Trends in neurosciences
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Adult oligodendrocyte precursor cells (OPCs) make up around 5-8% of the glial cell population in the CNS. Their function in the undamaged CNS is largely unknown, but their processes are in contact with nodes of Ranvier and synapses, suggesting a regulatory role at these structures. The cells divide slowly, and constitute approximately 70% of cells labelled following a pulse injection of bromodeoxyuridine. ⋯ However, remyelination fails during the later stages of multiple sclerosis, and it is not clear whether this is as a result of a depletion of adult OPCs, inhibition within the glial scar, or damage to the axons that prevents myelination. Adult OPCs are also activated and proliferate following other forms of CNS damage, such as mechanical injury, excitotoxicity and viral infection. The cells produce several of the chondroitin sulphate proteoglycans that might inhibit axon regeneration.
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Brain injury following transient or permanent focal cerebral ischaemia (stroke) develops from a complex series of pathophysiological events that evolve in time and space. In this article, the relevance of excitotoxicity, peri-infarct depolarizations, inflammation and apoptosis to delayed mechanisms of damage within the peri-infarct zone or ischaemic penumbra are discussed. While focusing on potentially new avenues of treatment, the issue of why many clinical stroke trials have so far proved disappointing is addressed. This article provides a framework that can be used to generate testable hypotheses and treatment strategies that are linked to the appearance of specific pathophysiological events within the ischaemic brain.
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Trends in neurosciences · Jul 1999
ReviewInnate and adaptive immune responses can be beneficial for CNS repair.
The limitation of immune responsiveness in the mammalian CNS has been attributed to the intricate nature of neuronal networks, which would appear to be more susceptible than other tissues to the threat of permanent disorganization when exposed to massive inflammation. This line of logic led to the conclusion that all forms of CNS inflammation would do more harm than good and, hence, the less immune intervention the better. ⋯ More recently, we found that autoimmune T cells that are specific for a component of myelin can protect CNS neurons from the catastrophic secondary degeneration, which extends traumatic lesions to adjacent CNS areas that did not suffer direct damage. The challenge, therefore, is to learn how to modify immune interactions in the traumatized CNS in order to promote its post-injury maintenance and repair.