Brain repair

Authors

  • A. COMPSTON

    Professor, Corresponding author
    1. University of Cambridge Neurology Unit, Addenbrooke's Hospital, and the Medical Research Council Cambridge Centre for Brain Repair, Cambridge, UK
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University of Cambridge Neurobiology Unit, Neurology Unit, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK.

Abstract

Abstract. Significant improvements in the treatment of common neurological diseases can be expected over the next few years from the application of advances now occurring in the basic neurosciences. In many disorders of the central nervous system, disability accumulates as a result of the degenerative process and its failure to repair. In part, this is because with differentiation, cells in the adult nervous system lose the ability to proliferate and migrate. A family of growth factors orchestrates proliferation, migration, differentiation and survival of neurones and glia; because certain of these growth factors also protect from injury cells which they support during development, there should soon be opportunities for limiting damage following a variety of insults and for rescuing degenerating neurones and glia. The discovery that axon regeneration is actively inhibited, perhaps in order to maintain stability in the complex systems and circuits that are established during development, suggests new strategies for enhancing axonal regeneration in spinal and head injury. Recruiting cells that are capable of restoring glial-neuronal interactions into areas of damage will be an important part of the brain repair strategy but it may prove possible to restore complex cellular arrangements through cell implantation only. Grafted neurones survive, produce appropriate neurotransmitters, form connections and restore some behaviours, but their relative inability to grow limits the degree of structural and functional repair that can be achieved; nevertheless, nerve cell implantation is now being used in the management of certain neurodegenerative diseases of the human central nervous system. There are also prospects for increasing the remyelination which occurs following acute inflammatory disease of the central nervous system, through the combination of immunological treatments that limit the disease process, growth factors that recruit oligodendrocytes and implantation of glial progenitors into demyelinated areas.

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