Brain-derived neurotrophic factor and the course of experimental cerebral malaria

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dc.contributor.authorLinares Gómez, María
dc.contributor.authorPatricia Marín-García
dc.contributor.authorSusana Pérez-Benavente
dc.contributor.authorJesús Sánchez-Nogueiro
dc.contributor.authorPuyet Catalina, Antonio
dc.contributor.authorBautista Santa Cruz, José Manuel
dc.contributor.authorDíez Martín, Amalia
dc.date.accessioned2024-01-29T18:23:25Z
dc.date.available2024-01-29T18:23:25Z
dc.date.issued2013
dc.description.abstractThe role of neurotrophic factors on the integrity of the central nervous system (CNS) during cerebral malaria (CM) infection remains obscure, but the long-standing neurocognitive sequelae often observed in rescued children can be attributed in part to the modulation of neuronal survival and synaptic plasticity. To discriminate the contribution of key responses in the time-sequence of the pathogenic events that trigger the development of neurocognitive malaria syndrome we defined four stages (I–IV) of the neurological progression of CM in C57BL/6 mice infected with Plasmodium berghei ANKA. Upregulation of ICAM-1, VCAM-1, e-selectin and p-selectin expression was detected in all cerebral regions before parasitized red blood cells (pRBC) accumulation. As the severity of symptoms increased, BDNF mRNA progressively diminished in several brain regions, earliest in the thalamus–hypothalamus, cerebellum, brainstem and cortex, and correlated with a four-stage disease sequence. Immunohistochemical confocal microscopy revealed changes in the BDNF distribution pattern, suggesting altered axonal transport. During CM progression, molecular markers of neurological infection and inflammation in the parasite and the host, respectively, were accompanied by a switch in the brain constitutive proteasome to the immunoproteasome, which could impede normal protein turnover. In parallel with BDNF downregulation, NCAM expression also diminished with increased CM severity. Together, these data suggest that changes in BDNF availability could be involved in the pathogenesis of CM.
dc.description.departmentDepto. de Bioquímica y Biología Molecular
dc.description.facultyFac. de Veterinaria
dc.description.refereedFALSE
dc.description.statuspub
dc.identifier.citationLinares, María, et al. «Brain-Derived Neurotrophic Factor and the Course of Experimental Cerebral Malaria». Brain Research, vol. 1490, enero de 2013, pp. 210-24. DOI.org (Crossref), https://doi.org/10.1016/j.brainres.2012.10.040.
dc.identifier.doi10.1016/j.brainres.2012.10.040
dc.identifier.essn1872-6240
dc.identifier.issn0006-8993
dc.identifier.officialurlhttps://doi.org/10.1016/j.brainres.2012.10.040
dc.identifier.pmid23123703
dc.identifier.urihttps://hdl.handle.net/20.500.14352/96249
dc.journal.titleBrain Research
dc.language.isoeng
dc.page.final224
dc.page.initial210
dc.relation.hasversionAM
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internationalen
dc.rights.accessRightsopen access
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subject.keywordBDNF
dc.subject.keywordCerebral malaria
dc.subject.keywordAdhesion molecule
dc.subject.keywordProteasome
dc.subject.keywordCytokine
dc.subject.ucmCiencias Biomédicas
dc.subject.unesco24 Ciencias de la Vida
dc.titleBrain-derived neurotrophic factor and the course of experimental cerebral malaria
dc.typejournal article
dc.volume.number1490
dspace.entity.typePublication
relation.isAuthorOfPublication855e6962-3ee2-4fc3-b110-96f1c20c5269
relation.isAuthorOfPublicationbe359210-ed21-4efe-8bbf-a176ae0cd618
relation.isAuthorOfPublication46789285-9ba2-4c31-a62a-91bd7f6011ef
relation.isAuthorOfPublicatione4352331-2f80-4b99-b08e-5de06d81bf89
relation.isAuthorOfPublication.latestForDiscovery855e6962-3ee2-4fc3-b110-96f1c20c5269
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