细胞铁缺乏症扰乱甲状腺激素调节的基因表达在发展的海马神经元中
Timothy R Monko1, Emma H Tripp1, Sierra E Burr1
1University of Minnesota, School of Medicine, Department of Pediatrics.
bioRxiv : the preprint server for biology
|July 3, 2023
概括
早期的铁缺乏会损害发育中的神经元中的甲状腺激素调节,可能导致持久的神经发育缺陷. 即使在铁补充后,一些基因表达模式也表明缺乏的持续影响.
科学领域:
- 神经科学是一个神经科学.
- 发展生物学 发展生物学
- 营养神经科学 营养神经科学
背景情况:
- 发育中的神经元需要足够的铁和甲状腺激素来实现最佳的新陈代谢和生长.
- 铁和甲状腺激素的早期缺乏是常见的,并且与神经发育障碍有关.
- 在生命早期缺铁会破坏甲状腺激素水平和大脑中的基因表达.
结论:
- 一个细胞内机制可能协调铁和甲状腺激素的活动,以调节神经元的能量生产和生长信号.
- 甲状腺激素依赖的神经发育过程的持续缺陷,即使在从早期的铁缺乏症中恢复过来之后,也可能发生.
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