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Decrease in APP and CP mRNA expression supports impairment of iron export in Alzheimer's disease patients

2015-10Journal article Restricted access
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dc.contributor.authorGuerreiro, Cláudia
dc.contributor.authorSilva, Bruno
dc.contributor.authorCrespo, Ângela
dc.contributor.authorMarques, Liliana
dc.contributor.authorCosta, Sónia
dc.contributor.authorTimóteo, Ângela
dc.contributor.authorMarcelino, Erica
dc.contributor.authorMaruta, Carolina
dc.contributor.authorVilares, Arminda
dc.contributor.authorMatos, Mafalda
dc.contributor.authorCouto, Frederico S.
dc.contributor.authorFaustino, Paula
dc.contributor.authorVerdelho, Ana
dc.contributor.authorGuerreiro, Manuela
dc.contributor.authorHerrero, Ana
dc.contributor.authorCosta, Cristina
dc.contributor.authorde Mendonça, Alexandre
dc.contributor.authorMartins, Madalena
dc.contributor.authorCosta, Luciana
dc.date.accessioned2015-09-17T12:11:42Z
dc.date.available2015-09-17T12:11:42Z
dc.date.issued2015-10
dc.description.abstractAlzheimer's disease (AD) is a neurodegenerative disorder of still unknown etiology and the leading cause of dementia worldwide. Besides its main neuropathological hallmarks, a dysfunctional homeostasis of transition metals has been reported to play a pivotal role in the pathogenesis of this disease. Dysregulation of iron (Fe) metabolism in AD has been suggested, particularly at the level of cellular iron efflux. Herein, we intended to further clarify the molecular mechanisms underlying Fe homeostasis in AD. In order to achieve this goal, the expression of specific Fe metabolism-related genes directly involved in Fe regulation and export was assessed in peripheral blood mononuclear cells (PBMCs) from 73AD patients and 74 controls by quantitative PCR. The results obtained showed a significant decrease in the expression of aconitase 1 (ACO1; P=0.007); ceruloplasmin (CP; P<0.001) and amyloid-beta precursor protein (APP; P=0.006) genes in AD patients compared with healthy volunteers. These observations point out to a significant downregulation in the expression of genes associated with ferroportin-mediated cellular Fe export in PBMCs from AD patients, when compared to controls. Taken together, these findings support previous studies suggesting impairment of Fe homeostasis in AD, which may lead to cellular Fe retention and oxidative stress, a typical feature of this diseasepor
dc.description.sponsorshipThis work was supported by Fundação para a Ciência e a Tecnologia (FCT): SFRH/BPD/29354/2006 to Madalena Martins, SFRH/BD/60718/ 2009 to BS, SFRH/BD/48671/2008 to LM, SFRH/BD/75710/2011 to CM and IMM/BI/7-2013 to Mafalda Matos; Fundação Astrazeneca (Research Grant awarded through the “Programme of Support to Research”); by the center grant to BioISI (Center Reference: UID/MULTI/04046/2013 from FCT/MCTES/PIDDAC, Portugal) and Instituto Nacional de Saúde Doutor Ricardo Jorge I.P.por
dc.identifier.citationBiochim Biophys Acta. 2015 Oct;1852(10 Pt A):2116-22. doi: 10.1016/j.bbadis.2015.07.017. Epub 2015 Jul 22.por
dc.identifier.doij.bbadis.2015.07.017
dc.identifier.issn0006-3002
dc.identifier.urihttp://hdl.handle.net/10400.18/3112
dc.language.isoengpor
dc.peerreviewedyespor
dc.publisherElsevierpor
dc.relation.publisherversionhttp://www.sciencedirect.com/science/article/pii/S0925443915002094por
dc.subjectAlzheimer's Diseasepor
dc.subjectCellular Iron Exportpor
dc.subjectGene Expressionpor
dc.subjectIron Homeostasispor
dc.subjectDeterminantes Imunológicos em Doenças Crónicaspor
dc.subjectDoenças Genéticaspor
dc.titleDecrease in APP and CP mRNA expression supports impairment of iron export in Alzheimer's disease patientspor
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage2122por
oaire.citation.startPage2116por
oaire.citation.titleBBA - Biochimica et Biophysica Acta - Molecular Basis of Diseasepor
oaire.citation.volume1852(10 Pt A)por
rcaap.rightsembargoedAccesspor
rcaap.typearticlepor

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