to their tissue-culture room, at Kyoto University in Japan. Under a microscope, they saw tiny clusters of cells — the culmination of five years of work and an achievement that Yamanaka hadn't even been sure was possible. Two weeks earlier, Takahashi had taken skin cells from adult mice and infected them with a virus designed to introduce 24 carefully chosen genes. Now, the cells had been transformed. They looked and behaved like embryonic stem (ES) cells — 'pluripotent' cells, with the ability to develop into skin, nerve, muscle or practically any other cell type. Yamanaka gazed at the cellular alchemy before him. “At that moment, I thought, 'This must be some kind of mistake',” he recalls. He asked Takahashi to perform the experiment again — and again. Each time, it worked. Over the next two months, Takahashi narrowed down the genes to just four that were needed to wind back the developmental clock. In June 2006, Yamanaka presented the results to a stunned room of scientists at the annual meeting of the International Society for Stem Cell Research in Toronto, Canada. He called the cells 'ES-like cells', but would later refer to them as induced pluripotent stem cells, or iPS cells. “Many people just didn't believe it,” says Rudolf Jaenisch, a biologist at the Massachusetts Institute of Technology in Cambridge, who was in the room. But Jaenisch knew and trusted Yamanaka's work, and thought it was “ingenious”. © 2016 Macmillan Publishers Limited,
By ALAN COWELL LONDON — When Muhammad Ali died last week, the memories spooled back inevitably to the glory days of the man who called himself the Greatest, a champion whose life intertwined with America’s traumas of race, faith and war. It was a chronicle of valor asserted in the most public of arenas scrutinized by an audience that spanned the globe. But there was another narrative, just as striking to some admirers, of a private courage beyond his klieg-lit renown. For the minority afflicted by Parkinson’s disease, Ali’s 30-year struggle with the same illness magnified the broader status he built from his boxing prowess as a black man who embraced radical Islam, refused to fight in Vietnam, earned the opprobrium of the establishment and yet emerged as an icon. “It was his longest bout, and one that ultimately he could not win,” the reporter Patrick Sawer wrote in The Telegraph, referring to Ali’s illness. Yet the affliction “only served to increase the worldwide admiration he had gained before the disease robbed him of his powers.” As a global superstar, Ali touched many lands, and Britain felt a particular bond. Boxing fans recalled his far-flung bouts — the “Rumble in the Jungle” against George Foreman in Zaire, as the Democratic Republic of Congo was then called, in 1974; “The Thrilla in Manila” in the Philippines against Joe Frazier a year later. But in Britain, his two defeats in the 1960s of Henry Cooper, a much-loved British heavyweight who died in 2011, and his feisty appearances in prime-time television interviews left an indelible mark. © 2016 The New York Times Company
Link ID: 22308 - Posted: 06.11.2016
By Esther Landhuis About 100 times rarer than Parkinson’s, and often mistaken for it, progressive supranuclear palsy afflicts fewer than 20,000 people in the U.S.—and two thirds do not even know they have it. Yet this little-known brain disorder that killed comic actor Dudley Moore in 2002 is quietly becoming a gateway for research that could lead to powerful therapies for a range of intractable neurodegenerative conditions including Alzheimer’s and chronic traumatic encephalopathy, a disorder linked to concussions and head trauma. All these diseases share a common feature: abnormal buildup of a protein called tau in the brains of patients. Progressive supranuclear palsy has no cure and is hard to diagnose. Although doctors may have heard of the disease, many know little about it. It was not described in medical literature until 1964 but some experts believe one of the earliest accounts of the debilitating illness appeared in an 1857 short story by Charles Dickens and his friend Wilke Collins: “A cadaverous man of measured speech. A man who seemed as unable to wink, as if his eyelids had been nailed to his forehead. A man whose eyes—two spots of fire—had no more motion than if they had been connected with the back of his skull by screws driven through them, and riveted and bolted outside among his gray hair. He had come in and shut the door, and he now sat down. He did not bend himself to sit as other people do, but seemed to sink bolt upright, as if in water, until the chair stopped him.” © 2016 Scientific American
By DENISE GRADY Muhammad Ali, who died on Friday after a long struggle with Parkinson’s disease, was given the diagnosis in 1984 when he was 42. The world witnessed his gradual decline over the decades as tremors and stiffness set in, replacing his athletic stride with a shuffle, silencing his exuberant voice and freezing his face into an expressionless mask. What is Parkinson’s disease? It is a progressive, incurable deterioration of the part of the brain that produces a chemical needed to carry signals to the regions that control movement. How common is Parkinson’s? About one million people in the United States, and between seven million and 10 million worldwide, are thought to have Parkinson’s, according to the Parkinson’s Disease Foundation. What causes it? Was boxing a factor for Ali? The exact cause is not known. As with many disorders, experts suspect a combination of genes and environment, meaning that people with a particular genetic makeup may be predisposed to the disease if they are exposed to certain environmental factors. Head injuries, such as those sustained repeatedly in boxing, are among the possible risk factors listed by the National Parkinson Foundation. So is exposure to certain pesticides. These factors have both been suggested as possible contributors in Muhammad Ali’s case. Can Parkinson’s disease be treated? Medication can ease the symptoms for a time, but the disease continues to progress. In some cases, implanted devices called deep-brain stimulators can also help with symptoms. But Parkinson’s is not curable. © 2016 The New York Times Company
