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Implications of glial nitric oxide in neurodegenerative diseases
dc.contributor.author | Yuste Jiménez, José Enrique | |
dc.contributor.author | Tarragon Cros, Ernesto | |
dc.contributor.author | Campuzano Brando, Carmen María | |
dc.contributor.author | Ros Bernal, Francisco | |
dc.date.accessioned | 2016-04-26T14:36:10Z | |
dc.date.available | 2016-04-26T14:36:10Z | |
dc.date.issued | 2015 | |
dc.identifier.citation | YUSTE, Jose Enrique, et al. Implications of glial nitric oxide in neurodegenerative diseases. Frontiers in cellular neuroscience, 2015, vol. 9. | ca_CA |
dc.identifier.issn | 1662-5102 | |
dc.identifier.uri | http://hdl.handle.net/10234/158967 | |
dc.description.abstract | Nitric oxide (NO) is a pleiotropic janus-faced molecule synthesized by nitric oxide synthases (NOS) which plays a critical role in a number of physiological and pathological processes in humans. The physiological roles of NO depend on its local concentrations, as well as its availability and the nature of downstream target molecules. Its double-edged sword action has been linked to neurodegenerative disorders. Excessive NO production, as the evoked by inflammatory signals, has been identified as one of the major causative reasons for the pathogenesis of several neurodegenerative diseases. Moreover, excessive NO synthesis under neuroinflammation leads to the formation of reactive nitrogen species and neuronal cell death. There is an intimate relation between microglial activation, NO and neuroinflammation in the human brain. The role of NO in neuroinflammation has been defined in animal models where this neurotransmitter can modulate the inflammatory process acting on key regulatory pathways, such as those associated with excitotoxicity processes induced by glutamate accumulation and microglial activation. Activated glia express inducible NOS and produce NO that triggers calcium mobilization from the endoplasmic reticulum, activating the release of vesicular glutamate from astroglial cells resulting in neuronal death. This change in microglia potentially contributes to the increased age-associated susceptibility and neurodegeneration. In the current review, information is provided about the role of NO, glial activation and age-related processes in the central nervous system (CNS) that may be helpful in the isolation of new therapeutic targets for aging and neurodegenerative diseases. | ca_CA |
dc.format.extent | 13 p. | ca_CA |
dc.format.mimetype | application/pdf | ca_CA |
dc.language.iso | eng | ca_CA |
dc.publisher | Frontiers Media | ca_CA |
dc.relation.isPartOf | Front. Cell. Neurosci., 17 August 2015 | ca_CA |
dc.rights | This Document is Protected by copyright and was first published by Frontiers. All rights reserved. it is reproduced with permission. Copyright © 2015 Yuste, Tarragon, Campuzano and Ros-Bernal. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. | ca_CA |
dc.rights | Attribution 4.0 Spain | * |
dc.rights.uri | http://creativecommons.org/licenses/by-sa/4.0/ | * |
dc.subject | Nitric oxide | ca_CA |
dc.subject | Neuroinflammation | ca_CA |
dc.subject | Neurodegenerative disorders | ca_CA |
dc.subject | Neuronal nitric oxide | ca_CA |
dc.subject | Neuronal death | ca_CA |
dc.title | Implications of glial nitric oxide in neurodegenerative diseases | ca_CA |
dc.type | info:eu-repo/semantics/article | ca_CA |
dc.identifier.doi | http://dx.doi.org/10.3389/fncel.2015.00322 | |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | ca_CA |
dc.relation.publisherVersion | http://journal.frontiersin.org/article/10.3389/fncel.2015.00322/full | ca_CA |
dc.type.version | info:eu-repo/semantics/publishedVersion |
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Excepto si se señala otra cosa, la licencia del ítem se describe como: This Document is Protected by copyright and was first published by Frontiers. All rights reserved. it is reproduced with permission. Copyright © 2015 Yuste, Tarragon, Campuzano and Ros-Bernal. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.