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    You are here : Home » MS Research News » Nerve And Brain Cells

    Nerve And Brain Cells

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    More news can be found in New Pathways Magazine, our bi-monthly publication, and also check daily at MSRC: Latest MS News.

    New light shed on nerve fibres in the brain by MRI research

    Nerves in the BrainWorld-leading experts in Magnetic Resonance Imaging from The University of Nottingham's Sir Peter Mansfield Magnetic Resonance Centre have made a key discovery which could give the medical world a new tool for the improved diagnosis and monitoring of neuro-degenerative diseases like multiple sclerosis.

    The new study, published in the Proceedings of the National Academy of Science, reveals why images of the brain produced using the latest MRI techniques are so sensitive to the direction in which nerve fibres run.

    The white matter of the brain is made up of billions of microscopic nerve fibres that pass information in the form of tiny electrical signals. To increase the speed at which these signals travel, each nerve fibre is encased by a sheath formed from a fatty substance, called myelin. Previous studies have shown that the appearance of white matter in magnetic resonance images depends on the angle between the nerve fibres and the direction of the very strong magnetic field used in an MRI scanner.

    Based on knowledge of the molecular structure of myelin, the Nottingham physicists devised a new model in which the nerve fibres are represented as long thin hollow tubes with special (anisotropic) magnetic properties. This model explains the dependence of image contrast on fibre orientation in white matter and potentially allows information about the nerve fibres (such as their size and direction) to be inferred from magnetic resonance images.

    Research Fellow Dr Samuel Wharton said: "While most MRI-based research focuses on tissue measurements at the millimetre length scale, our experimental scans on healthy human volunteers and modelling of the myelin sheath shows that much more detailed microscopic information relating to the size and direction of nerve fibres can be generated using fairly simple imaging techniques. The results will give clinicians more context in which to recognise and identify lesions or abnormalities in the brain and will also help them to tailor different types of scan to a particular patient."

    Head of the School of Physics and Astronomy, Professor Richard Bowtell added "These results should be an important boost to the world of biomedical imaging which is a key research priority here at The University of Nottingham. We have a strong heritage of groundbreaking work in MRI at the Sir Peter Mansfield Magnetic Resonance Centre and the work was carried out using our 7T scanner which is the strongest magnetic field system for scanning human subjects in the UK."

    Dr Nikolaos Evangelou, Clinical Associate Professor specialising in multiple sclerosis at the Nottingham University Hospitals Trust said: "This research opens new avenues of looking at the nerve fibres in the brain. The more we understand about the nerves and the myelin around them, the more successful we are in studying brain diseases, such as multiple sclerosis. The recent advances in our understanding and treatments of MS are based on basic, solid research such as the one presented by Dr Wharton and Bowtell."

    The research will give scientists and clinicians all over the world a better understanding of the effects of nerve fibres and their orientation in magnetic resonance imaging and has potentially useful applications in the diagnosis and monitoring of brain and nervous system diseases like multiple sclerosis where there are known links to myelin loss.

    Source: MedPage Today © MediLexicon International Ltd 2004-2012 (06/11/12)

    Protein could undo MS nerve damage

    Brain Nerve CellA protein that helps regenerate the protective covering around nerve cells is a “strong candidate” for drug development for diseases like multiple sclerosis, say researchers.

    They have identified previously unrecognized properties of the naturally occuring protein, also finding that it enhances brain cell formation and survival.

    The protein, pigment epithelium-derived factor (PEDF), has well-known anti-tumor generating properties. But its role in promoting growth of a type of brain cell and regenerating the protective myelin sheaths around nerve cells had not been known, the researchers say.

    “Our investigation found that PEDF plays a key role in accelerating regeneration of the myelin sheath,” says study senior author David Pleasure, professor of neurology and pediatrics, and director of the Institute for Pediatric Regenerative Medicine, a collaborative initiative of the University of California, Davis, School of Medicine and Shriners Hospitals for Children Northern California.

    “That makes PEDF a strong drug-therapy candidate, because it appears to encourage the regeneration of a type of brain cell called oligodendocyte and is able to repair the damage caused by demyelinative diseases, including MS.”

    Pleasure and his colleagues identified PEDF’s functions on the adult central nervous system under both normal and pathological conditions in mouse-model research.

