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Mechanisms of Neurodegeneration and Axonal Dysfunction in Progressive Multiple Sclerosis

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dc.contributor.author Correale, Jorge
dc.contributor.author Marrodán, Mariano
dc.contributor.author Ysrraelit, María Célica
dc.date.accessioned 2020-02-07T14:28:44Z
dc.date.available 2020-02-07T14:28:44Z
dc.date.issued 2019-02-20
dc.identifier.citation Correale, J., Marrodan, M., Ysrraelit, M.C. Mechanisms of Neurodegeneration and Axonal Dysfunction in Progressive Multiple Sclerosis. Biomedicines 2019 Feb 20;7(1):14. doi: 10.3390/biomedicines7010014. en_US
dc.identifier.uri https://doi.org/10.3390/biomedicines7010014
dc.identifier.uri https://repositorio.fleni.org.ar/handle/123456789/181
dc.description.abstract Multiple Sclerosis (MS) is a major cause of neurological disability, which increases predominantly during disease progression as a result of cortical and grey matter structures involvement. The gradual accumulation of disability characteristic of the disease seems to also result from a different set of mechanisms, including in particular immune reactions confined to the Central Nervous System such as: (a) B-cell dysregulation, (b) CD8⁺ T cells causing demyelination or axonal/neuronal damage, and (c) microglial cell activation associated with neuritic transection found in cortical demyelinating lesions. Other potential drivers of neurodegeneration are generation of oxygen and nitrogen reactive species, and mitochondrial damage, inducing impaired energy production, and intra-axonal accumulation of Ca2+, which in turn activates a variety of catabolic enzymes ultimately leading to progressive proteolytic degradation of cytoskeleton proteins. Loss of axon energy provided by oligodendrocytes determines further axonal degeneration and neuronal loss. Clearly, these different mechanisms are not mutually exclusive and could act in combination. Given the multifactorial pathophysiology of progressive MS, many potential therapeutic targets could be investigated in the future. This remains however, an objective that has yet to be undertaken. en_US
dc.language.iso eng en_US
dc.publisher MDPI en_US
dc.rights info:eu-repo/semantics/openAccess
dc.rights.uri https://creativecommons.org/licenses/by/2.5/ar/
dc.subject Autoimmunity en_US
dc.subject Autoinmunidad en_US
dc.subject Axons en_US
dc.subject Demyelinating Diseases en_US
dc.subject Enfermedades Desmielinizantes en_US
dc.subject Mitochondria en_US
dc.subject Mitocondrias en_US
dc.subject Multiple Sclerosis en_US
dc.subject Esclerosis Múltiple en_US
dc.subject Nerve Degeneration en_US
dc.subject Degeneración Nerviosa en_US
dc.title Mechanisms of Neurodegeneration and Axonal Dysfunction in Progressive Multiple Sclerosis en_US
dc.type info:eu-repo/semantics/publishedVersion
dc.type info:eu-repo/semantics/article en_US
dc.description.fil Fil: Correale, Jorge. Fleni. Departamento de Neurología. Servicio de Neuroinmunología y Enfermedades Desmielinizantes; Argentina.
dc.description.fil Fil: Marrodán, Mariano. Fleni. Departamento de Neurología. Servicio de Neuroinmunología y Enfermedades Desmielinizantes; Argentina.
dc.description.fil Fil: Ysrraelit, María Célica. Fleni. Departamento de Neurología; Argentina.
dc.relation.ispartofVOLUME 7
dc.relation.ispartofNUMBER 14
dc.relation.ispartofCOUNTRY Suiza
dc.relation.ispartofCITY Basilea
dc.relation.ispartofTITLE Biomedicines
dc.relation.ispartofISSN 2227-9059
dc.type.snrd info:ar-repo/semantics/artículo es_ES


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