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Decrease of β-amyloid peptide precursor and ceruloplasmin mRNA levels in patients with Alzheimer’s disease support impairment of cellular iron efflux in this pathology

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dc.contributor.authorSilva, Bruno
dc.contributor.authorGuerreiro, Cláudia
dc.contributor.authorC. Crespo, Ângela
dc.contributor.authorMarques, Liliana
dc.contributor.authorMarcelino, Erica
dc.contributor.authorMaruta, Carolina
dc.contributor.authorCosta, Sónia
dc.contributor.authorTimóteo, Ângela
dc.contributor.authorVilares, Arminda
dc.contributor.authorSimões Couto, Frederico
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.accessioned2015-02-17T17:14:17Z
dc.date.available2015-02-17T17:14:17Z
dc.date.issued2014-09
dc.descriptionThis research was supported by the Fundação para a Ciência e a Tecnologia (FCT) [SFRH/BPD/29354/2006 to MM, SFRH/BD/60718/2009 to BS, and SFRH/BD/48671/2008 to LM]; Fundação Astrazeneca (Research Grant awarded through the “Programme of Support to Research”); Instituto Nacional de Saúde Dr. Ricardo Jorge; Portuguese Ministry of Health (Research Grant 53/2007 of the “Comissão de Fomento da Investigação em Cuidados de Saúde”); Lundbeck Portugal, Lda (Research Grant).por
dc.description.abstractIntroduction: Alzheimer’s disease (AD) is the most common neurodegenerative disorder and the leading cause of dementia worldwide. Because of the clinical interest in its early diagnosis and prediction of patient evolution and prognosis, the identification of AD biomarkers is of crucial importance. Several lines of evidence implicate an imbalance of the redox-active biometals in AD. Metal-catalyzed hydroxyl radicals are potent mediators of cellular injury and are central to the oxidative injury hypothesis of AD pathogenesis [1,2]. Importantly, previous genetic and biochemical studies in AD patients support a concerted systemic iron metabolism dysregulation, namely at the level of cellular iron efflux [3]. Herein, we intended to further understand the molecular mechanisms underlying iron homeostasis in this pathology. In order to achieve this goal, the expression of specific iron metabolism-related genes directly involved in iron metabolism regulation and cellular iron export was measured in peripheral blood mononuclear cells from AD patients and healthy controls. Also, serum ceruloplasmin (CP) concentration and its oxidase activity were measured in all participants in the study, given the known role of this oxidase in facilitating iron exit from cells. Through this study we expect to further clarify the contribution of iron metabolism disruption to the etiopathogenesis of AD.por
dc.identifier.urihttp://hdl.handle.net/10400.18/2886
dc.language.isoengpor
dc.subjectDeterminantes Imunológicos em Doenças Crónicaspor
dc.subjectAlzheimer’s diseasepor
dc.subjectIron Metabolismpor
dc.titleDecrease of β-amyloid peptide precursor and ceruloplasmin mRNA levels in patients with Alzheimer’s disease support impairment of cellular iron efflux in this pathologypor
dc.typeconference object
dspace.entity.typePublication
oaire.citation.conferencePlaceVerona, Italy.por
oaire.citation.titleEuropean Iron Club, 10-14 September 2014por
rcaap.rightsembargoedAccesspor
rcaap.typeconferenceObjectpor

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