    The study was conducted in male and female wild-type mice that were continuously infused with a PEDF/saline suspension. Control mice received daily infusions of saline alone. The study found that in the PEDF infused mice, the PEDF receptor was expressed in various areas of the brain, including the corpus callosum and subventricular zone, reflecting the extensive effects of PEDF.

    “What’s unique about our findings is that we demonstrated that the continuous administration of recombinant PEDF into the normal adult mouse brain enhances production of glial cells in a critical portion of the brain,” says Jiho Sohn, a post-doctoral scholar and lead study author.

    “In addition, we noted the maturation of oligodendrocyte progenitors in the bundle of nerve fibers that connect the left and right hemispheres of the brain.” The study also documented that PEDF infusion enhances production of oligodendroglial progenitor cells from endogenous neural stem cells in mice with corpus callosum demyelinative lesions.

    Multiple sclerosis is one of several disease conditions brought about by demyelination, or damage to the protective sheath around nerve cells.

    Demyelination impairs the conduction of signals in the affected nerves, causing impairment in sensation, movement, cognition, or other functions depending on which nerves are involved.

    Multiple sclerosis is believed to be caused by the body’s immune system attacking the myelin coating on the nerves. There are more than 2.5 million people world-wide with multiple sclerosis, for which there is no cure.

    The study is published in The Journal of Neuroscience. Other study authors contributed from Cornell University, UC Davis, University of Tokyo, and Northwestern University.

    The study was funded by the National Institutes of Health, National Multiple Sclerosis Society, Shriners Hospitals for Children, and a postdoctoral fellowship grant to Sohn from the California Institute for Regenerative Medicine.

    Full Text

    Source: Futurity © 2009-2012 Futurity.org (05/10/12)

    Discovery of immune cells that protect against MS offers hope for new treatment

    Dendritic CellsIn multiple sclerosis, the immune system attacks nerves in the brain and spinal cord, causing movement problems, muscle weakness and loss of vision. Immune cells called dendritic cells, which were previously thought to contribute to the onset and development of multiple sclerosis, actually protect against the disease in a mouse model, according to a study published by Cell Press in the August issue of the journal Immunity. These new insights change our fundamental understanding of the origins of multiple sclerosis and could lead to the development of more effective treatments for the disease.

    "By transfusing dendritic cells into the blood, it may be possible to reduce autoimmunity," says senior study author Ari Waisman of University Medical Center of Johannes Gutenberg University Mainz. "Beyond multiple sclerosis, I can easily imagine that this approach could be applied to other autoimmune diseases, such as inflammatory bowel disease and psoriasis."

    In an animal model of multiple sclerosis known as experimental autoimmune encephalomyelitis (EAE), immune cells called T cells trigger the disease after being activated by other immune cells called antigen-presenting cells (APCs). Dendritic cells are APCs capable of activating T cells, but it was not known whether dendritic cells are the APCs that induce EAE.

    In the new study, Waisman and his team used genetic methods to deplete dendritic cells in mice. Unexpectedly, these mice were still susceptible to EAE and developed worse autoimmune responses and disease clinical scores, suggesting that dendritic cells are not required to induce EAE and other APCs stimulate T cells to trigger the disease. The researchers also found that dendritic cells reduce the responsiveness of T cells and lower susceptibility to EAE by increasing the expression of PD-1 receptors on T cells.

    "Removing dendritic cells tips the balance toward T cell-mediated autoimmunity," says study author Nir Yogev of University Medical Center of Johannes Gutenberg University Mainz. "Our findings suggest that dendritic cells keep immunity under check, so transferring dendritic cells to patients with multiple sclerosis could cure defects in T cells and serve as an effective intervention for the disease."

    Source: Science Codex (17/08/12)

    Limiting multiple sclerosis related axonopathy by blocking Nogo receptor and CRMP-2 phosphorylation

    Brain CellsMultiple sclerosis involves demyelination and axonal degeneration of the central nervous system. The molecular mechanisms of axonal degeneration are relatively unexplored in both multiple sclerosis and its mouse model, experimental autoimmune encephalomyelitis.

    We previously reported that targeting the axonal growth inhibitor, Nogo-A, may protect against neurodegeneration in experimental autoimmune encephalomyelitis; however, the mechanism by which this occurs is unclear.

