Neurocognitive Dysfunctions in Iron Deficiency Patients

Abstract

In this chapter, the authors described the actuality of the investigations of neurocognitive dysfunctions in patients with iron deficiency. In infants, the incidence of iron deficiency is 73%; the probability of its transition to iron deficiency anemia is very high. The development of myelin at an early age reduces the production of myelin, and the formation of g-aminobutyric acid worsens the metabolism of dopamine in the striatal brain, which leads to slowing of motor function and behavioral problems in the child. Children with iron deficiency conditions are prone to developmental delays, reduced school performance, and behavioral disorders. In older adults, cognitive dysfunctions depend on complications of the vascular nature, complicated by comorbid iron deficiency. Concomitant pathology also influences iron homeostasis. The regulating mechanisms of iron deficiency, as the same cognitive deficiency, despite the age involve more than 200 proteins from iron homeostasis, appropriate cofactors: derivatives of vitamin B, copper, manganese, zinc ions, enzymes, cell growth factors, etc. All these partners could influence separately or together to the development of iron deficiency and a complication of it neurocognitive dysfunctions. The combination of iron deficiency anemia and iron deficiency with comorbid pathology often exacerbates cognitive problems and requires a weighted approach to the choice of therapeutic correction tactics.