Links for Keyword: Regeneration

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By Katherine Harmon Researchers have been searching for decades for a way to mend damage to the spinal cord, an injury that can lead to life-long paralysis. Even the smallest of breaks in these crucial central nerve fibers can result in the loss of leg, arm and other bodily functions. And attempts to prompt healing, through stem cells or growth factors, have yet to achieve widespread success. Previous research had been stepping closer to encouraging neuronal growth—which usually stops after physical maturation. And a 2008 study coauthored by Zhigang He, a neurologist at Children's Hospital Boston, announced success in shutting down a gene that stops neuron cell growth, thus enticing damaged nerves to start growing again. Through that process, the team was able to reestablish a severed optical nerve connection in mice. A new study, coauthored in part by He and other members of the 2008 team, demonstrates that voluntary movement can be reestablished in mice with spinal cord damage after removing a common enzyme that regulates the neuronal cell growth. The results were published online August 8 in Nature Neuroscience (Scientific American is part of Nature Publishing Group). The removed enzyme PTEN, a phosphatase and tensin homolog, helps to dictate activity in the mTOR pathway, which plays a role in cell growth. During maturation, PTEN is activated, halting cell regeneration, but after removing it from a group of experimental mice with spinal cord injury, the neurons grew as they did in the development phase. © 2010 Scientific American,

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 14338 - Posted: 08.09.2010

By NICHOLAS WADE Two research reports published Friday offer novel approaches to the age-old dream of regenerating the body from its own cells. Animals like newts and zebra fish can regenerate limbs, fins, even part of the heart. If only people could do the same, amputees might grow new limbs and stricken hearts be coaxed to repair themselves. But humans have very little regenerative capacity, probably because of an evolutionary trade-off: suppressing cell growth reduced the risk of cancer, enabling humans to live longer. A person can renew his liver to some extent, and regrow a fingertip while very young, but not much more. In the first of the two new approaches, a research group at Stanford University led by Helen M. Blau, Jason H. Pomerantz and Kostandin V. Pajcini has taken a possible first step toward unlocking the human ability to regenerate. By inactivating two genes that work to suppress tumors, they got mouse muscle cells to revert to a younger state, start dividing and help repair tissue. What is true of mice is often true of humans, and although scientists are a long way from being able to cause limbs to regenerate, the research is attracting attention. Jeremy Brockes, a leading expert on regeneration at University College London, said the report was “an excellent paper.” Though there is a lot still to learn about the process, “it is hard to imagine that it will not be informative for regenerative medicine in the future,” he said. Copyright 2010 The New York Times Company

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory, Learning, and Development
Link ID: 14329 - Posted: 08.07.2010

By Nikhil Swaminathan Often spinal cord injuries result in the severing of the long nerve fibers connecting the brain to the spinal cord, disrupting one's ability to walk, among other things. But even with the primary top-to-bottom signal highway rendered out of order, the nervous system can, over time, reroute itself, finding neural detours and side streets that restore movement, according to a new study out of the University of California, Los Angeles (U.C.L.A.). "It's been known for some time that after certain types of lesions, animals and human[s] will recover their ability to walk," notes Michael Sofroniew, a professor of neurobiology at U.C.L.A.'s David Geffen School of Medicine. For instance, if the long nerve fibers on only one side of the spinal cord are damaged, "the previous explanation is that the other [intact] side was able to activate things," he adds. Recent work in Sofroniew's lab contradicts that theory. Using mice, the U.C.L.A. researchers first severed the nerve fibers coming from the brain to one side of lumbar spinal cord (in the lower back), which controls walking. This resulted in a complete loss of movement in the corresponding hind limb, causing the animal to drag it along when it moved. Over a period of 10 weeks, Sofroniew says, "the swing of the injured leg starts coming back and gets to become 80 percent of normal," on average. © 1996-2007 Scientific American Inc.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 11172 - Posted: 06.24.2010

