2015
DOI: 10.3945/jn.114.201798
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Fetal Iron Deficiency and Genotype Influence Emotionality in Infant Rhesus Monkeys

Abstract: MAOA × ID interactions support the role of monoamine neurotransmitters in prenatal ID effects in rhesus monkeys and the potential involvement of common human polymorphisms in determining the pattern of neurobehavioral effects produced by inadequate prenatal nutrition.

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Cited by 8 publications
(6 citation statements)
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“…Because of high Fe requirements in both the fetus and the mother, maternal ID is a common condition in pregnancy ( 36 , 37 ) . The rationale for identifying it as a risk factor in infant neurodevelopment is that the fetus receives reduced placental transfer of Fe, causing either reduced Fe stores for the important 1st month of postnatal brain development, when Fe requirements in the infant are largely met by the inborn stores ( 24 , 38 ) , or direct prenatal compromise during fetal brain development ( 6 , 9 , 39 ) . The magnitude of this risk has previously been considered low, because of the efficient Fe uptake mechanism in the placenta.…”
Section: Discussionmentioning
confidence: 99%
“…Because of high Fe requirements in both the fetus and the mother, maternal ID is a common condition in pregnancy ( 36 , 37 ) . The rationale for identifying it as a risk factor in infant neurodevelopment is that the fetus receives reduced placental transfer of Fe, causing either reduced Fe stores for the important 1st month of postnatal brain development, when Fe requirements in the infant are largely met by the inborn stores ( 24 , 38 ) , or direct prenatal compromise during fetal brain development ( 6 , 9 , 39 ) . The magnitude of this risk has previously been considered low, because of the efficient Fe uptake mechanism in the placenta.…”
Section: Discussionmentioning
confidence: 99%
“…One well understood example that relates maternal diet to CNS pathologies is spina bifida, caused by insufficient folic acid in early pregnancy. While less understood, abnormalities in the levels of central minerals potentially begin in utero (3,4). Examples of neurological disorders where imbalances of micronutrients have been identified in adulthood include Alzheimer's, Parkinson's and Huntington's diseases (5)(6)(7).…”
Section: Introductionmentioning
confidence: 99%
“…Therefore, the decrease of irisin levels in this study due to IDA reveals impairment in the molecular mechanisms driving neuron homeostasis. Moreover, the decrease recorded in MAO-A can be explained because iron is a key factor for MAO activity, and monoamine neurotransmitter synthesis requires the iron-dependent enzymes tyrosine and tryptophan hydroxylase, which is a finding that has been correlated with later behavioral consequences in juvenile monkeys, influencing brain function [35]. IDA also decreased oxytocin, which is a hypothalamic neuropeptide involved in regulating social behavior, and has a key role in physiological conditions and brain diseases.…”
Section: Discussionmentioning
confidence: 99%