Several observations suggest that iron is an essential factor in myelination and oligodendrocyte biology. However, the specific role of iron in these processes remains to be elucidated. This role could be as an essential cofactor in metabolic processes or as a transcriptional or translational regulator. In this study, we used animals models each with a unique defect in iron availability, storage, or transfer to test the hypothesis that disruptions in these mechanisms affect myelinogenesis and myelin composition. Disruption of iron availability either by limiting dietary iron or by altering iron storage capacity resulted in a decrease in myelin proteins and lipids but not the iron content of myelin. Among the integral myelin proteins, proteolipid protein was most consistently affected, suggesting that limiting iron to oligodendrocytes results not only in hypomyelination but also in a decrease in myelin compaction. Mice deficient in transferrin must receive transferrin injections beginning at birth to remain viable, and these mice had increases in all of the myelin components and in the iron content of the myelin. This finding indicates that the loss of endogenous iron mobility in oligodendrocytes could be overcome by application of exogenous transferrin. Overall, the results of this study demonstrate how myelin composition can be affected by loss of iron homeostasis and reveal specific chronic changes in myelin composition that may affect behavior and attempts to rescue myelin deficits.
"e, deri ve mukozalarda önemli değişiklikler ortaya çıkmaktadır (Ağaoğlu 2010). Demirin, pek çok biyolojik işlevi yanında, miyelinizasyon, oligodendrositlerin gelişimi, nörotransmitter sentezi gibi nörobiyolojik süreçler üzerine olan etkisi oldukça önemlidir (Lozoff ve ark. 1987, Beard ve ark. 1993, Connor ve Menzies 1996, Roncagliolo ve ark. 1998, Ortiz ve ark. 2004). Demir eksikliğinin, santral sinir sistemi üzerine olan etkileri; halsizlik, aktivite azalması, irritabilite, iletişim bozuklukları, okul başarısında düşme, mental-motor gelişim testlerinde performans düşüklüğü, kognitif performansta azalma, papil ödem olarak sıralanabilir (Ekici 2012). Demir eksikliğinin, psikomotor gelişim ve öğrenme"
[Show abstract][Hide abstract] ABSTRACT: Dikkat eksikliği ve hiperaktivite bozukluğu, tıp literatüründe en iyi araştırılmış bozukluklardan biri olmasına rağmen, etiyolojisi halen net olarak açıklığa kavuşturulamamıştır. Dikkat eksikliği ve hiperaktivite bozukluğu’nun küratif şekilde tedavi edilmesi için bozukluk ile ilişkili etmenlerin net olarak aydınlatılması oldukça önemlidir. Literatür incelendiğinde, demir eksikliğinin dikkat eksikliği ve hiperaktivite bozukluğu patofizyolojisi için bir risk faktörü olabileceği belirtilmekle birlikte, konu ile ilgili şu ana kadar yapılan çalışmalarda çelişkili sonuçlar elde edildiği gözlenmektedir. Bu yazıda, dikkat eksikliği ve hiperaktivite bozukluğu patofizyolojisinde etkili olduğu düşünülen demir ve demirle ilişkili parametrelerin kan düzeyleri ile ilgili literatürdeki, çocuk ve ergen yaş grubunda, ülkemizde ve yurt dışında yapılmış konu ile ilgili çalışmaların incelenmesi, genel özelliklerinin derlenmesi ve sonuçlarının sunulması amaçlanmıştır.
"Effects on myelination Iron is needed for myelination Features of AD include white matter hyperintensity, axonal, neurite and synaptic changes Impaired neurotransmission Ortiz et al., 2004; Bartzokis et al., 2007; Baeten et al., 2010; Romero et al., 2010; Paling et al., 2012 staining is not covered here, but has been recently reviewed with a focus on neurobiology (Que et al., 2008). "
[Show abstract][Hide abstract] ABSTRACT: Alzheimer’s disease (AD) is the leading cause of dementia in the elderly. AD represents a complex neurological disorder which is best understood as the consequence of a number of interconnected genetic and lifestyle variables, which culminate in multiple changes to brain structure and function. At a molecular level, metal dyshomeostasis is frequently observed in AD due to anomalous binding of metals such as Iron (Fe), Copper (Cu) and Zinc (Zn), or impaired regulation of redox-active metals which can induce the formation of cytotoxic reactive oxygen species and neuronal damage. Neuroimaging of metals in a variety of intact brain cells and tissues is emerging as an important tool for increasing our understanding of the role of metal dysregulation in AD. Several imaging techniques have been used to study the cerebral metallo-architecture in biological specimens to obtain spatially resolved data on chemical elements present in a sample. Hyperspectral techniques, such as particle-induced X-ray emission (PIXE), energy dispersive X-ray spectroscopy (EDS), X-ray fluorescence microscopy (XFM), synchrotron X-ray fluorescence (SXRF), secondary ion mass spectrometry (SIMS), and laser ablation inductively coupled mass spectrometry (LA-ICPMS) can reveal relative intensities and even semi-quantitative concentrations of a large set of elements with differing spatial resolution and detection sensitivities. Other mass spectrometric and spectroscopy imaging techniques such as laser ablation electrospray ionisation mass spectrometry (LA ESI-MS), MALDI imaging mass spectrometry (MALDI-IMS), and Fourier transform infrared spectroscopy (FTIR) can be used to correlate changes in elemental distribution with the underlying pathology in AD brain specimens. The current review aims to discuss the advantages and challenges of using these emerging elemental and molecular imaging techniques, and highlight clinical achievements in AD research using bioimaging techniques.
"With iron in being integral part of numerous cellular metabolic activities  , its homeostasis is controlled by a large group of iron-regulatory proteins, but it excess in the body becomes potentially toxic to the cell because mammals lack a regulatory pathway for its excretion . Erythrocytes besides spleen and liver contain the majority of body iron as a component of hemoglobin and circulate throughout the body for vital redox biological processes. "
[Show abstract][Hide abstract] ABSTRACT: To gain insight into the hepatohistological alterations in noninjured rat liver, Nerium oleander (N.O.) leaves extract was injected intramuscularly to induce an acute phase reaction (APR). Histopathological changes were studied after 3, 12, and 24 h time course of sterile muscle abscess. Tissue integrity and any infiltration of inflammatory cells in the liver were investigated by Hematoxylin and Eosin and ED1 peroxidase stainings. The administration of N.O. leaves extract (10 mL/kg) in H & E stained sections showed a general vacuolization of cytoplasm resulting loss of polarity with prominent nucleoli after 3 h of induction. At 12 h, eccentric nuclei were also observed in the sections. Marked infiltration of leucocytes with predominate macrophages was also found after 24 h as seen by ED1 positive staining. In the present study, a possible relationship between serum hepcidin and total iron level was also investigated in vivo. An early increase of hepcidin and total iron level (3 h) with a maximum at 12 h (P < 0.01; P < 0.001) was observed. These changes indicate that sterile muscle abscess may induce APR resulting in hepatic damage which is evident with the recruitment of inflammatory cells into the organ.
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