J Neurochem. 2007 Nov 6 [Epub ahead of print].
CSF Proteomic Analysis Reveals Persistent Iron Deficiency-Induced Alterations in Nonhuman Primate Infants.
Geguchadze RN, Coe CL, Lubach GR, Clardy TW, Beard JL, Connor JR.
Department of Neurosurgery, The Pennsylvania State University College of Medicine, Milton S. Hershey Medical Center, 500 University Drive, Hershey, PA, USA.

Iron deficiency anemia (IDA) during infancy results in long term neurological consequences, yet the mediating mechanisms remain unclear. Infant monkeys become naturally anemic during the first 6 months of life, presenting an opportunity to determine the effect of developmental iron deficiency. After weaning, animals were chosen randomly for supplementation with oral iron or, fed a standard commercial chow diet. The control group was never iron deficient. Iron deficiency anemia was corrected by 12 months in both groups, as indicated by hematological parameters. Cerebrospinal fluid was collected for proteomic analysis at 12 months of age to assess the impact of developmental iron deficiency on the brain. The CSF proteome for both formerly iron deficient groups was similar and revealed twelve proteins whose expression was altered at least two-fold. These proteins were identified by MALDI-TOF spectrometry and included prostaglandin D synthase, olfactory receptors and GFAP. Thus the proteomic analysis reveals a persistent effect of iron deficiency and provides insights into reports of disturbed sleep, hypomyelination and other behavioral alterations associated with iron deficiency. Furthermore, alterations in the CSF proteome despite normal hematologic parameters indicate that there is a hierarchical system that prioritizes repletion of red cell mass at the expense of the brain.

Categories: 2007, Iron, Iron deficiency anemia, Gene expression, Epigenetics, Sleep architecture, Myelination