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Please use this identifier to cite or link to this item: http://hdl.handle.net/10400.18/837

Título: Crosstalk between iron and copper metabolism in Alzheimer's disease: any news?
Autor: Costa, Luciana
Palavras-chave: Determinantes Imunológicos em Doenças Crónicas
Issue Date: 17-Apr-2011
Editora: Instituto Nacional de Saúde Doutor Ricardo Jorge, IP
Resumo: Alzheimer’s disease (AD) is the most frequent neurodegenerative disorder affecting up to 15 million individuals worldwide. The distinction between normal aging and AD is a relevant step to combat this disease efficiently. Thus, the identification of biomarkers and genetic factors underlying AD pathology is extremely important. Oxidative injury in the brain, mediated by the imbalance of redox-active metals, iron (Fe) and copper (Cu), has been recognized to contribute to the pathology of AD. Accumulation of Fe in the brain is a consistent observation in AD and has been extensively investigated. In fact, a link between congenital Fe overload (haemochromatosis, HFE) and AD has been proposed. The presence of the HFE mutation in AD strongly supports the idea that Fe imbalance in the brain contributes to the disease, and its prevalence indicates that it could be an important risk factor. On the other hand, abnormalities in the synthesis of ceruloplasmin (Cp) have been associated with various neurodegenerative diseases. Cp is an oxidase containing 95% of circulating Cu that has been implicated in maintaining Fe homeostasis in the central nervous system (CNS) and in its protection from Fe-mediated free radical injury. Although the liver is the predominant source of serum circulating Cp, extrahepatic Cp expression has been demonstrated in many tissues. Particularly, a glycosylphosphatidylinositol (GPI)-anchored form of Cp (GPI-Cp) was previously shown to be expressed in the mammalian CNS. Recent results from our group showed that human peripheral blood mononuclear cells constitutively express both secreted Cp and the GPI-Cp isoforms. The exact function of this GPI-linked form is unknown, but previous studies suggested its potential role in Fe mobilization in the blood-brain barrier. From early observations that low circulating serum Cp levels serve as a marker for Wilson’s disease to the characterization of aceruloplasminemia as a neurodegenerative disorder associated with a complete lack of serum Cp, the link between Cp and neuropathy has strengthened. Importantly, the demonstration that Cp acts in concert with Fe transporters during Fe cellular efflux suggest that elucidation of the mechanisms of Fe and Cu trafficking and metabolism within the nervous system may be an important step to understand the pathogenesis of AD. In this presentation, new insights into the putative functional crosstalk between Fe and Cu metabolism and oxidative stress in the pathogenesis of AD will be presented. The results obtained by our group and the hypothesis raised during the ongoing research project on this topic will be discussed.
Descrição: Palestra por convite
URI: http://hdl.handle.net/10400.18/837
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