WASHINGTON - It’s a delicate and daring experiment: Could doctors switch a leg nerve to make it operate the bladder instead? Families of a few U.S. children whose spina bifida robs them of the bladder control that most people take for granted dared to try the procedure — and early results suggest the surgery indeed may help, in at least some patients. With the technique, pioneered in China, the kids are supposed to scratch or pinch their thigh to signal the bladder to empty every few hours. But surprisingly, some youngsters instead are starting to feel those need-to-go sensations that their birth defect had always prevented. “It feels like this little chill kind of thing in me,” marvels 9-year-old Billy Kraser of Scranton, Pa. “When he goes in there and he’s dry and he’s clean, it’s such a triumph,” adds his mother, Janice Kraser. “I’ll hear him going, ‘Yesss!”’ The U.S. pilot study consists of just nine spina bifida patients and still is tracking how they fare — no one is finished healing yet. But already desperate families are lining up for a chance at this nerve rerouting, even as William Beaumont Hospital in Royal Oak, Mich., is trying to raise money to expand the study and provide better evidence. © 2008 Microsoft

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 12220 - Posted: 06.24.2010

by Wendy Zukerman Rats with damaged spines can walk again thanks to acupuncture. But it's not due to improvements in their energy flow or "chi". Instead, the ancient treatment seems to stop nerve cell death by reducing inflammation. Acupuncture's scientific credentials are growing. Trials show that it improves sensory and motor functions in people with spinal cord injuries. To find out why, Doo Choi and his colleagues at Kyung Hee University in Seoul, South Korea, damaged the spines of 75 rats. One-third were given acupuncture in two locations: Shuigou – between their snout and mouth, and Yanglingquan – in the upper hind leg. Others received no treatment or "simulated acupuncture". After 35 days, the acupuncture group were able to stand at a steeper incline than the others and walk better. Staining their paws with ink revealed that their forelimb-hindlimb coordination was fairly consistent and that there was very little toe dragging, whereas the control groups still dragged their feet. The rats in the acupuncture group also had less nerve cell death and lower levels of proteins known to induce inflammation after spinal cord injury and make neural damage worse. One explanation is that sharp needles prompt a stress response that dampens down inflammation. In humans, the inflammation that follows spinal cord injury is known to be responsible for nerve cell death. © Copyright Reed Business Information Ltd

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 14015 - Posted: 06.24.2010

Helen Phillips A study of the "miraculous" recovery of a man who spent 19 years in a minimally conscious state has revealed the likely cause of his regained consciousness. The findings suggest the human brain shows far greater potential for recovery and regeneration then ever suspected. It may also help doctors predict their patients’ chances of improvement. But the studies also highlight gross inadequacies in the system for diagnosing and caring for patients in vegetative or minimally conscious states. In 1984, 19-year-old Terry Wallis was thrown from his pick-up truck during an accident near his home in Massachusetts, US. He was found 24 hours later in a coma with massive brain injuries. Within a few weeks he had stabilised in a minimally conscious state, which his doctors thought would last indefinitely. It did indeed persist for 19 years. Then, in 2003, he started to speak. Over a three day period, Wallis regained the ability to move and communicate, and started getting to know his now 20 year old daughter – a difficult process considering he believed himself to be 19, and that Ronald Reagan was still president. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 15: Language and Our Divided Brain
Link ID: 9089 - Posted: 06.24.2010

WEST LAFAYETTE, Ind. – A successful method for healing spinal injuries in dogs has been developed by Purdue University researchers, offering hope for preventing human paralysis. Lab tests have shown that an injection of a liquid polymer known as polyethylene glycol (PEG), if administered within 72 hours of serious spinal injury, can prevent most dogs from suffering permanent spinal damage. Even when the spine is initially damaged to the point of paralysis, the PEG solution prevents the nerve cells from rupturing irrevocably, enabling them to heal themselves. "Nearly 75 percent of the dogs we treated with PEG were able to resume a normal life," said Richard Borgens, Mari Hulman George Professor of Applied Neuroscience and director of the Center for Paralysis Research in Purdue's School of Veterinary Medicine. "Some healed so well that they could go on as though nothing had happened." The research, performed at Purdue, Indiana University—Purdue University Indianapolis, and Texas A&M University, appears in the December issue of the Journal of Neurotrauma.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 6520 - Posted: 06.24.2010

