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Dev Neurosci. 2002;24(2-3):197-207.

Iron deficiency during embryogenesis and consequences for oligodendrocyte generation in vivo.

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Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah, USA.


One of the hallmarks of the pathology of iron deficiency in children is neurological disabilities that are often associated with hypomyelination. It has been hypothesized that this amyelination is mainly due to a disruption of myelin generation during the early postnatal stages when oligodendrocytes mature to generate myelin producing cell. In addition to these suggestions, we have previously provided in vitro data showing that iron affects both the proliferation and differentiation of glial precursor cells leading to a disruption in the generation of oligodendrocytes. We now present evidence demonstrating in vivo that iron deficiency during pregnancy affects the iron levels of various brain tissues in the developing fetus and disrupts not only the proliferation of their glial precursor cells but also disturbs the generation of oligodendrocytes from these precursor cells. In addition, we show that iron deficiency during embryogenesis affects glial lineage cells in a tissue-specific manner. Our studies offer the possibility to begin to comprehend whether any effects that occur during embryogenesis might have an influence on the establishment of the pathological defects that occur as a consequence of iron deficiency.

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