By Claire Thomas How does the brain cope when, several years after having both hands amputated, a person suddenly receives two new hands? Surprisingly well, it seems. In a study out today, researchers provide the most detailed picture yet of how the brain reorganizes itself to accommodate foreign appendages. And in a result that they are still trying to explain, the scientists found that in two such double-hand transplants, the left hand reconnected with the brain more quickly than did the right. A group of French and Australian doctors performed the world's first hand transplant in 1998, and the same team repeated the feat on both hands 2 years later. Studies carried out since then indicate that the brain reorganizes itself in response to these new appendages. However, the work looked only at coarse hand movements that mainly used nontransplanted muscles. Wanting to learn more about how the brain copes with donor hands, cognitive neuroscientist Angela Sirigu of the French National Research Agency in Lyon and colleagues looked at two right-handed men, one age 20 and the other 42, who recently had left and right hand transplants to replace hands amputated following work injuries 3 to 4 years ago. After extensive training, both men are now able to perform a range of complex tasks with the foreign appendages, from dialing a phone number to using tools such as screwdrivers and pliers to rewire an electrical outlet. The researchers found that both men's motor cortexes--the region of the brain responsible for carrying out muscle movement--had reorganized themselves in response to the new hands. After a person loses a hand, the region of the motor cortex that controls hand movement shrinks and rewires itself to control the upper arm, a property called plasticity. But when Sirigu and colleagues used transcranial magnetic stimulation--a technique that employs magnetic fields to excite neurons in the brain--to stimulate specific fragments of the motor cortex, they found that the "hand areas" in the motor cortex of both men had reassumed their original "wiring." © 2009 American Association for the Advancement of Science.

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 12726 - Posted: 06.24.2010

The U.S. Food and Drug Administration has given the green light to human clinical trials of an embryonic stem-cell-based therapy for spinal cord injuries, a biotechnology firm said Friday. The regulator has given permission to Geron Corp. of Menlo Park, Calif., to inject embryonic stem cells into eight to 10 people recently paralyzed due to spinal cord injuries. The research aims to regrow nerve tissue. President Barack Obama, who took office on Tuesday, was expected to reverse former president George W. Bush's executive order that restricted federal funding on research involving human embryonic stem cells. Advocates of embryonic stem cell research say it could lead to potential treatments for diseases such as Alzheimer's, Parkinson's and cancer by restoring organ and tissue function. Scientists say embryonic stem cells are the most useful type because they have the potential to become any type of cell within the body. But the research is controversial since embryos are destroyed to obtain the stem cells. Dr. Thomas Okarma, president and CEO of Geron, said the injections will be made in the spine. Several medical centres around the U.S. will participate in the research, which he said has not received U.S. government funding. © CBC 2009

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 15: Language and Lateralization
Link ID: 12481 - Posted: 06.24.2010

by Alison Motluk RATS with breathing problems caused by damage to their nerves have had normal breathing restored by bursts of visible light aimed onto the spinal cord. This achievement raises hopes that a miniature light source implanted near the spine might one day allow people with similar injuries to breathe normally. In 2005, Ed Boyden at the Massachusetts Institute of Technology infected neurons in Petri dishes with viruses carrying the ChR2 gene, which codes for a light-sensitive protein called channelrhodopsin-2. The neurons started expressing the protein, and this allowed the researchers to use pulses of light to control when the neurons fired (Nature Neuroscience, vol 8, p 1263). "The nerve cells think they are photoreceptors," says neuroscientist Jerry Silver at Case Western Reserve University in Cleveland, Ohio. Silver has now taken things a step further with a study to investigate how this light-operated neuronal switch might be used to restore function lost as a result of nerve damage. His team cut part way through the spinal cords of rats at the second vertebra from the top, where the neck pivots, severing the connection between the spinal cord and the nerves that control one side of the diaphragm. This prevented messages from the brain getting to the diaphragm, leaving the animals with problems breathing. Similar injuries are the leading cause of death in people with spinal cord damage. © Copyright Reed Business Information Ltd