For the first time, researchers have used human embryonic stem cells to create new insulating tissue for nerve fibers in a live animal model – a finding that has potentially important implications for treatment of spinal cord injury and multiple sclerosis. Researchers at the UC Irvine Reeve-Irvine Research Center used human embryonic stem cells to create cells called oligodendrocytes, which are the building blocks of the myelin tissue that wraps around and insulates nerve fibers. This tissue is critical for maintenance of proper nerve signaling in the central nervous system, and, when it is stripped away through injury or disease, sensory and motor deficiencies and, in some cases, paralysis result. In this study, neurologist Hans Keirstead and colleagues at UCI and the Geron Corporation devised a novel technique that allows human embryonic stem cells to differentiate into high-purity, early-stage oligodendrocyte cells. The researchers then injected these cells into the spinal cords of mice genetically engineered to have no myelin tissue. After transplantation into mice, the early-stage cells formed into full-grown oligodendrocyte cells and migrated to appropriate neuronal sites within the spinal cord. More importantly, the researchers discovered the oligodendrocyte cells forming patches of myelin’s basic protein, and they observed compact myelin tissue wrapping around neurons in the spinal cord. These studies demonstrated that the oligodendrocytes derived from human embryonic stem cells can function in a living system. © Copyright 2002-2004 UC Regents

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 6468 - Posted: 06.24.2010

CHAPEL HILL -- Scientists at the University of North Carolina at Chapel Hill have discovered key steps involved in regulating nerve growth and regeneration that may have implications for spinal cord research. The new research, published in the June 24 issue of the journal Neuron, for the first time describes how nerve growth factor (NGF) stimulates a sequence of proteins – a molecular pathway – that promotes nerve growth. "It is the first study to show the link between NGF and the building blocks that form the axon," said Dr. William Snider, professor of neurology and cell and molecular physiology at UNC's School of Medicine and director of the UNC Neuroscience Center. Axons are long tendrils, or processes, that extend from nerve cells to form connections with other nerve cells, muscles and the skin. Injury to the peripheral nervous system – that portion of the nervous system outside the brain and spinal cord – typically results in spontaneous regeneration and repair. However, this is not the case with the spinal cord, where disruption of connections from injury leads to paralysis

Related chapters from BP7e: Chapter 19: Language and Hemispheric Asymmetry; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 15: Language and Our Divided Brain; Chapter 5: The Sensorimotor System
Link ID: 5734 - Posted: 06.24.2010

Two-pronged approach synergizes growth BOSTON -- Researchers at Children's Hospital Boston and Harvard Medical School have advanced a decades-old quest to get injured nerves to regenerate. By combining two strategies – activating nerve cells' natural growth state and using gene therapy to mute the effects of growth-inhibiting factors – they achieved about three times more regeneration of nerve fibers than previously attained. The study involved the optic nerve, which connects nerve cells in the retina with visual centers in the brain, but the Children's team has already begun to extend the approach to nerves damaged by spinal cord injury, stroke, and certain neurodegenerative diseases. Results appear in the February 18th Journal of Neuroscience. Normally, injured nerve fibers, known as axons, can't regenerate. Axons conduct impulses away from the body of the nerve cell, forming connections with other nerve cells or with muscles. One reason axons can't regenerate has been known for about 15 years: Several proteins in the myelin, an insulating sheath wrapped around the axons, strongly suppress growth. Over the past two years, researchers have developed techniques that disable the inhibitory action of myelin proteins, but this approach by itself has produced relatively little axon growth.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 15: Language and Our Divided Brain
Link ID: 4992 - Posted: 06.24.2010

