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dc.contributor.authorRodríguez Arellano, José Julio
dc.contributor.authorWitton, J.
dc.contributor.authorOlabarria, M.
dc.contributor.authorNoristani, H.N.
dc.contributor.authorVerkhratsky, Alexei
dc.date.accessioned2014-03-31T17:13:23Z
dc.date.available2014-03-31T17:13:23Z
dc.date.issued2010-01
dc.identifier.citationCell Death & Disease 1 : (2010) // e1es
dc.identifier.issn2041-4889
dc.identifier.urihttp://hdl.handle.net/10810/11884
dc.description.abstractThe formation of cerebral senile plaques composed of amyloid beta peptide (A beta) is a fundamental feature of Alzheimer's disease (AD). Glial cells and more specifically microglia become reactive in the presence of A beta. In a triple transgenic model of AD (3 x Tg-AD), we found a significant increase in activated microglia at 12 (by 111%) and 18 (by 88%) months of age when compared with non-transgenic (non-Tg) controls. This microglial activation correlated with A beta plaque formation, and the activation in microglia was closely associated with A beta plaques and smaller A beta deposits. We also found a significant increase in the area density of resting microglia in 3 x Tg-AD animals both at plaque-free stage (at 9 months by 105%) and after the development of A plaques (at 12 months by 54% and at 18 months by 131%). Our results show for the first time that the increase in the density of resting microglia precedes both plaque formation and activation of microglia by extracellular A beta accumulation. We suggest that AD pathology triggers a complex microglial reaction: at the initial stages of the disease the number of resting microglia increases, as if in preparation for the ensuing activation in an attempt to fight the extracellular A beta load that is characteristic of the terminal stages of the disease. Cell Death and Disease (2010) 1, e1; doi:10.1038/cddis.2009.2; published online 14 January 2010es
dc.description.sponsorshipSupported by the Alzheimer's Research Trust (UK) Programme Grant ART/PG2004A/1 to AV and JJR; and the Grant Agency of the Czech Republic GACR 309/09/1696 to JJR and GACR 305/08/1384 to AV.es
dc.language.isoenges
dc.publisherNature Publishing Groupes
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.subjectmicrogliaes
dc.subjectAlzheimer's diseasees
dc.subjecthippocampuses
dc.subjectplasticityes
dc.subjectbeta-amyloides
dc.subjectmouse modeles
dc.subjectin-vivoes
dc.subjectinflammatory responsees
dc.subjectamyloid plaqueses
dc.subjectA betaes
dc.subjectbraines
dc.subjectcellses
dc.subjectmicees
dc.subjectsystemes
dc.subjectdysfunctiones
dc.titleIncrease in the density of resting microglia precedes neuritic plaque formation and microglial activation in a transgenic model of Alzheimer's diseasees
dc.typeinfo:eu-repo/semantics/articlees
dc.rights.holderThis is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits distribution and reproduction in any medium, provided the original author and source are credited. This license does not permit commercial exploitation without specific permission.es
dc.relation.publisherversionhttp://www.nature.com/cddis/journal/v1/n1/full/cddis20092a.htmles
dc.identifier.doi10.1038/cddis.2009.2
dc.departamentoesNeurocienciases_ES
dc.departamentoeuNeurozientziakes_ES
dc.subject.categoriaCELL BIOLOGY
dc.subject.categoriaONCOLOGY
dc.subject.categoriaMEDICINE
dc.subject.categoriaIMMUNOLOGY AND MICROBIOLOGY
dc.subject.categoriaCELLULAR AND MOLECULAR NEUROSCIENCE


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