No abstract

ET among breast cancer patients seems to negatively alter the cognitive outcomes of breast cancer patients. However, the methodological heterogeneity of the included studies, as well as the relatively small follow-up period, render imperative the conduct of further studies in the field.

AbstractIron deficiency (ID) is a major public health problem worldwide among children aged 0–12 months. Several factors seem to contribute to the iron-deficient state in infancy, including insufficient antenatal and neonatal iron supplementation, exclusive breastfeeding, and early umbilical cord clamping after birth. The most concerning complications of ID, except for anemia, are related to altered long-term neurodevelopment. Clinical studies have shown a negative impact of ID anemia on fetal and neonatal behavior including impairments of motor maturity, autonomic response, memory/learning, and mood. ID-induced defects during infancy seem to persist later in life, even after ID treatment. The underlying mechanisms involve dysfunctional myelination, neurotransmission alterations, and altered synaptogenesis and/or dendritogenesis. The purpose of the present review is to summarize these mechanisms and to provide recommendations for future clinical research in the field.

Westernization of dietary habits has led to a progressive reduction in dietary intake of n‐3 polyunsaturated fatty acids (n‐3 PUFAs). Low maternal intake of n‐3 PUFAs has been linked to neurodevelopmental disorders, conditions in which myelination processes are abnormal, leading to defects in brain functional connectivity. Only little is known about the role of n‐3 PUFAs in oligodendrocyte physiology and white matter development. Here, we show that lifelong n‐3 PUFA deficiency disrupts oligodendrocytes maturation and myelination processes during the postnatal period in mice. This has long‐term deleterious consequences on white matter organization and hippocampus‐prefrontal functional connectivity in adults, associated with cognitive and emotional disorders. Promoting developmental myelination with clemastine, a first‐generation histamine antagonist and enhancer of oligodendrocyte precursor cell differentiation, rescues memory deficits in n‐3 PUFA deficient animals. Our findings identify a novel mechanism through which n‐3 PUFA deficiency alters brain functions by disrupting oligodendrocyte maturation and brain myelination during the neurodevelopmental period.