Browsing by Subject "Myelin"

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    De- and remyelination in the CNS white and grey matter induced by cuprizone: The old, the new, and the unexpected
    (F. Hernández y J.F. Madrid. Murcia: Universidad de Murcia, Departamento de Biología Celular e Histología., 2011) Skripuletz, Thomas; Gudi, Viktoria; Hackstette, Diane; Stangel, Martin
    The copper chelator cuprizone (bis-cyclohexanone oxaldihydrazone) was established as a neurotoxin in rodents in 1966 by Carlton. During the following years the usefulness of cuprizone feeding in mice to induce oligodendrocyte death with secondary demyelination of the superior cerebellar peduncles was described by Blakemore. In 1998 the cuprizone model experienced a renaissance as the group of Matsushima described the effects of cuprizone on the white matter of the cerebrum and focussed on demyelination in the corpus callosum, where the extent of demyelination could be scored more easily and consistently. Since then the toxic cuprizone model has been widely used to study experimental de- and remyelination in the corpus callosum. Recently, we and others have extended these studies and have shown several new aspects characteristic for this model. Many lessons can be learned from these recent findings that have implications for the basic understanding of remyelination and the design of remyelinating and neuroprotective strategies in demyelinating diseases of the CNS. Although the model is often mentioned in the context of multiple sclerosis, it must always be kept in mind that this model has a fundamentally different induction of demyelination. We highlight the important findings delineated from this model and critically discuss both the advantages and the shortcomings of cuprizone induced demyelination.
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    Myeloid cell distribution and activity in multiple sclerosis
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Moliné-Velázquez, Verónica; Vila-del Sol, Virginia; de Castro, Fernando; Clemente, Diego
    Multiple sclerosis (MS) is a demyelinating disease in which an exacerbated immune response provokes oligodendrocyte loss and demyelination, the hallmarks of this neurological disease. The destruction of myelin due to the uncontrolled activity of the invading immune cells leads to the formation of MS plaques. Among the different leukocytes that participate in the immune response associated with MS, the role of myeloid cells has been analyzed extensively (i.e. macrophages, dendritic cells -DCs- and neutrophils). Hence, in this review we will summarize what is known about the distribution, expression and markers available to study myeloid cells, and their histopathology, not only in a standard animal model of MS (autoimmune experimental encephalomyelitis -EAE) but also in MS tissue. In this review, we will not only refer to mature myeloid cells but also to the undifferentiated and almost unexplored myeloid-derived suppressor cells (MDSCs). The active role of MDSCs in the prompt resolution of an immune episode is gaining importance, yet is still the subject of some debate. Finally, the similarities and differences between MS and EAE are discussed, particularly in terms of myeloid cell phenotype, activity and the markers used.