Iron deficiency in early life is associated with delayed development as assessed by a number of clinical trials using similar global scales of development; this poor development during infancy persists in most cases after iron therapy has corrected iron status. If iron deficiency occurs in preschool and older children, the consequences appear reversible with treatment. The biologic understanding of this relationship between development, brain iron status, and functioning is sparse though animal studies repeatedly demonstrate alterations in dopamine metabolism and in the myelination process. Dietary iron deficiency can rapidly deplete brain iron concentrations and repletion is able to normalize them. Residual alterations in striatal dopamine metabolism and myelin production persist if neonatal animals are used. Future studies with more specific measures of neurodevelopment in iron-deficient human infants, and animal models, will allow investigators to more clearly define causal roles of brain iron in neural development and functioning.

中文翻译：

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铁的状态和神经功能。

生命早期的铁缺乏与发育迟缓有关，这是通过许多使用相似的全球发展规模的临床试验评估得出的；在大多数情况下，铁疗法纠正了铁的状况后，婴儿期的这种不良发展仍然存在。如果学龄前和较大的儿童出现铁缺乏症，那么治疗带来的后果似乎是可逆的。尽管动物研究反复证明了多巴胺代谢和髓鞘形成过程中的变化，但对发育，脑铁状态和功能之间这种关系的生物学了解很少。饮食中的铁缺乏会迅速耗尽脑中铁的浓度，补充可使它们恢复正常。如果使用新生动物，则纹状体多巴胺代谢和髓磷脂产生的残留变化仍然存在。