NEURONS IMPLANTED IN STROKE-DAMAGED BRAIN TISSUE SHOW FUNCTION, SAY UNIVERSITY OF PITTSBURGH RESEARCHERS
PITTSBURGH, – An imaging study of neurons implanted in damaged areas of the brains of stroke patients in the hopes of restoring function has shown the first signs of cellular growth, say University of Pittsburgh researchers. Positron Emission Tomography (PET) scans taken six months after surgery to implant LBS-neurons showed a greater than 10 percent increase in metabolic activity in the damaged parts of some patients' brains compared to scans taken just a week prior to surgery. The increased metabolism corresponds with better performance on standardized stroke tests for behavioral and motor function. The study was funded by Layton BioScience Inc. © 2001 UPMC Health System

Related chapters from BP7e: Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 15: Language and Our Divided Brain
Link ID: 471 - Posted: 06.24.2010

By Rachel Ehrenberg A blue dye found in Gatorade and Rocket Pops could play a protective role in the cellular mayhem that follows spinal cord injury. In rats, the dye — known as FD&C Blue No.1 — appears to block a molecule that floods the injury site and kills nerve cells, a team reports in the July 28 Proceedings of the National Academy of Sciences. Rats dosed with the dye after injury showed greater improvement in motor skills than rats not receiving the dye. And the food colorant’s low toxicity suggests a new approach for treating spinal cord trauma in humans, injuries for which there are few therapies. “It’s not a cure,” says neuroscientist Maiken Nedergaard of the University of Rochester Medical Center in Rochester, N.Y., who led the new study. “I don’t think that anything can cure this, but for the patient it could be a big improvement.” The results are impressive and realistic, comments Lynne Weaver, a neuroscientist at the Robarts Research Institute in London, Canada. Weaver notes that the side effects of any new potential therapy must be considered, but “the principle is interesting.” ATP, for adenosine triphosphate, is known as the energy currency of cells, and the molecule is used like a battery whenever cells need to get stuff done. But a few years ago Nedergaard and her colleagues reported that ATP has a darker side. It wreaks havoc when the central nervous system is injured, flooding the injury site and hitting a receptor that sits on some immune system cells. ATP binds to this receptor, called P2X7, resulting in a cascade of events that leads to cell death. © Society for Science & the Public 2000 - 2009

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 15: Language and Our Divided Brain
Link ID: 13103 - Posted: 06.24.2010

Heidi Ledford Tadpoles can achieve something that humans may only dream of: pull off a tadpole's thick tail or a tiny developing leg, and it'll grow right back — spinal cord, muscles, blood vessels and all. Now researchers have discovered the key regulator of the electrical signal that convinces Xenopus pollywogs to regenerate amputated tails. The results, reported this week in Development, give some researchers hope for new approaches to stimulating tissue regeneration in humans1. Researchers have known for decades that an electrical current is created at the site of regenerating limbs. Furthermore, applying an external current speeds up the regeneration process, and drugs that block the current prevent regeneration. The electrical signals help to tell cells what type to grow into, how fast to grow, and where to position themselves in the new limb. To investigate, Michael Levin and his colleagues at the Forsyth Center for Regenerative and Developmental Biology in Boston, Massachusetts, sorted through libraries of drug compounds to find ones that prevent tail regeneration but do not interfere with wound healing. One such drug, they found, blocks a molecular pump that transports protons across cell membranes; this kind of proton flow creates a current. ©2007 Nature Publishing Group

Related chapters from BP7e: Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 15: Language and Our Divided Brain
Link ID: 10024 - Posted: 06.24.2010

ATLANTA ( — When Yadong Wang, a chemist by training, first ventured into nerve regeneration two years ago, he didn’t know that his peers would have considered him crazy. His idea was simple: Because neural circuits use electrical signals often conducted by neurotransmitters (chemical messengers) to communicate between the brain and the rest of the body, he could build neurotransmitters into the material used to repair a broken circuit. The neurotransmitters could coax the neurons in the damaged nerves to regrow and reconnect with their target organ. Strange though his idea might have seemed to others in his field, Wang, an assistant professor in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University, discovered that he could integrate dopamine, a type of neurotransmitter, into a polymer to stimulate nerve tissues to send out new connections. The discovery is the first step toward the eventual goal of implanting the new polymer into patients suffering from neurological disorders, such as Alzheimer's, Parkinson’s or epilepsy, to help repair damaged nerves. The findings were published online the week of Oct. 30 in the Proceedings of the National Academy of Sciences (PNAS). “We showed that you could use a neurotransmitter as a building block of a polymer,” said Wang. “Once integrated into the polymer, the transmitter can still elicit a specific response from nerve tissues.” ©2006 Georgia Institute of Technology