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 12237 - Posted: 06.24.2010

By Lucy Elkins The human brain: Numerous system which link up and work together The human brain is the most complex organ in the body and contains 20 billion cells, responsible for everything from dreaming and movement to appetite and emotions. It consists mainly of grey matter - the brain cells or neurons where information is processed. It also contains white matter - the nerve fibres which, like electric cables, send out chemical messengers and relay information between the cells. In fact, the brain contains more nerve fibres than there are wires in the entire international telephone network and sometimes the brain's 'wires' can become crossed, as a result of injury, illness or genetics. Scientists used to think a brain injury resulted in permanent damage to the brain's functions, but new research suggests this is not necessarily the case. 'When one area of our brain is damaged we now know from scans that the functions of that area are distributed elsewhere,' says Dr Keith Muir, a senior lecturer in neuroscience at Glasgow University. © 2008 Associated Newspapers Ltd

Related chapters from BN: Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 15: Language and Lateralization
Link ID: 11928 - Posted: 06.24.2010

Scientists from three western Canadian universities are using a microchip as they try to encourage nerves cells to reconnect the brain, spinal cord, and the body. If they succeed, the research could mean "a new life for people with brain or spinal cord injuries," said Naweed Syed, research director at the University of Calgary's Hotchkiss Brain Institute, in a release Thursday. Using a microchip to encourage nerve cells to reconnect could help people with brain or spinal cord injuries, said Naweed Syed, research director of the University of Calgary's Hotchkiss Brain Institute. (University of Calgary/Ken Bendiktsen) The chip could also help people with degenerative diseases, said University of Saskatchewan neuroscientist Valerie Verge. The team is close to knowing how to use computer chips to facilitate the regeneration process, she said. The Canadian Institutes of Health Research gave the team, the Western Canada Regeneration Initiative, a $2.25-million grant Thursday to boost their research. Brain surgeons, electrical engineers, neurologists, and neuroscience researchers from the universities of Calgary, Alberta and Saskatchewan are working on the project. © CBC 2008

Related chapters from BN: Chapter 19: Language and Lateralization; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 15: Language and Lateralization; Chapter 5: The Sensorimotor System
Link ID: 11397 - Posted: 06.24.2010

Marlowe Hood, -- Tiny nerves crisscrossing the spine can bypass crippling injuries recently written off as irreversible, scientists reported in a study published Monday. Experiments conducted on mice at the University of California in Los Angeles showed for the first time that the central nervous system can rewire itself to create small neural pathways between the brain and the nerve cells that control movement. This startling discovery could one day open the way to new therapies for damaged spinal cords and perhaps address conditions stemming from stroke and multiple sclerosis, according to the study. Normally, the brain relays messages that control walking or running via neural fibers called axons. When these long nerves are crushed or severed -- in a road crash or sports accident, for example -- these lines of communication are cut, resulting in reduced movement or paralysis. "Not long ago, it was assumed that the brain was hard-wired at birth and that there was no capacity to adapt to damage," explained neurobiologist Michael Sofroniew, who led the research. © 2008 Discovery Communications

Related chapters from BN: Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 15: Language and Lateralization
Link ID: 11179 - Posted: 06.24.2010

More than half of the 185,000 amputations in the U.S. each year are a result of diabetes, a disease that plagues an estimated 20.8 million Americans -- seven percent of the population -- and is on the rise. Diabetic neuropathy, nerve damage that causes a loss of sensation in the hands and feet, can allow small injuries to go unnoticed and become severely infected. Tight control of blood sugar can keep neuropathy at bay, but there is no cure. "There are a variety of medications that are available now that can help with the pain but unfortunately, there's nothing available to help with numbness or prevention of nerve damage," says diabetes specialist Mark Kipnes, MD, director of the Diabetes and Glandular Disease Research Clinic in San Antonio, Texas. But now Kipnes is leading the first human testing of a new drug that might prevent or even reverse such damage. Designed by researchers at Sangamo Biosciences, it uses a natural protein that turns on the patient's own gene for helping nerve growth. As the researchers wrote in the journal "Diabetes," tests on diabetic rats showed that repeated treatments with the drug led to increasingly improved nerve function. © ScienCentral, 2000-2006.

