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Contribution of Neurons and Glial Cells to Complement-Mediated Synapse Removal during Development, Aging and in Alzheimer’s Disease

dc.contributor.authorLuchena Moreno, Celia ORCID
dc.contributor.authorZuazo Ibarra, Jone
dc.contributor.authorAlberdi Alfonso, Elena María ORCID
dc.contributor.authorMatute Almau, Carlos José
dc.contributor.authorCapetillo González de Zarate, Estibaliz
dc.date.accessioned2020-05-05T10:20:41Z
dc.date.available2020-05-05T10:20:41Z
dc.date.issued2018
dc.identifier.citationMediators of inflammation 2018 : (2018) // Article ID 2530414es_ES
dc.identifier.issn0962-9351
dc.identifier.issn1466-1861
dc.identifier.urihttp://hdl.handle.net/10810/43013
dc.description.abstractSynapse loss is an early manifestation of pathology in Alzheimer's disease (AD) and is currently the best correlate to cognitive decline. Microglial cells are involved in synapse pruning during development via the complement pathway. Moreover, recent evidence points towards a key role played by glial cells in synapse loss during AD. However, further contribution of glial cells and the role of neurons to synapse pathology in AD remain not well understood. This review is aimed at comprehensively reporting the source and/or cellular localization in the CNS-in microglia, astrocytes, or neurons-of the triggering components (C1q, C3) of the classical complement pathway involved in synapse pruning in development, adulthood, and AD.es_ES
dc.description.sponsorshipThe authors thank Dr. Baleriola at Achucarro Basque Center for Neuroscience (Bilbao, Spain) and Dr. Sole-Domenech and Dr. Pipalia at Weill Cornell Medical College (Cornell University, New York, USA) for the helpful and critical revision of the manuscript. This study was supported by CIBERNED and by grants from Ministerio de Economia y Competitividad (SAF2016-75292-R), Gobierno Vasco (PIBA PI-2016-1-009-0016 and ELKARTEK 2016-00033), Ikerbasque, Basque Foundation for Science, and Universidad del Pais Vasco/Euskal Herriko Unibertsitatea UPV/EHU. Jone Zuazo held a fellowship from Gobierno Vasco and Celia Luchena from Fundacion Tatiana Perez de Guzman el Bueno.es_ES
dc.language.isoenges_ES
dc.publisherHindawies_ES
dc.relationinfo:eu-repo/grantAgreement/MINECO/SAF2016-75292-Res_ES
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.subjectamyloid-beta-peptidees_ES
dc.subjectgenome-wide associationes_ES
dc.subjectA-betaes_ES
dc.subjectmouse modelses_ES
dc.subjectmultiple-sclerosises_ES
dc.subjectneurofibrillary tangleses_ES
dc.subjectdystrophic neuriteses_ES
dc.subjectreactive astrocyteses_ES
dc.subjectidentifies variantses_ES
dc.subjectanaphylatoxin C3Aes_ES
dc.titleContribution of Neurons and Glial Cells to Complement-Mediated Synapse Removal during Development, Aging and in Alzheimer’s Diseasees_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.rights.holder2018 Celia Luchena et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.es_ES
dc.rights.holderAtribución 3.0 España*
dc.relation.publisherversionhttps://www.hindawi.com/journals/mi/2018/2530414/es_ES
dc.identifier.doi10.1155/2018/2530414
dc.departamentoesNeurocienciases_ES
dc.departamentoeuNeurozientziakes_ES


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2018 Celia Luchena et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Except where otherwise noted, this item's license is described as 2018 Celia Luchena et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.