Utilize este identificador para referenciar este registo: http://hdl.handle.net/10400.18/3112
Título: Decrease in APP and CP mRNA expression supports impairment of iron export in Alzheimer's disease patients
Autor: Guerreiro, Cláudia
Silva, Bruno
Crespo, Ângela
Marques, Liliana
Costa, Sónia
Timóteo, Ângela
Marcelino, Erica
Maruta, Carolina
Vilares, Arminda
Matos, Mafalda
Couto, Frederico S.
Faustino, Paula
Verdelho, Ana
Guerreiro, Manuela
Herrero, Ana
Costa, Cristina
de Mendonça, Alexandre
Martins, Madalena
Costa, Luciana
Palavras-chave: Alzheimer's Disease
Cellular Iron Export
Gene Expression
Iron Homeostasis
Determinantes Imunológicos em Doenças Crónicas
Doenças Genéticas
Data: Out-2015
Editora: Elsevier
Citação: Biochim Biophys Acta. 2015 Oct;1852(10 Pt A):2116-22. doi: 10.1016/j.bbadis.2015.07.017. Epub 2015 Jul 22.
Resumo: Alzheimer'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 disease
Peer review: yes
URI: http://hdl.handle.net/10400.18/3112
DOI: j.bbadis.2015.07.017
ISSN: 0006-3002
Versão do Editor: http://www.sciencedirect.com/science/article/pii/S0925443915002094
Aparece nas colecções:DPSPDNT - Artigos em revistas internacionais
DGH - Artigos em revistas internacionais



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