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 8975 - Posted: 06.24.2010

Whether it's from surgery, an accident or stroke, when the brain is injured, the damage is usually permanent. Most of the time, the cells of the brain don't grow back. But two researchers at Massachusetts Institute of Technology are working to change that. "The problem we're trying to solve with the research is how to reconnect disconnected parts of the brain," says one of the researchers, neuroscientist Rutledge Ellis-Behnke. He and professor Gerald Schneider of the M.I.T. Department of Brain and Cognitive Sciences are using nanotechnology to create tiny bridges that can help brain cells grow back together. The bridges assemble themselves from protein fragments called peptides, which are injected into the injured area. The bridges are similar to the normal structures among brain cells. "It would be easy to fool an anatomist into thinking that this was part of the brain," says Schneider about these bridges that are smaller than the width of a human hair. He adds that "it's functioning like it's part of the natural material that fills spaces between the nerve cells in the brain." The peptide nano-bridges are not permanent. After a while they dissolve. © ScienCentral, 2000-2006.

Related chapters from BN: Chapter 19: Language and Lateralization; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 15: Language and Lateralization; Chapter 4: Development of the Brain
Link ID: 8809 - Posted: 06.24.2010

Prashant Nair TWO antibodies that enabled the severed spinal nerves of rats to be regenerated are to be tested in humans. The antibodies have helped rats with damaged spinal cords to walk again, by blocking the action of Nogo, a protein that stops nerve cells sprouting new connections. But there were concerns about whether blocking Nogo would lead to uncontrolled neuronal rewiring in the brain or spinal cord and it was also unclear how such a therapy could be given to humans. Now Martin Schwab and his colleagues at the University of Zurich in Switzerland have infused two antibodies, 11C7 and 7B12, into the damaged spinal cords of rats. An osmotic mini-pump connected to a fine catheter was used to deliver the antibodies directly into the cerebrospinal fluid surrounding the injured part of the spinal cord - a method of delivery that could easily be applied to humans, they say. The antibodies triggered regeneration of axons, the fine thread-like extensions that connect neurons, and enabled injured rats to swim, cross the rungs of a ladder without slipping and traverse a narrow beam (Annals of Neurology, vol 58, p 706). Moreover, the antibodies did not cause hyperalgesia, a condition in which even a simple touch is sensed as pain - a sign that would have indicated wrong neuronal connections had been made. © Copyright Reed Business Information Ltd.

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 8518 - Posted: 06.24.2010

The central nervous system in adult mammals is notoriously bad at healing itself. Once severed, the axons that connect one neuron to another can't regrow. That's why people regain little, if any, movement or sensation after a spinal cord injury. Now, researchers have made a promising discovery. In the 7 October Science, they identify a class of drugs--including one already on the market for treating cancer--that promote axon regeneration in rodents. In the new study, Zhigang He, and Vuk Koprivica at Children's Hospital in Boston along with colleagues tested about 400 small molecules on cultured rodent neurons, hoping to identify ones that promoted the growth of new axonlike extensions. Most of the compounds did nothing, but several compounds that blocked a cell surface protein called the epidermal growth factor receptor (EGFR) had impressive effects. To test the compounds on nerve injuries in live animals, the researchers crushed an optic nerve in adult mice then packed the nerve with foam soaked with one of the EGFR blockers. Two weeks after the injury, the treated mice showed a ninefold increase in axon regeneration compared to untreated animals. Additional work by He's team suggests that the compounds block two kinds of molecular signals: inhibitory molecules embedded in the myelin insulation on axons and inhibitory signals spewed out by support cells that form a scar around the site of injury. "It's a really unexpected finding," says Marie Filbin, a neurobiologist at Hunter College in New York City. She and other experts say they never suspected that EGFR might have a role in thwarting regeneration. The study "identifies a novel target for therapeutic interventions," Filbin says. © 2005 by the American Association for the Advancement of Science.