Related chapters from BP7e: Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 15: Language and Our Divided Brain
Link ID: 9570 - Posted: 06.24.2010

By Lauran Neergaard, The Associated Press WASHINGTON — Injections of human stem cells seem to directly repair some of the damage caused by spinal cord injury, according to research that helped partially paralyzed mice walk again. The experiment, reported Monday, isn't the first to show that stem cells offer tantalizing hope for spinal cord injury — other scientists have helped mice recover, too. But the new work went an extra step, suggesting the connections that the stem cells form to help bridge the damaged spinal cord are key to recovery. Surprisingly, they didn't just form new nerve cells. They also formed cells that create the biological insulation that nerve fibers need to communicate. A number of neurological diseases, such as multiple sclerosis, involve loss of that insulation, called myelin. "The actual cells that we transplanted, the human cells, are the ones that are making myelin," explained lead researcher Aileen Anderson of the University of California, Irvine. "We're extremely excited about these cells." The research is reported in Monday's issue of Proceedings of the National Academy of Sciences. Stem cells are building blocks that turn into different types of tissue. Embryonic stem cells in particular have made headlines recently, as scientists attempt to harness them to regenerate damaged organs or other body parts. They're essentially a blank slate, able to turn into any tissue given the right biochemical instructions. © Copyright 2005 USA TODAY

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory, Learning, and Development
Link ID: 7930 - Posted: 06.24.2010

By Cory Hatch People who suffer from brain or spinal cord trauma often have few options beyond physical therapy and hope; injuries to the central nervous system rarely heal and often worsen over time. But recently, researchers from Helsinki, Finland, found a tiny chunk of protein that not only keeps these cells alive but also encourages new cells to grow. The protein—called KDI tri-peptide (KDI)—could someday lead to new treatment options for people suffering from a wide range of neurological problems from spinal cord injury to Alzheimer's disease, says researcher Pivi Liesi. In earlier studies, Liesi and her colleagues found that rats with damaged spinal cords could walk again after three months when they injected KDI near the injury. The protein also shows promise for human cells, at least in the petri dish. How does KDI work? Liesi's most recent research, which appeared July 25 on the Journal of Neuroscience Research website, found that the KDI protein prevents cell death by blocking a substance called glutamate. Normally, glutamate helps cells communicate with one another for learning and memory. However, glutamate is toxic to injured neural cells, causing the cells to take in too much calcium and die. This cell death by glutamate occurs in many different types of nervous system injuries and diseases, including Alzheimer's disease, Lou Gehrig's disease, and spinal cord injuries. Copyright © 2005 U.S.News & World Report

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory, Learning, and Development
Link ID: 7708 - Posted: 06.24.2010

Could a chemical cousin of antifreeze someday help people with spinal cord injuries walk again? Researchers at Purdue University are studying this in dogs with paralyzed hind legs. They injected 19 injured dogs with a drug called polyethylene glycol (PEG)—a nontoxic liquid polymer related to antifreeze—on top of providing them with the standard drugs, surgery and rehab, and showed that PEG targets damaged nerve cells, protecting some of the injured cells from progressive damage and death. "The dogs that come in that receive conventional management, that is, just surgery and rehabilitation, about 15 to 20 percent of those dogs will have some quality of life just through spontaneous repair," says Richard Borgens, director of Purdue University Center for Paralysis Research, who reported his findings in the Journal of Neurotrauma. "But most of them, about 80 percent, will remain paraplegic for the rest of their lives. What this [PEG] compound does when we inject it is it reverses those odds, it really goes from about 20-80 to 80-20; about 80 percent are leading very normal lives, good quality of life, and only about 20 percent have any kind of real problem at the end of the study time, which was, we followed them out to about a year." In the study, 13 of the 19 dogs (about 68 percent) injected with PEG regained use of their hind legs and were able to walk within eight weeks. The dogs were injected twice—when they were brought into the lab (within three days of their injuries), and then after standard surgery and steroids to reduce inflammation. In a group of 24 dogs that only received the standard treatment, only about 25 percent regained a similar level of mobility and 62 percent remained paraplegic. © ScienCentral, 2000- 2005.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 6805 - Posted: 06.24.2010

