Early-Life Iron Deficiency Anemia Programs the Hippocampal Epigenomic Landscape

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 i...

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Autores principales: Amanda K. Barks, Shirelle X. Liu, Michael K. Georgieff, Timothy C. Hallstrom, Phu V. Tran
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Lenguaje:EN
Publicado: MDPI AG 2021
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Acceso en línea:https://doaj.org/article/38e76bbf21414a4aa88fdbc41102cf1f
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spelling oai:doaj.org-article:38e76bbf21414a4aa88fdbc41102cf1f2021-11-25T18:34:42ZEarly-Life Iron Deficiency Anemia Programs the Hippocampal Epigenomic Landscape10.3390/nu131138572072-6643https://doaj.org/article/38e76bbf21414a4aa88fdbc41102cf1f2021-10-01T00:00:00Zhttps://www.mdpi.com/2072-6643/13/11/3857https://doaj.org/toc/2072-6643Iron 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.Amanda K. BarksShirelle X. LiuMichael K. GeorgieffTimothy C. HallstromPhu V. TranMDPI AGarticleperinatal iron deficiencyneurodevelopmentepigeneticsJARIDsTETscognitionNutrition. Foods and food supplyTX341-641ENNutrients, Vol 13, Iss 3857, p 3857 (2021)
institution DOAJ
collection DOAJ
language EN
topic perinatal iron deficiency
neurodevelopment
epigenetics
JARIDs
TETs
cognition
Nutrition. Foods and food supply
TX341-641
spellingShingle perinatal iron deficiency
neurodevelopment
epigenetics
JARIDs
TETs
cognition
Nutrition. Foods and food supply
TX341-641
Amanda K. Barks
Shirelle X. Liu
Michael K. Georgieff
Timothy C. Hallstrom
Phu V. Tran
Early-Life Iron Deficiency Anemia Programs the Hippocampal Epigenomic Landscape
description 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.
format article
author Amanda K. Barks
Shirelle X. Liu
Michael K. Georgieff
Timothy C. Hallstrom
Phu V. Tran
author_facet Amanda K. Barks
Shirelle X. Liu
Michael K. Georgieff
Timothy C. Hallstrom
Phu V. Tran
author_sort Amanda K. Barks
title Early-Life Iron Deficiency Anemia Programs the Hippocampal Epigenomic Landscape
title_short Early-Life Iron Deficiency Anemia Programs the Hippocampal Epigenomic Landscape
title_full Early-Life Iron Deficiency Anemia Programs the Hippocampal Epigenomic Landscape
title_fullStr Early-Life Iron Deficiency Anemia Programs the Hippocampal Epigenomic Landscape
title_full_unstemmed Early-Life Iron Deficiency Anemia Programs the Hippocampal Epigenomic Landscape
title_sort early-life iron deficiency anemia programs the hippocampal epigenomic landscape
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/38e76bbf21414a4aa88fdbc41102cf1f
work_keys_str_mv AT amandakbarks earlylifeirondeficiencyanemiaprogramsthehippocampalepigenomiclandscape
AT shirellexliu earlylifeirondeficiencyanemiaprogramsthehippocampalepigenomiclandscape
AT michaelkgeorgieff earlylifeirondeficiencyanemiaprogramsthehippocampalepigenomiclandscape
AT timothychallstrom earlylifeirondeficiencyanemiaprogramsthehippocampalepigenomiclandscape
AT phuvtran earlylifeirondeficiencyanemiaprogramsthehippocampalepigenomiclandscape
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