Pregnancy-related neurodevelopmental disorders: Exploring potential timelines and locations where they might originate in a fetus's brain development
In a groundbreaking study, researchers from the University of Rochester have uncovered the potential link between gestational iron deficiency and cognitive impairments in children. The study, published in the journal Development, reveals that iron is crucial during fetal development for various brain-related processes, and a deficiency in iron can negatively impact the development of neuronal progenitor cells.
Iron plays a vital role in oxygen transport, myelination, energy production, and the functioning of neurotransmitters such as dopamine and GABA. These processes are essential for proper neuronal differentiation and maturation. When iron is deficient during gestation, neuronal progenitor cells may not proliferate or differentiate optimally, potentially impairing brain growth and the formation of neural circuits critical for cognitive functions.
Although a meta-analysis found no significant short-term effects of maternal anemia on neonatal cognitive and motor functions, the long-term neurodevelopmental consequences remain uncertain and warrant further study. The lack of iron can specifically impair processes like myelination, leading to suboptimal neuronal connectivity, which is linked to poorer cognitive performance and motor skills later in childhood.
To better understand the mechanisms behind this, Margot Mayer-Proschel's lab is establishing a human model of iron deficiency using brain organoids. Brain organoids are a mass of cells that represent a brain and can be instructed to form specific regions of the ganglionic eminences of the embryonic human brain. The human model will help understand cellular targets of the prevalent nutritional deficiency, iron, which has limited impact with iron supplementation after birth.
Using this human model, the researchers found that a specific progenitor cell pool was disrupted in embryonic brains exposed to gestational iron deficiency (GID), suggesting that GID affects the behavior of embryonic progenitor cells, causing the creation of a suboptimal network of specialized neurons later in life. This study aims to determine the relevance of findings in the mouse model for the human system and find new cellular targets for GID that are not present in mouse models.
The lab of Margot Mayer-Proschel has identified a new embryonic neuronal progenitor cell target for GID. Understanding such cellular targets of this prevalent nutritional deficiency will be imperative to make changes to how we think of maternal health. It's crucial to note that iron deficiency is still prevalent in pregnant mothers and young children, and mothers with low iron levels during pregnancy have a higher risk of giving birth to a child with cognitive impairments like autism, attention deficit syndrome, and learning disabilities.
This research was supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development at the National Institute of Health, the Toxicology training grant of the Environmental Health Department at the University of Rochester, the New York Stem Cell Training Grant, and the Kilian J. and Caroline F. Schmitt Foundation through the Del Monte Institute for Neuroscience Pilot Program. The human brain's cells begin developing before the physical brain's formation, and a network of cells' early organizing plays a significant role in brain health throughout a lifetime.
In conclusion, the study provides valuable insights into the impact of gestational iron deficiency on cognitive development. Early nutritional status, including adequate maternal and infant iron, is critical to supporting healthy brain development and cognitive outcomes. Further research is needed to fully understand the mechanisms behind this link and to develop effective strategies for preventing and managing gestational iron deficiency.
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