1. Decrease in APP and CP mRNA expression supports impairment of iron export in Alzheimer's disease patients
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Paula Faustino, Carolina Maruta, Ângela Timóteo, Cristina Costa, Madalena Martins, Cláudia Guerreiro, Alexandre de Mendonça, Arminda Vilares, Sónia Costa, Ana Herrero, Erica Marcelino, Frederico Simões do Couto, Liliana Marques, Mafalda Matos, Manuela Guerreiro, Ana Verdelho, Luciana Costa, Bruno Silva, and Ângela C. Crespo
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Iron ,Gene Expression ,Iron Homeostasis ,medicine.disease_cause ,Alzheimer's Disease ,Aconitase ,Pathogenesis ,Downregulation and upregulation ,Iron homeostasis ,Gene expression ,medicine ,Homeostasis ,Cellular Iron Export ,Molecular Biology ,biology ,Cellular iron export ,Alzheimer's disease ,medicine.disease ,3. Good health ,Doenças Genéticas ,Immunology ,biology.protein ,Molecular Medicine ,Alzheimer disease ,Ceruloplasmin ,Oxidative stress ,Determinantes Imunológicos em Doenças Crónicas - Abstract
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
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