Utilize este identificador para referenciar este registo: http://hdl.handle.net/10400.18/2886
Título: 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
Autor: Silva, Bruno
Guerreiro, Cláudia
C. Crespo, Ângela
Marques, Liliana
Marcelino, Erica
Maruta, Carolina
Costa, Sónia
Timóteo, Ângela
Vilares, Arminda
Simões Couto, Frederico
Faustino, Paula
Verdelho, Ana
Guerreiro, Manuela
Herrero, Ana
Costa, Cristina
de Mendonça, Alexandre
Martins, Madalena
Costa, Luciana
Palavras-chave: Determinantes Imunológicos em Doenças Crónicas
Alzheimer’s disease
Iron Metabolism
Data: Set-2014
Resumo: Introduction: 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.
Descrição: This 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).
URI: http://hdl.handle.net/10400.18/2886
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