Abstract
Iron deficiency (ID) anemia is the foremost micronutrient deficiency worldwide, affecting around 40% of pregnant women and young children. ID during the prenatal and early postnatal periods has a pronounced effect on neurodevelopment, resulting in long-term effects such as cognitive impairment and increased risk for neuropsychiatric disorders. Treatment of ID has been complicated as it does not always resolve the long-lasting neurodevelopmental deficits. In animal models, developmental ID results in abnormal hippocampal structure and function associated with dysregulation of genes involved in neurotransmission and synaptic plasticity. Dysregulation of these genes is a likely proximate cause of the life-long deficits that follow developmental ID. However, a direct functional link between iron and gene dysregulation has yet to be elucidated. Iron-dependent epigenetic modifications are one mechanism by which ID could alter gene expression across the lifespan. The jumonji and AT-rich interaction domain-containing (JARID) protein and the Ten-Eleven Translocation (TET) proteins are two families of iron-dependent epigenetic modifiers that play critical roles during neural development by establishing proper gene regulation during critical periods of brain development. Therefore, JARIDs and TETs can contribute to the iron-mediated epigenetic mechanisms by which early-life ID directly causes stable changes in gene regulation across the life span.
Highlights
Increasing evidence indicates that early-life adverse events can have a lasting impact on physiological and mental health [1,2]
iron deficiency (ID) during the fetal and early childhood periods has a significant effect on neurodevelopment, resulting in cognitive, socio-emotional, and learning and memory deficits that last into early adulthood [5,6]
Parallel studies in pre-clinical models have shown that early-life ID results in abnormal hippocampal structure, function, and gene expression acutely during the period of rapid neurodevelopment and persistently into adulthood despite prompt iron therapy after diagnosis [9,10,11,12,13,14,15,16,17,18]
Summary
Increasing evidence indicates that early-life adverse events (e.g., malnutrition) can have a lasting impact on physiological and mental health [1,2]. Choline supplementation during late fetal or early postnatal life has been shown to mitigate behavioral abnormalities in models of genetic and early-life environmental insults, including ID [24,29,30,31,32,33]. Like supplements such as folic acid, betaine, vitamin B12, and L-methionine, choline is a methyl donor for Sadenosylmethionine (SAM), which is a substrate for DNA and histone methylation.
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