Link ID: 22284 - Posted: 06.06.2016
By Gretchen Reynolds A weekly routine of yoga and meditation may strengthen thinking skills and help to stave off aging-related mental decline, according to a new study of older adults with early signs of memory problems. Most of us past the age of 40 are aware that our minds and, in particular, memories begin to sputter as the years pass. Familiar names and words no longer spring readily to mind, and car keys acquire the power to teleport into jacket pockets where we could not possibly have left them. Some weakening in mental function appears to be inevitable as we age. But emerging science suggests that we might be able to slow and mitigate the decline by how we live and, in particular, whether and how we move our bodies. Past studies have found that people who run, weight train, dance, practice tai chi, or regularly garden have a lower risk of developing dementia than people who are not physically active at all. There also is growing evidence that combining physical activity with meditation might intensify the benefits of both pursuits. In an interesting study that I wrote about recently, for example, people with depression who meditated before they went for a run showed greater improvements in their mood than people who did either of those activities alone. But many people do not have the physical capacity or taste for running or other similarly vigorous activities. So for the new study, which was published in April in the Journal of Alzheimer’s Disease, researchers at the University of California, Los Angeles, and other institutions decided to test whether yoga, a relatively mild, meditative activity, could alter people’s brains and fortify their ability to think. © 2016 The New York Times Company
Keyword: Learning & Memory
Link ID: 22270 - Posted: 06.01.2016
by Bruce Bower For a landmark 1977 paper, psychologist Andrew Meltzoff stuck his tongue out at 2- to 3-week-old babies. Someone had to do it. After watching Meltzoff razz them for 15 seconds, babies often stuck out their own tongues within the next 2½ minutes. Newborns also tended to respond in kind when the young researcher opened his mouth wide, pushed out his lips like a duck and opened and closed the fingers of one hand. Meltzoff, now at the University of Washington in Seattle, and a colleague were the first to report that babies copy adults’ simple physical deeds within weeks of birth. Until then, most scientists assumed that imitation began at around 9 months of age. Newborns don’t care that imitation is the sincerest form of flattery. For them, it may be a key to interacting with (and figuring out) those large, smiley people who come to be known as mommy and daddy. And that’s job number one for tykes hoping to learn how to talk and hang out with a circle of friends. Meltzoff suspected that babies enter the world able to compare their own movements — even those they can feel but not see, such as a projecting tongue — to corresponding adult actions. Meltzoff’s report has inspired dozens of papers on infant imitation. Some have supported his results, some haven’t. A new report, published May 5 in Current Biology, falls in the latter group. The study of 106 Australian babies tracked from 1 to 9 weeks of age concludes that infants don’t imitate anyone. © Society for Science & the Public 2000 - 201
Keyword: Development of the Brain
Link ID: 22246 - Posted: 05.25.2016
By Ian Randall As if you needed another reason to hate the gym, it now turns out that exercise can exhaust not only your muscles, but also your eyes. Fear not, however, for coffee can perk them right up again. During strenuous exercise, our muscles tire as they run out of fuel and build up waste products. Muscle performance can also be affected by a phenomenon called “central fatigue,” in which an imbalance in the body’s chemical messengers prevents the central nervous system from directing muscle movements effectively. It was not known, however, whether central fatigue might also affect motor systems not directly involved in the exercise itself—such as those that move the eyes. To find out, researchers gave 11 volunteers a carbohydrate solution either with a moderate dose of caffeine—which is known to stimulate the central nervous system—or as a placebo without, during 3 hours of vigorous cycling. After exercising, the scientists tested the cyclists with eye-tracking cameras to see how well their brains could still control their visual system. The team found that exercise reduced the speed of rapid eye movements by about 8%, impeding their ability to capture new visual information. The caffeine—the equivalent of two strong cups of coffee—was sufficient to counteract this effect, with some cyclists even displaying increased eye movement speeds, the team reports today in Scientific Reports. So it might be a good idea to get someone else to drive you home after that marathon. © 2016 American Association for the Advancement of Science.
