Please use this identifier to cite or link to this item: https://hdl.handle.net/11000/31210
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dc.contributor.authorLopez-Font, Inmaculada-
dc.contributor.authorIborra Lázaro, Guillermo-
dc.contributor.authorSánchez-Valle, Raquel-
dc.contributor.authorMolinuevo, José Luis-
dc.contributor.authorCuchillo-Ibañez, Inmaculada-
dc.contributor.authorSáez-Valero, Javier-
dc.date.accessioned2024-02-07T10:23:43Z-
dc.date.available2024-02-07T10:23:43Z-
dc.date.created2018-12-12-
dc.identifier.citationClinica Chimica Acta 490 (2019) 6–11es_ES
dc.identifier.issn1873-3492-
dc.identifier.issn0009-8981-
dc.identifier.urihttps://hdl.handle.net/11000/31210-
dc.description.abstractReelin is a glycoprotein associated with synaptic plasticity and neurotransmission. The malfunctioning of reelin signaling in the brain is likely to contribute to the pathogenesis of Alzheimer's disease (AD). Reelin binding to Apolipoprotein E receptor 2 (ApoER2) activates downstream signaling and induces the proteolytic cleavage of ApoER2, resulting in the generation of soluble fragments. To evaluate the efficiency of reelin signaling in AD, we have quantified the levels of reelin and soluble ectodomain fragments of ApoER2 (ectoApoER2) in the cerebrospinal fluid (CSF). CSF from sporadic AD patients (sAD; n = 14, age 54-83 years) had lower levels of ecto-ApoER2 (~31% reduction; p = .005) compared to those in the age-matched controls (n = 10, age 61-80), and a higher reelin/ecto-ApoER2 ratio. In contrast, autosomal dominant AD patients, carriers of PSEN1 mutations (ADAD; n = 7, age 31-49 years) had higher ecto-ApoER2 levels (~109% increment; p = .001) and a lower reelin/ecto-ApoER2 ratio than the non-mutation carriers from the same families (n = 7, age 25-47 years). Our data suggest that the levels of ecto-ApoER2 in CSF could be a suitable read-out of an impaired reelin signaling in AD, but also indicate differences between sAD and ADAD.es_ES
dc.formatapplication/pdfes_ES
dc.format.extent6es_ES
dc.language.isoenges_ES
dc.publisherElsevieres_ES
dc.rightsinfo:eu-repo/semantics/closedAccesses_ES
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectReelines_ES
dc.subjectApoER2es_ES
dc.subjectAutosomal-dominant ADes_ES
dc.subjectCSFes_ES
dc.subjectProteolytic fragmentes_ES
dc.subjectSporadic ADes_ES
dc.titleCSF-ApoER2 fragments as a read-out of reelin signaling: Distinct patterns in sporadic and autosomal-dominant Alzheimer diseasees_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.contributor.instituteInstitutos de la UMH::Instituto de Neurocienciases_ES
dc.relation.publisherversionhttps://doi.org/10.1016/j.cca.2018.12.012es_ES
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Instituto de Neurociencias


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