    We now show that the collapsin response mediator protein 2 (CRMP-2), an important tubulin-associated protein that regulates axonal growth, is phosphorylated and hence inhibited during the progression of experimental autoimmune encephalomyelitis in degenerating axons.

    The phosphorylated form of CRMP-2 (pThr555CRMP-2) is localized to spinal cord neurons and axons in chronic-active multiple sclerosis lesions. Specifically, pThr555CRMP-2 is implicated to be Nogo-66 receptor 1 (NgR1)-dependent, since myelin oligodendrocyte glycoprotein (MOG)35–55-induced NgR1 knock-out (ngr1−/−) mice display a reduced experimental autoimmune encephalomyelitis disease progression, without a deregulation of ngr1−/− MOG35–55-reactive lymphocytes and monocytes.

    The limitation of axonal degeneration/loss in experimental autoimmune encephalomyelitis-induced ngr1−/− mice is associated with lower levels of pThr555CRMP-2 in the spinal cord and optic nerve during experimental autoimmune encephalomyelitis.

    Furthermore, transduction of retinal ganglion cells with an adeno-associated viral vector encoding a site-specific mutant T555ACRMP-2 construct, limits optic nerve axonal degeneration occurring at peak stage of experimental autoimmune encephalomyelitis.

    Therapeutic administration of the anti-Nogo(623–640) antibody during the course of experimental autoimmune encephalomyelitis, associated with an improved clinical outcome, is demonstrated to abrogate the protein levels of pThr555CRMP-2 in the spinal cord and improve pathological outcome.

    We conclude that phosphorylation of CRMP-2 may be downstream of NgR1 activation and play a role in axonal degeneration in experimental autoimmune encephalomyelitis and multiple sclerosis. Blockade of Nogo-A/NgR1 interaction may serve as a viable therapeutic target in multiple sclerosis.

    Full text

    Steven Petratos, Ezgi Ozturk, Michael F. Azari, Rachel Kenny, Jae Young Lee, Kylie A. Magee, Alan R. Harvey, Courtney McDonald, Kasra Taghian, Leon Moussa, Pei Mun Aui, Christopher Siatskas, Sara Litwak, Michael G. Fehlings, Stephen M. Strittmatter and Claude C. A. Bernard

    Source: Brain Copyright © 2012 Guarantors of Brain (08/05/12)

    Neuroscientists discover key protein responsible for controlling nerve cell protection

    Nerve Cells A key protein, which may be activated to protect nerve cells from damage during heart failure or epileptic seizure, has been found to regulate the transfer of information between nerve cells in the brain. The discovery, made by neuroscientists at the University of Bristol and published in Nature Neuroscience and PNAS, could lead to novel new therapies for stroke and epilepsy.

    The research team, led by Professor Jeremy Henley and Dr Jack Mellor from Bristols Medical School, has identified a protein, known as SUMO, responsible for controlling the chemical processes which reduce or enhance protection mechanisms for nerve cells in the brain.

    These key proteins produce subtle responses to the brains activity levels to regulate the amount of information transmitted by kainate receptors - responsible for communication between nerve cells and whose activation can lead to epileptic seizures and nerve cell death.

    Protein function is controlled by altering their structure in processes that can be independent or inter-related including phosphorylation, ubiquitination and SUMOylation. In the present work it is shown that phosphorylation of kainate receptors on its own promotes their activity. However, phosphorylation also facilitates SUMOylation of kainate receptors that reduces their activity. Thus there is a dynamic and delicate interplay between phosphorylation and SUMOylation that regulates kainate receptor function.

    This fine balance between phosphorylation and SUMOylation is dependent on brain activity levels where damaging activity that occurs during stroke or epilepsy will enhance SUMOylation and therefore reduce kainate receptor function to protect nerve cells.

    Dr Mellor, Senior Lecturer from the Universitys School of Physiology and Pharmacology, said: Kainate receptors are a somewhat mysterious but clearly very important group of proteins that are known to be involved in a number of diseases including epilepsy. However, we currently know little about what makes kainate receptors so important. Likewise, we also know that SUMO proteins play an important role in neuroprotection. These findings provide a link between SUMO and kainate receptors that increases our understanding of the processes that nerve cells use to protect themselves from excessive and abnormal activity.