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 8002 - Posted: 06.24.2010

Michael Hopkin Computer scientists have created a hat that can read your thoughts. It allows you to stroll down a virtual street. All you have to do is think about walking. Called a brain-computer interface, the device detects activity in certain brain areas linked to movement, and uses the signals to mimic that movement in a virtual world. The technology could one day help paralysed patients to move robotic arms, or help sufferers of motor neuron disease to type out words on a virtual keyboard. "Just thinking about movement activates the same neurons as actually moving," explains Gert Pfurtscheller of Graz University of Technology in Austria, who has been working on the device for around four years. By picking up on these bursts of nerve activity, the computer can decide whether you are thinking about moving your hands or feet, and react accordingly. The technology detects brain waves by using electrodes placed at strategic points on the scalp; they are positioned over brain areas known to be involved in moving specific body parts. The computer can then distinguish between signals corresponding to different types of movement. Previously, accurate detection of local brain activity has required electrodes to be implanted in the brain. This technique has allowed recipients to control robots and even send e-mails (see "Paralysed man sends e-mail by thought ") . The new device, presented at the Presence 2005 technology meeting in London last week1, achieves a similar feat using non-invasive methods. ©2005 Nature Publishing Group

Related chapters from BN: Chapter 1: Introduction: Scope and Outlook; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 20: ; Chapter 5: The Sensorimotor System
Link ID: 7960 - Posted: 06.24.2010

Carl T. Hall, Chronicle Science Writer New evidence from mouse studies suggests that stem cells may help cure paralysis in cases of spinal cord injury. So that raises an obvious question: When can they be tried in humans? The answer: No time soon. That may be disappointing to paralyzed individuals with untreatable spinal cord damage, as well as champions of California's Proposition 71 stem cell research program, all anxious to see real treatments develop from the hype of regenerative medicine. But experts warn it would be a big mistake to rush into clinical trials before settling the many scientific and ethical issues clouding the future of stem cell biology. "I fully understand the impatience of patients, spinal cord injury patients in particular, who are desperate for some form of treatment. But there is risk proceeding too quickly here," said Dr. Arnold Kriegstein, a neurologist who serves as director of a stem cell and tissue biology program at UCSF. "The whole field could be damaged by the outcome of one failed early trial," he said. "I am not saying (a human trial) shouldn't be done, but we should really be cautious about it." ©2005 San Francisco Chronicle

Related chapters from BN: 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 4: Development of the Brain
Link ID: 7957 - Posted: 06.24.2010

Unlike people, fish can regrow damaged nerve fibers in their central nervous systems. Now a study may have found the reason: The creatures lack a protein called Nogo-A that prevents nerve regeneration in mammals. Axons, or nerve fibers, are the transmission lines that conduct electrical signals throughout the body. The fibers are protected by sheaths of myelin, a fatty insulator that speeds the electrical impulses along. Damaged axons in the brain and spinal cord of mammals don't regenerate, and spinal cord injuries can therefore lead to permanent paralysis. Fish are luckier: They can regrow the axons in their central nervous system, but curiously this regeneration stops if their nerve endings come into contact with mammalian myelin. Because a protein in mammalian myelin called Nogo-A is known to inhibit central nervous system axon growth in mammals, a team of researchers led by biologist Claudia Stürmer at the University of Konstanz in Germany wondered if fish might be missing this protein. When the researchers exposed goldfish axons to rat Nogo-A, the nerves stopped growing. Furthermore, a comparison of genomes between ten species of fish, including zebrafish and pufferfish, and humans revealed that fish lack the genetic information to make Nogo-A or a similar inhibitor. The team reports its findings in the August issue of Molecular Biology and Evolution. The paper's careful study of fish phylogeny supports an existing notion that Nogo-A may be a recent evolutionary development that correlates with more complex nervous systems and more complex functions, says Stephen Strittmatter, a neurologist at Yale University in New Haven, Connecticut. "It's an important addition to our growing understanding of the role these inhibitors play," he says. --CAROLYN GRAMLING Copyright © 2005 by the American Association for the Advancement of Science.

