Gestational Iron deficiency
The majority of data that support this novel hypothesis come from our studies that are focused on iron deficiency, one of the world most prevalent nutritional deficiencies. In this paradigm we have shown for the first time that embryonic CNS tissue is not protected from iron deficiency during pregnancy, as commonly thought, and that early glial precursor cell populations are highly sensitive to changes in tissue iron concentrations. Thus, iron deprivation may lead to a failure to produce proper myelin by perturbing normal development of the precursor cell and oligodendrocyte populations that are responsible for axon myelination (Morath and Mayer-Proschel, 2001, Dev. Biol, 2002, Dev. Neurosci). Support for this hypothesis comes also from the observation that iron deficiency-associated defects cannot be cured by application of dietary iron during postnatal development. (see for summary Figure 2).
We have established rat and mouse models of gestation iron deficiency with and without anemia and focus on two ages of development where sufficient iron seems to be critically important for specific biological processes: (i) early embryonic telencephalic development and (ii) myelination of the auditory nerve postnatally.
In the early embryo we are especially interested in the impact of insufficient maternal iron on embryonic patterning. We have discovered that important signaling cascades that are responsible for setting up a dorsal ventral gradient are impaired in iron deficiency embryos. We are currently investigating the molecular mechanism that is involved in this impairment.
In postnatal development we focused on the auditory nerve due to the ease by which auditory function can be measured in a non invasive manner. We have discovered a novel phenotype of demyelination that is associated with iron deficiency and affects not only myelination itself but the cross talk between axons and oligodendrocytes. The research in this area is now focused on extending these studies to other brain regions and to decipher the mechanism by which iron deficiency disrupts axon- glial interactions.
For work that involves auditory testing we collaborate with Dr. Josef Walton.
University of Rochester
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