    Professor Henley added: This work is important because it gives a new perspective and a deeper understanding of how the flow of information between cells in the brain is regulated. The team has found that by increasing the amount of SUMO attached to kainate receptors which would reduce communication between the cells could be a way to treat epilepsy by preventing over-excitation of the brains nerve cells.

    The research follows on from previous findings published in Nature that discovered SUMO proteins target the brains kainate receptors altering their cellular location.

    The research teams comprised academics from the University of Bristols MRC Centre for Synaptic Plasticity and the Division of Neuroscience in the School of Physiology & Pharmacology and the School of Biochemistry. This work was supported by the Wellcome Trust, Biotechnology and Biological Sciences Research Council (BBSRC), European Research Council (ERC), Medical Research Council (MRC) and EMBO.

    Source: Scientist Live ©2012 Setform Limited (27/04/12)

    Breakthrough in nerve mapping gives hope for neurologists

    NeuronsA breakthrough in the mapping of monkey nerve fibers might lead to early diagnosis and improved treatment for neurological diseases in humans, according to Taiwanese research published Friday.

    "The structure of nerve fibers, we have found, follows a checker-board pattern," said Tseng Wen-yih, a biomedical expert from National Taiwan University, at a press conference held to announce the publication of the findings in a peer-reviewed journal.

    Neurological disorders such as schizophrenia, hyperactive disorder, autism, dementia and epilepsy can be triggered when a deviation occurs in the brain's "wiring system," he said.

    Unlike the common portrayal of brain nerve fibers as branches of a tree that spread in every direction, Tseng said his team found that fiber bundles constitute an orderly three-dimensional grid that more resembles intricately woven cloth.

    "The findings took us by surprise," Tseng told reporters. "We have uncovered a clear blueprint of brain fibers."

    Tseng and a group of scientists from around the world, including some from Harvard University, have been working together for years to uncover fiber trajectories, and their latest findings were published in the journal Science on March 30.

    The study was based on the brains of monkeys from six different species, but current magnetic resonance imaging (MRI) technology needs improvement to fully sketch out the fiber pathways of living humans, Tseng said.

    Nevertheless, the discovery could yield many applications, including the understanding and prevention of neurological disorders in humans.

    Taking autism as an example, Tseng said that the fiber bundles in sufferers in areas of cognition and language processing seem abnormal.

    If a more sophisticated MRI machine could be designed, doctors would be able to diagnose patients more quickly and precisely, he added.

    The blueprint could also serve as a guideline for the assessment of drug efficiency on patients, he added.

    Tseng said he is in negotiations with local hospitals to take his findings to the stage of clinical trials.

    Describing the discovery as "revolutionary," Yang Pan-chyr, dean of National Taiwan University's College of Medicine, said scientists could work on the findings and further explain how the brain works.

    Source: Focus Taiwan (30/03/12)

    Researchers report potential MS breakthrough

    LIFCaltech researchers report a possible breakthrough in multiple sclerosis medicine in the latest issue of the Journal of Neuroscience.

    Scientists led by Paul Patterson, the Biaggini Professor of Biological Sciences at Caltech, have found a way to use tissue from the brain to help heal neurons damaged by the disease. The scientists developed a gene therapy to stimulate production of specialized nerve cells called oligodendrocytes that make material that protects neurons.

    The therapy uses leukemia inhibitory factor (LIF), a naturally occurring protein.

    “We're using the brain's own progenitor cells as a way to boost repair," Benjamin Deverman, a postdoctoral biology student at Caltech and lead author of the paper, said in a statement.

    "This new application of LIF is an avenue of therapy that has not been explored in human patients with MS," Deverman said, adding the therapy might also help spinal-cord injury patients. Patterson and Deverman, who’ve done their initial research on mice, plan to develop their research to bring it closer to potential human clinical trials.

    More information: The work done in this study, "Exogenous Leukemia Inhibitory Factor Stimulates Oligodendrocyte Progenitor Cell Proliferation and Enhances Hippocampal Remyelination," was funded by the California Institute for Regenerative Medicine, the National Institutes of Neurological Disorders and Stroke, and the McGrath Foundation.

    Source: Pasadena Sun © Copyright Pasadena Sun 2012 (10/02/12)

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