Related chapters from BN: 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 4: Development of the Brain
Link ID: 7741 - Posted: 06.24.2010

A PIONEERING treatment has allowed paralysed dogs to regain some movement. The results have raised hopes that the method will work in people too. So far, nine dogs paralysed in road accidents or by spinal disc injuries have been treated by veterinary surgeons Robin Franklin and Nick Jeffery of the University of Cambridge. Within a month, all regained the ability to make jerky movements in their hind legs, Jeffery told a meeting in Birmingham, UK, this week, although they are only slowly gaining the ability to support their own weight. Many different approaches to treating spinal injuries are being explored, but promising results in small animals such as rats have often not been repeated in larger animals. That is one of the reasons why the dog results are exciting, says Geoffrey Raisman of the Institute of Neurology at University College London, one of the pioneers of the method used by the Cambridge team. "I think that these findings in dogs are directly relevant to the human situation," he says. "Of course, we canıt know for sure without doing the work but it is a very good indicator that we can expect the same effects. We are hoping to start similar trials in humans within a couple of years." In Australia, three patients have already been treated using the same method (New Scientist, 12 July 2002, p 18). But the results will not be revealed until 2007. © Copyright Reed Business Information Ltd.

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 7192 - Posted: 06.24.2010

Damaged optic nerves - which run from the eye to the brain - have been regrown for the first time by scientists working with mice. The researchers believe the technique might one day restore sight to people whose optic nerves have been damaged by injury or glaucoma. It could even help regenerate other nerves in the body, they say. A team led by Dong Feng Chen, at the Schepens Eye Research Institute in Boston, US, combined two genetic modifications to regrow the optic nerve after it was damaged. First they turned on a gene called BCL-2, which promotes growth and regeneration of the optic nerve in young mice. This gene is normally turned off shortly before birth. They then bred those animals with other mice carrying genetic mutations that reduce scar tissue in injured nerves. The researchers crushed the optic nerves shortly after birth, and found that in young mice - less than 14 days old - between 40% and 70% of the injured optic nerve fibres regrew to reach their target destinations in the brain. No regrowth was seen in injured mice without the genetic modifications. That suggests the mice may have regained some vision, Chen told New Scientist, although the study cannot prove it did. © Copyright Reed Business Information Ltd.

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 15: Language and Lateralization
Link ID: 6929 - Posted: 06.24.2010

By PAUL ELIAS, AP Biotechnology Writer IRVINE, Calif. - So far, not a single person has been helped by human embryonic stem cells. But in cramped university labs, a young neurobiologist with movie star good looks, a Carl Sagan-like fondness for the popular media and an entrepeneur's nose for profits is getting tantalizingly close. Hans Keirstead is making paralyzed rats walk again by injecting them with healthy brain cells sussed from a reddish soup of human embryonic stem cells he and his colleagues have created. Keirstead hopes to apply his therapy to humans by 2006. If his ambitious timetable keeps to schedule, Keirstead's work will be the first human embryonic stem cell treatment given to humans. "I have been shocked, thrilled and humbled at the progress that I have made," Keirstead, 37, said in an interview in his University of California-Irvine office, which is dominated by a 4- by 8-foot collage of famous rock stars created by his artist brother. "I just want to see one person who is bettered by something that I created." Keirstead has been turning stem cells into specialized cells that help the brain's signals traverse the spinal cord. Those new cells have repaired damaged rat spines several weeks after they were injured. For the last two years, he has shown dramatic video footage of walking healed rats to scientific gatherings and during campaign events to promote California's $3 billion bond measure to fund stem cell work, which passed in November. Copyright © 2004 The Associated Press. Copyright © 2004 Yahoo! Inc.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 5: The Sensorimotor System
Link ID: 6611 - Posted: 06.24.2010