Using a precisely targeted laser, researchers have snipped apart a single neuron in the roundworm C. elegans — an achievement that opens a new avenue for studying nerve regeneration in this genetically manipulable animal. Indeed, their initial studies have demonstrated that the severed nerves of worms are capable of regenerating and regaining full function. According to the researchers, studying nerve regeneration in the worm could provide answers to questions that are not accessible currently by doing experiments in more complex animals, including mice and zebrafish. “Until now there has been little study of nerve regeneration using genetic methodology, because most studies have been done on higher vertebrate organisms.” Yishi Jin A research team that included Yishi Jin, a Howard Hughes Medical Institute investigator at the University of California, Santa Cruz (UCSC), Andrew Chisholm, also of UCSC, and Adela Ben-Yakar, who was at Stanford University and is now at the University of Texas at Austin, reported its achievement in the December 16, 2004, issue of the journal Nature. Other co-authors are from Stanford University and UCSC. © 2004 Howard Hughes Medical Institute

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 6591 - Posted: 06.24.2010

Christopher Reeve, best known for his role as Superman, remained in the limelight in recent years as an advocate of increased funding and research for spinal cord injuries and other central nervous system disorders. Left paralyzed from the neck down by a fall from his horse in 1995, Reeve focused his efforts through the Christopher Reeve Paralysis Foundation. He was one of an estimated 250,000 people in the U.S. living with spinal cord injuries. Martin Schwab, a neuroscientist at The Brain Research Institute at the University of Zurich, Switzerland, and an international team of researchers have spent much of the last twenty years studying why the nerve fibers of the spinal cord and the brain don't re-grow or regenerate themselves after injury in the same way as other tissues of the body. "If you destroy a large part of the muscle tissue in a muscle, or of your liver, this tissue can re-generate," Schwab explains. "This is what is not occurring in the central nervous system." During early childhood development, the nervous system, which consists of around 10 billion nerve cells, each one having between a thousand and ten thousand connections with other nerve cells, develops and forms an incredibly complex network. Having become stabilized, the adult central nervous system—the brain and the spinal cord—are relatively hard-wired, allowing only small changes during learning or adaptation. So when part of this system is damaged by injury or disease such as stroke, the loss of function associated with the damage is permanent. "Once you are paraplegic due to an accident which has injured your spinal cord, you remain in a wheelchair all your life," Schwab says. © ScienCentral, 2000- 2004.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 6337 - Posted: 06.24.2010

Some of the 250,000 Americans who have been paralyzed by spinal cord injuries are pressing medical researchers for a cure. The most prominent is actor and director Christopher Reeve, who was paralyzed after a fall from his horse in 1995. At a symposium on spinal cord research at Rockefeller University, held on November 24, 2003, Reeve commented on "a certain frustration" that he and other paralyzed patients feel over the current pace of American research, which has been hampered by political debate over the use of stem cells. "I think that we need to inject more urgency into the whole process here," Reeve observed. Another speaker at the Rockefeller symposium was Michael Di Scipio, 34, who was paralyzed after a diving accident in July 1999, when he was 29. A single father, he says his two young children have been injured, too—by what he can't do: "Not being able to run around and play with them, hold them, tickle them, tuck them in, give them a kiss good night. Things we're supposed to do as parents." One reason that prospects for recovery are dim at present for patients with spinal cord injury is that unlike other cells, nerve cells, or neurons in the central nervous system (the brain and spinal cord) are unique in that they cannot replicate themselves in their mature state. So repairing spinal cords means finding a way to get nerve cells to grow back across the gap in a spinal cord that has been severed. © ScienCentral, 2000-2004.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 5636 - Posted: 06.24.2010