Link ID: 22243 - Posted: 05.25.2016
By D. T. Max When a spinal cord is damaged, location is destiny: the higher the injury, the more severe the effects. The spine has thirty-three vertebrae, which are divided into five regions—the coccygeal, the sacral, the lumbar, the thoracic, and the cervical. The nerve-rich cord traverses nearly the entire length of the spine. The nerves at the bottom of the cord are well buried, and sometimes you can walk away from damage to these areas. In between are insults to the long middle region of the spine, which begins at the shoulders and ends at the midriff. These are the thoracic injuries. Although they don’t affect the upper body, they can still take away the ability to walk or feel below the waist, including autonomic function (bowel, bladder, and sexual control). Injuries to the cord in the cervical area—what is called “breaking your neck”—can be lethal or leave you paralyzed and unable to breathe without a ventilator. Doctors who treat spinal-cord-injury patients use a letter-and-number combination to identify the site of the damage. They talk of C3s (the cord as it passes through the third cervical vertebra) or T8s (the eighth thoracic vertebra). These morbid bingo-like codes help doctors instantly gauge the severity of a patient’s injury. Darek Fidyka, who is forty-one years old, is a T9. He was born and raised in Pradzew, a small farming town in central Poland, not far from Lodz. ... Several of the wounds punctured his lungs, and one nearly cut his spinal cord in half. As Fidyka lay on the ground, he felt his body change. “I can remember very vividly losing feeling in my legs, bit by bit,” he says. “It started in the upper part of the spine and was moving down slowly while I lay waiting for the ambulance to arrive.”
Link ID: 22230 - Posted: 05.19.2016
A bionic body is closer than you think By Dwayne Godwin, Jorge Cham Dwayne Godwin is a neuroscientist at the Wake Forest University School of Medicine. Jorge Cham draws the comic strip Piled Higher and Deeper at www.phdcomics.com. © 2016 Scientific American
Link ID: 22222 - Posted: 05.17.2016
Dara Mohammadi As the small motorboat chugs to a halt, three travellers, wind-beaten from the three-hour journey along the Atrato river, step on to the muddy banks of Bellavista, an otherwise inaccessible town in the heart of the heavily forested north-west of Colombia. They swing their hessian bags – stuffed with bedsheets, dried beans and cuddly toys – to their shoulders and clamber up a dusty path. Tucked inside the bag of one of the travellers, neuropsychologist Sonia Moreno, is the reason they are here: a wad of unfinished, hand-drawn charts of family trees. The people whose names are circled on the charts have Huntington’s disease, an incurable genetic brain disorder that usually starts between the ages of 35 and 45 years. It begins with personality changes that can make them aggressive, violent, uninhibited, anxious and depressed. The disease progresses slowly, robbing them first of the control of their body, which jerks and twists seemingly of its own will, and then their ability to walk, talk and think until, about 20 years after the symptoms first begin, they die. Their children, each of whom has a 50% chance of inheriting the disease, watch and wait to see if it will happen to them. It is in this way that the disease strangles families. With Moreno is Ignacio Muñoz-Sanjuan, vice president of translational biology at CHDI Foundation, a US nonprofit research organisation that aims to find ways to prevent or slow down the progression of the disease. The foundation spent $140m–$150m (£97m-£104m) on research last year, but Muñoz-Sanjuan is not here on official business. He’s here for Factor-H, an initiative he founded four years ago to help with the other end of the problem – poor families with Huntington’s struggling in Latin America. © 2016 Guardian News and Media Limited o