Christopher Reeve's death saddened many, but those who work in the field of spinal cord injury felt it on another level. "I think that he is probably the most courageous person I have ever met in my life," says Margaret "Jo" Velardo, a neuroscientist at the Evelyn F. & William L. McKnight Brain Institute of the University of Florida. "I think there was sort of a generalized denial on the part of everybody that somehow he really was going to live longer and he was going to make good his pledge of walking again. So the death was unexpected and also it made us sad because he was an icon of hope and now, he's gone." Velardo's research into the genes that could heal spinal cord injuries was published in the Journal of Neuroscience the week Reeve died. She was in the process of putting together a package of materials to send him when she heard of his death. "I really admit that I cried all day on Sunday when he died," she recounts. "I had made a pledge to him about this work that we were doing...so it added to my sadness because I felt that I would have liked him to have seen the work before he died." Studying the spinal cords of rats, her research group used computer chips containing genetic material, called microarrays, to see what genes are turned on or off in the injured tissues from hours to months after injury. The microarrays let the researchers see 8,000 genes simultaneously. © ScienCentral, 2000- 2004.

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 6426 - Posted: 06.24.2010

Paula Gould Damaged spinal cords in mice have been encouraged to grow back by blocking a scar-causing molecule. The result suggests a fresh approach to treatments for sufferers of spinal cord injury. Spinal cord injuries have long been considered incurable because the affected nerve cells do not grow back. Depending on the site and severity of damage, patients can be left paralysed and unable to control important bodily functions. But in recent years, scientists seeking to reverse spinal cord damage have been pursuing a number of different approaches. These include transplanting cells to stimulate growth, removing factors that inhibit repair and using biocompatible materials to 'bridge' gaps between damaged nerve ends. One major barrier to nerve regrowth is scar tissue. Now researchers from the University of Melbourne seem to have found a way to prevent this scarring, which they publish in this week's Journal of Neuroscience1. The team found that mice bred without a molecule called EphA4 produce very little scar tissue around damaged spinal nerves. The researchers believe this is because EphA4 plays an important role in activating cells known as astrocytes, which are responsible for scar-tissue formation. ©2004 Nature Publishing Group

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 6394 - Posted: 06.24.2010

Each year, more than 11,000 people will become paralyzed in the United States. It happens in a split second, but it changes lives forever. Researchers are constantly looking for ways to reverse the condition. Now there is a promising discovery that could put them on the fast track. Neuroscientist Mary Bartlett Bunge has found her passion at the Miami Project to cure paralysis. "These are the most exciting findings that I have seen in my laboratory in my 15 years on the Miami Project." In a three-year study, Bunge restored walking ability in paralyzed rats to up to 70 percent normal function. "To see something for the first time is a creative and thrilling experience." The therapy combines three treatments believed to help paralysis. One of those treatments is schwann cells. "Schwann cells enable regeneration of neuro-fibers in the peripheral nervous system that is in your legs and arms." Copyright ©2004 TWEAN Newschannel of Raleigh, L.L.C.

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 6209 - Posted: 06.24.2010

By Aileen Constans Despite advances in knowledge about the mechanisms of nerve injury and repair, regeneration strategies for peripheral and central nervous system (PNS and CNS) damage are still in their infancies. "Neuroscientists are very good at finding out, okay, this enzyme would work or this trophic factor would work, but translating that to a controlled application that will help lead to clinical translation is a different story," says Ravi Bellamkonda, a biomedical engineer at Georgia Institute of Technology, Atlanta. Recently a group at the Miami Project to Cure Paralysis, University of Miami School of Medicine, combined Schwann cell grafts with elevation of cAMP levels to promote axonal growth and improve functional recovery in spinal cord-injured rats.1 Yet such successes are few and far between. A growing number of researchers are turning to tissue engineering as a promising strategy. Incorporating knowledge of the biochemical environment necessary for nerve regeneration with the development of artificial and biological scaffolds that guide regrowth, neural tissue engineering aims to bridge gaps in peripheral nerves, bypass scar tissue in damaged spinal cords, or replace damaged and diseased brain. © 2004, The Scientist LLC, All rights reserved.

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 5678 - Posted: 06.24.2010