The Effects of Early-Life Iron Deficiency on Brain Energy Metabolism
Iron deficiency (ID) is one of the most prevalent nutritional deficiencies in the world. Iron deficiency in the late fetal and newborn period causes abnormal cognitive performance and emotional regulation, which can persist into adulthood despite iron repletion. Potential mechanisms contributing to...
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2020-06-01
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Series: | Neuroscience Insights |
Online Access: | https://doi.org/10.1177/2633105520935104 |
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doaj-f38face72fc4445199e4023e0890511f2020-11-25T03:52:02ZengSAGE PublishingNeuroscience Insights2633-10552020-06-011510.1177/2633105520935104The Effects of Early-Life Iron Deficiency on Brain Energy MetabolismThomas W BastianRaghavendra RaoPhu V TranMichael K GeorgieffIron deficiency (ID) is one of the most prevalent nutritional deficiencies in the world. Iron deficiency in the late fetal and newborn period causes abnormal cognitive performance and emotional regulation, which can persist into adulthood despite iron repletion. Potential mechanisms contributing to these impairments include deficits in brain energy metabolism, neurotransmission, and myelination. Here, we comprehensively review the existing data that demonstrate diminished brain energetic capacity as a mechanistic driver of impaired neurobehavioral development due to early-life (fetal-neonatal) ID. We further discuss a novel hypothesis that permanent metabolic reprogramming, which occurs during the period of ID, leads to chronically impaired neuronal energetics and mitochondrial capacity in adulthood, thus limiting adult neuroplasticity and neurobehavioral function. We conclude that early-life ID impairs energy metabolism in a brain region- and age-dependent manner, with particularly strong evidence for hippocampal neurons. Additional studies, focusing on other brain regions and cell types, are needed.https://doi.org/10.1177/2633105520935104 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Thomas W Bastian Raghavendra Rao Phu V Tran Michael K Georgieff |
spellingShingle |
Thomas W Bastian Raghavendra Rao Phu V Tran Michael K Georgieff The Effects of Early-Life Iron Deficiency on Brain Energy Metabolism Neuroscience Insights |
author_facet |
Thomas W Bastian Raghavendra Rao Phu V Tran Michael K Georgieff |
author_sort |
Thomas W Bastian |
title |
The Effects of Early-Life Iron Deficiency on Brain Energy Metabolism |
title_short |
The Effects of Early-Life Iron Deficiency on Brain Energy Metabolism |
title_full |
The Effects of Early-Life Iron Deficiency on Brain Energy Metabolism |
title_fullStr |
The Effects of Early-Life Iron Deficiency on Brain Energy Metabolism |
title_full_unstemmed |
The Effects of Early-Life Iron Deficiency on Brain Energy Metabolism |
title_sort |
effects of early-life iron deficiency on brain energy metabolism |
publisher |
SAGE Publishing |
series |
Neuroscience Insights |
issn |
2633-1055 |
publishDate |
2020-06-01 |
description |
Iron deficiency (ID) is one of the most prevalent nutritional deficiencies in the world. Iron deficiency in the late fetal and newborn period causes abnormal cognitive performance and emotional regulation, which can persist into adulthood despite iron repletion. Potential mechanisms contributing to these impairments include deficits in brain energy metabolism, neurotransmission, and myelination. Here, we comprehensively review the existing data that demonstrate diminished brain energetic capacity as a mechanistic driver of impaired neurobehavioral development due to early-life (fetal-neonatal) ID. We further discuss a novel hypothesis that permanent metabolic reprogramming, which occurs during the period of ID, leads to chronically impaired neuronal energetics and mitochondrial capacity in adulthood, thus limiting adult neuroplasticity and neurobehavioral function. We conclude that early-life ID impairs energy metabolism in a brain region- and age-dependent manner, with particularly strong evidence for hippocampal neurons. Additional studies, focusing on other brain regions and cell types, are needed. |
url |
https://doi.org/10.1177/2633105520935104 |
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