Rae Ellen Bichell For Tim Goliver and Luther Glenn, the worst illness of their lives started in the same way — probably after having a stomach bug. Tim was 21 and a college student at the University of Michigan. He was majoring in English and biology and active in the Lutheran church. "I was a literature geek," says Tim. "I was really looking forward to my senior year and wherever life would take me." Luther was in his 50s. He'd spent most of his career as a U.S. military policeman and was working in security in Washington, D.C. He'd recently separated from his wife and had just moved into a new house with his two daughters, who were in their 20s. Both men recovered from their stomach bugs, but a few days later they started to feel sluggish. "Here we are trying to unpack, prepare ourselves for new life together and I'm flat out, dead tired," says Luther. He fell asleep in the car one morning and never made it out of the garage. Then he fell in the bathroom. For Tim, it started to feel like running a marathon just to lift a spoonful of soup. One morning, he tried to comb his hair and realized he couldn't lift his arm above his shoulder. "At that moment I started to freak out," he says. Both men got so weak that their families had to wheel them into the emergency room in wheelchairs. They got the same diagnosis: Guillain-Barre syndrome, a neurological disorder which can leave people paralyzed for weeks. © 2016 npr
By Nicholas Bakalar Exposure to pesticides may increase the risk for amyotrophic lateral sclerosis, also known as Lou Gehrig’s disease, a new study has found. The study, in JAMA Neurology, included 156 patients with A.L.S. and 128 controls. All participants completed questionnaires providing information on age, sex, ethnicity, education, marital status, residential history, occupational history, smoking and military service. The researchers used the information on residence and occupation to estimate long-term exposure to pesticides, and then took blood samples to determine serum levels of 122 persistent environmental pollutants. The scientists divided exposure into four time periods: ever exposed, exposed in the last 10 years, exposed 10 to 30 years ago, and exposed more than 30 years ago. Exposure to pesticides at any time was associated with a fivefold increased relative risk for A.L.S. compared to no exposure. Even exposure more than 30 years ago tripled the risk. Military service was associated with double the risk, confirming findings of previous studies. “This is an association, not causality,” cautioned the senior author, Dr. Eva L. Feldman, a professor of neurology at the University of Michigan. “We found that people with A.L.S. were five times more likely to have been exposed to pesticides, but we don’t want people to conclude that pesticides cause A.L.S.” © 2016 The New York Times Company
By Dan Kiefer I’m on the heavy bag, throwing left jabs, ignoring the relentless blare of Kanye’s “Drive Slow, Homie” played at a volume that would raise the dead. I punch to a one-two count: left jab, right cross. I’m working as hard as I’ve ever worked, and even in this unheated gym I sweat as if it’s a sauna. Finally, the bell rings. It feels as if I’ve been at it for an hour; actually, three minutes have passed. The ensuing one-minute break seems to last four seconds. Let’s be clear: Boxing, even when the opponent is only a heavy bag, is a brutal sport. But brutality is needed, even welcome, when you’re facing a progressive, incurable neurological disease. I have Parkinson’s disease, and it causes my body to just freeze up. Weirdly enough, boxing helps me get unstuck. All 12 of us in this class bear the unmistakable signs of Parkinson’s disease. I spot a dapper, cheerful white-haired fellow shaking like a leaf (tremor). Next, a balding, heavyset guy stumbling forward awkwardly on his toes (dystonia, or muscle cramping). Then I see myself in a mirror: a man in a white T-shirt, khaki shorts and Nike running shoes, standing still, seemingly paralyzed. I’m in the midst of a Parkinson’s freeze (an extreme form of bradykinesia, or slow movement). Although Parkinson’s is generally thought of as an old-person’s disease, I was diagnosed with a young-onset version 18 years ago, at age 35. Since then, I’ve taken every sort of medication known to science. I’ve had brain surgery — two tiny electrodes were implanted deep in my brain to stimulate an area affected by Parkinson’s — which unquestionably have helped treat some of my symptoms. But medicine and surgery have not cured my freezing and falling, my gait and balance issues that worsen as my disease progresses: When walking across a busy street, I may suddenly, inexplicably come to a full stop as the light is about to change. Even the slightest downhill slope of a path causes me to fall forward.
