DPSPDNT - Palestras
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- Identificação de factores de susceptibilidade para os Distúrbios do Espectro do AutismoPublication . Moura Vicente, Astrid
- Metals, immune system and diseasePublication . Costa, LucianaCeruloplasmin (CP) is an abundant copper (Cu)-containing plasma glycoprotein that participates in the acute phase reaction to stress. Despite its physiologic role(s) remains unknown, CP antioxidant activity by promoting iron mobilization or scavenging free radicals and thus preventing metal-catalyzed free-radical tissue damage has been widely described. In this presentation, we show human peripheral blood lymphocytes (huPBL) express two distinct CP transcripts: a secreted and a membrane GPI-anchored form. Particularly, we suggest that expression of CP in immune cells could represent an integral part of host response to immunological stress and could contribute to the increase of plasma CP levels observed during acute-phase conditions. Also, we show that the CP protein is localized at huPBL surface and its expression is highly specific to the NK cell lymphocyte subset, suggesting an important role for huPBL-associated CP in the relationship between innate immunity and oxidative biology. As a ferroxidase, CP converts the reduced ferrous iron to oxidized ferric non-toxic form facilitating the movement of iron from cells to the blood. There is also increasing experimental evidence that CP can also function as an extracellular protective enzyme against oxidative stress. In this context, the physiologic relevance of CP expressed by immune cells in iron homeostasis, particularly in oxyradical overload pathologic conditions, is discussed. The functional link between copper/iron metabolism and immunity in specific pathologies related to cardiovascular, neurologic and inflammatory conditions will be presented.
- Crosstalk between iron and copper metabolism in Alzheimer's disease: any news?Publication . Costa, LucianaAlzheimer’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.
- Autism Genome ProjectPublication . Moura Vicente, Astrid
- Estudo Português de Hipercolesterolemia FamiliarPublication . Bourbon, Mafalda
- Molecular Genetics of AutismPublication . Moura Vicente, Astrid
- PharmacogenomicsPublication . Moura Vicente, Astrid
- Transplantação – História, organização, legislação e polémicasPublication . Alves, Helena
- Relationship between copper, iron and immune system: Alzheimer’s disease as a clinical modelPublication . Costa, LucianaThe involvement of metals in a wide range of biological pathways, have been previously extensively described. However, during the last decade there has been a surge of interest in the research of the metabolic links between immunological processes, copper (Cu) and iron (Fe) metabolism. 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 as Cu and Fe has been recognized to contribute to the pathology of AD. Accumulation of Fe in the brain is a consistent observation in AD. 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 and in its protection from Fe-mediated free radical injury. 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 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.
- Schistosoma haematobium e cancro da bexiga: a verdade escondidaPublication . Botelho, Mónica