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Optimized Analysis of DNA Methylation and Gene Expression from Small, Anatomically-defined Areas of the Brain

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Early-Life Iron Deficiency Anemia Programs the Hippocampal Epigenomic Landscape.

Amanda K Barks¹, Shirelle X Liu¹, Michael K Georgieff¹

¹Department of Pediatrics, University of Minnesota, Minneapolis, MN 55455, USA.

|November 27, 2021

Summary

Iron deficiency anemia in early life can cause lasting neurodevelopmental deficits by altering gene expression. Iron-dependent epigenetic modifiers like JARID and TET proteins may explain how this occurs.

Keywords:

JARIDs TETs cognition epigenetics neurodevelopment perinatal iron deficiency

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Area of Science:

Neuroscience
Developmental Biology
Genetics

Background:

Iron deficiency (ID) anemia is a global health issue, particularly impacting pregnant women and young children.
Early-life ID can lead to irreversible neurodevelopmental deficits, including cognitive impairment and neuropsychiatric disorders.
Existing treatments for ID do not always reverse these long-term neurological consequences.

Purpose of the Study:

To investigate the functional link between iron deficiency and gene dysregulation in the brain.
To explore the role of iron-dependent epigenetic modifications in mediating the effects of early-life ID.
To identify specific epigenetic modifiers involved in iron-mediated neurodevelopmental changes.

Main Methods:

Utilized animal models of developmental iron deficiency.
Examined hippocampal structure and function in affected models.
Investigated gene expression patterns related to neurotransmission and synaptic plasticity.
Focused on the role of iron-dependent epigenetic modifiers, specifically JARID and TET proteins.

Main Results:

Developmental ID in animal models resulted in abnormal hippocampal structure and function.
Observed dysregulation of genes critical for neurotransmission and synaptic plasticity.
Identified iron-dependent epigenetic modifiers (JARID and TET proteins) as key players in neural development.
These modifiers are implicated in establishing gene regulation during critical developmental periods.

Conclusions:

Early-life iron deficiency can cause stable, life-long changes in gene regulation across the lifespan.
Iron-dependent epigenetic mechanisms involving JARID and TET proteins are a likely cause of these persistent neurodevelopmental deficits.
Understanding these mechanisms offers potential targets for mitigating the long-term effects of developmental iron deficiency.