Iron is an essential micronutrient that plays crucial roles in molecular oxygen (O2) transport, DNA replication, and mitochondrial function among other processes. As such, iron dyshomeostasis in the form of iron deficiency (ID) or iron overload is detrimental to human health. Humans and other mammals have evolved intricate mechanisms that tightly regulate iron metabolism and maintain iron homeostasis. The interplay between the peptide hormone hepcidin and the iron exporter ferroportin (FPN) is key in maintaining systemic iron balance. ID has long been associated with significant adverse consequences including anemia, compromised immunity, and increased susceptibility to microbial infections, especially in children. Moreover, numerous clinical and experimental findings have long suggested that ID during pregnancy, infancy, or early childhood may hinder brain development and function. The spectrum of cognitive domains that could be affected by ID covers memory, attention, problem-solving, spatial awareness, sensorimotor functions, and socio-emotional skills among others. The mechanism(s) underlying the link between ID and poor cognition in children are poorly understood. However, defective synthesis of neurotransmitters like dopamine and serotonin, defective neuronal myelination, and poor neurotransmission are likely contributors. Defective development and function in other organ systems like the cardiovascular and immune systems may amplify the negative effects of ID on cognition. This chapter discusses the link between ID and poor cognition in preschool and schoolchildren with special emphasis on the biological aspects of ID and how it impacts brain development and function.