Link ID: 22198 - Posted: 05.10.2016
By Jocelyn Kaiser Gene therapy is living up to its promise of halting a rare, deadly brain disease in young boys. In a new study presented in Washington, D.C., yesterday at the annual meeting of the American Society of Gene and Cell Therapy, all but one of 17 boys with adrenoleukodystrophy (ALD) remained relatively healthy for up to 2 years after having an engineered virus deliver into their cells a gene to replenish a missing protein needed by the brain. The results, which expand on an earlier pilot study, bring this ALD therapy one step closer to the clinic. About one in 21,000 boys are born with ALD, which is caused by a flaw in a gene on the X chromosome that prevents cells from making a protein that the cells need to process certain fats—females have a backup copy of the gene on their second X chromosome. Without that protein, the fats build up and gradually destroy myelin sheaths that protect nerves in the brain. In the cerebral form of ALD, which begins in childhood, patients quickly lose vision and mobility, usually dying by age 12. The disease achieved some degree of fame with the 1992 film Lorenzo’s Oil, inspired by a family’s struggle to prolong their son’s life with a homemade remedy. The only currently approved treatment for ALD is a bone marrow transplant -- white blood cells in the marrow go to the brain and turn into glial cells that produce normal ALD proteins. But bone marrow transplants carry many risks, including immune rejection, and matching donors can’t always be found. As an alternative, in the late 2000s, French researchers treated the bone cells of two boys with a modified virus carrying the ALD gene. They reported in Science in 2009 that this halted progression of the disease. © 2016 American Association for the Advancement of Science
Laura Sanders Iron, says aging expert Naftali Raz, is like the Force. It can be good or bad, depending on the context. When that context is the human brain, though, scientists wrangle over whether iron is a dark force for evil or a bright source of support. Some iron is absolutely essential for the brain. On that, scientists agree. But recent studies suggest to some researchers that too much iron, and the chemical reactions that ensue, can be dangerous or deadly, especially to nerve cells in the vulnerable brain area that deteriorates with Parkinson’s disease. Yet other work raises the possibility that those cells die because of lack of iron, rather than too much. “There are a lot of surprises in this field,” says iron biologist Nancy Andrews of Duke University. The idea that too much iron is dangerous captivates many researchers, including analytical neurochemist Dominic Hare of the University of Technology Sydney. “All of life is a chemical reaction,” he says, “so the start of disease is a chemical reaction as well.” And as Raz points out, reactions involving iron are both life-sustaining and dangerous. “Iron is absolutely necessary for conducting the very fundamental business in every cell,” says Raz, of Wayne State University in Detroit. It helps produce energy-storing ATP molecules. And that’s a dirty job, throwing off dangerous free radicals that can cause cellular mayhem as energy is made. But those free radicals are not the most worrisome aspect of iron, Hare believes. “The reaction that is much more dangerous is the reaction you get when iron and dopamine come together,” he says. © Society for Science & the Public 2000 - 2016.
