Department of Pediatrics Neonatology Division, University of Minnesota, Minneapolis, MN 55455, USA.
Adv Nutr. 2011 Mar;2(2):112-21. doi: 10.3945/an.110.000190. Epub 2011 Mar 10.
Iron deficiency (ID) is the most common nutrient deficiency, affecting 2 billion people and 30% of pregnant women and their offspring. Early life ID affects at least 3 major neurobehavioral domains, including speed of processing, affect, and learning and memory, the latter being particularly prominent. The learning and memory deficits occur while the infants are iron deficient and persist despite iron repletion. The neural mechanisms underlying the short- and long-term deficits are being elucidated. Early ID alters the transcriptome, metabolome, structure, intracellular signaling pathways, and electrophysiology of the developing hippocampus, the brain region responsible for recognition learning and memory. Until recently, it was unclear whether these effects are directly due to a lack of iron interacting with important transcriptional, translational, or post-translational processes or to indirect effects such as hypoxia due to anemia or stress. Nonanemic genetic mouse models generated by conditionally altering expression of iron transport proteins specifically in hippocampal neurons in late gestation have led to a greater understanding of iron's role in learning and memory. The learning deficits in adulthood likely result from interactions between direct and indirect effects that contribute to abnormal hippocampal structure and plasticity.
缺铁（ID）是最常见的营养缺乏症，影响了 20 亿人，包括 30%的孕妇及其后代。生命早期的缺铁会影响至少 3 个主要的神经行为领域，包括处理速度、情感和学习记忆，后者尤为突出。学习和记忆缺陷发生在婴儿缺铁时，尽管补充了铁，但这些缺陷仍然存在。目前正在阐明导致短期和长期缺陷的神经机制。早期缺铁会改变发育中的海马体的转录组、代谢组、结构、细胞内信号通路和电生理学，海马体是负责识别学习和记忆的大脑区域。直到最近，人们还不清楚这些影响是直接由于缺乏与重要转录、翻译或翻译后过程相互作用的铁，还是由于贫血或应激引起的缺氧等间接影响。通过在妊娠后期特异性改变铁转运蛋白在海马神经元中的表达而产生的非贫血基因小鼠模型，使人们对铁在学习和记忆中的作用有了更深入的了解。成年后的学习缺陷可能是直接和间接影响相互作用的结果，导致异常的海马体结构和可塑性。