Link ID: 22173 - Posted: 05.03.2016
By ANDREW POLLACK In a confrontation between the hopes of desperate patients and clinical trial data, advisers to the Food and Drug Administration voted on Monday not to recommend approval of what would become the first drug for Duchenne muscular dystrophy. The negative votes came despite impassioned pleas from patients, parents and doctors who insisted that the drug, called eteplirsen, was prolonging the ability of boys with the disease to walk well beyond when they would normally be in wheelchairs. The problem was that the drug’s manufacturer, Sarepta Therapeutics, was trying to win approval based on a study involving only 12 patients without an adequate placebo control. The advisory panel voted 7 to 3, with three abstentions, that the clinical data did not meet the F.D.A. requirements for well controlled studies necessary for approval. However, some of the panel members had trouble reconciling the often compelling patient testimony with the F.D.A. legal requirements. “I was just basically torn between my mind and my heart,” said Richard P. Hoffmann, a pharmacist who was the consumer representative on the committee and who abstained. Dr. Bruce I. Ovbiagele, chairman of neurology at the Medical University of South Carolina, voted against approval but said, “Based on all I heard, the drug definitely works, but the question was framed differently.” On another question of whether the drug could qualify for so-called accelerated approval, a lower hurdle, the panel voted 7 to 6 against the drug. The F.D.A., which does not have to follow the advice of its advisory panels, is scheduled to decide whether to approve eteplirsen by May 26. © 2016 The New York Times Company
Melissa Davey Researchers have developed the world’s first blood test that can detect the abnormal metabolism of blood cells in people with Parkinson’s disease, which means the blood test could be used to diagnose the disorder. At present the only way to diagnose Parkinson’s disease, a degenerative neurological condition, is through ordering a range of tests and scans to rule out other disorders, combined with examining symptoms. Patients are often diagnosed only after they have developed symptoms and brain cells have already been destroyed. While there is no cure for Parkinson’s, early detection allows treatment with medication and physiotherapy to begin, which may slow the deterioration of motor functions in patients. Because diagnosing the disease is a process of elimination, and the symptoms mimic those of other neurological disorders, patients are also at risk being diagnosed and treated for the wrong disease. The group of Australian researchers from La Trobe University believe their blood test will enable doctors to detect Parkinson’s disease with unprecedented reliability and lead to earlier treatment. Their findings are under review by an international medical journal. © 2016 Guardian News and Media Limited
Link ID: 22120 - Posted: 04.20.2016
By BENEDICT CAREY Five years ago, a college freshman named Ian Burkhart dived into a wave at a beach off the Outer Banks in North Carolina and, in a freakish accident, broke his neck on the sandy floor, permanently losing the feeling in his hands and legs. On Wednesday, doctors reported that Mr. Burkhart, 24, had regained control over his right hand and fingers, using technology that transmits his thoughts directly to his hand muscles and bypasses his spinal injury. The doctors’ study, published by the journal Nature, is the first account of limb reanimation, as it is known, in a person with quadriplegia. Doctors implanted a chip in Mr. Burkhart’s brain two years ago. Seated in a lab with the implant connected through a computer to a sleeve on his arm, he was able to learn by repetition and arduous practice to focus his thoughts to make his hand pour from a bottle, and to pick up a straw and stir. He was even able to play a guitar video game. “It’s crazy because I had lost sensation in my hands, and I had to watch my hand to know whether I was squeezing or extending the fingers,” Mr. Burkhart, a business student who lives in Dublin, Ohio, said in an interview. His injury had left him paralyzed from the chest down; he still has some movement in his shoulders and biceps. The new technology is not a cure for paralysis. Mr. Burkhart could use his hand only when connected to computers in the lab, and the researchers said there was much work to do before the system could provide significant mobile independence. But the field of neural engineering is advancing quickly. Using brain implants, scientists can decode brain signals and match them to specific movements. Previously, people have learned to guide a cursor on a screen with their thoughts, monkeys have learned to skillfully use a robotic arm through neural signals and scientists have taught monkeys who were partly paralyzed to use an arm with a bypass system. This new study demonstrates that the bypass approach can restore critical skills to limbs no longer directly connected to the brain. © 2016 The New York Times Company
Link ID: 22106 - Posted: 04.14.2016
For decades, it was thought that scar-forming cells called astrocytes were responsible for blocking neuronal regrowth across the level of spinal cord injury, but recent findings challenge this idea. According to a new mouse study, astrocyte scars may actually be required for repair and regrowth following spinal cord injury. The research was funded by the National Institutes of Health, and published in Nature. “At first, we were completely surprised when our early studies revealed that blocking scar formation after injury resulted in worse outcomes. Once we began looking specifically at regrowth, though, we became convinced that scars may actually be beneficial,” said Michael V. Sofroniew, M.D., Ph.D., professor of neurobiology at the University of California, Los Angeles, and senior author of the study. “Our results suggest that scars may be a bridge and not a barrier towards developing better treatments for paralyzing spinal cord injuries.” Neurons communicate with one another by sending messages down long extensions called axons. When axons in the brain or spinal cord are severed, they do not grow back automatically. For example, damaged axons in the spinal cord can result in paralysis. When an injury occurs, astrocytes become activated and go to the injury site, along with cells from the immune system and form a scar. Scars have immediate benefits by decreasing inflammation at the injury site and preventing spread of tissue damage. However, long-term effects of the scars were thought to interfere with axon regrowth.