Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin, Heilongjiang Province 150081, China; Key Lab of Etiology and Epidemiology, Education Bureau of Heilongjiang Province and Ministry of Health (23618504), Harbin, Heilongjiang 150081, China; Heilongjiang Provincial Key Lab of Trace Elements and Human Health, Harbin, Heilongjiang 150081, China.
Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin, Heilongjiang Province 150081, China; Key Lab of Etiology and Epidemiology, Education Bureau of Heilongjiang Province and Ministry of Health (23618504), Harbin, Heilongjiang 150081, China; Heilongjiang Provincial Key Lab of Trace Elements and Human Health, Harbin, Heilongjiang 150081, China.
Neuroscience. 2024 Oct 18;558:22-29. doi: 10.1016/j.neuroscience.2024.08.011. Epub 2024 Aug 11.
Fluorosis is a global public health concern. Prolonged exposure to excessive fluoride causes fluoride accumulation in the hippocampus, resulting in cognitive dysfunction. Cell death is necessary for maintaining tissue function and morphology, and changes in the external morphology of nerve cells and the function of many internal organelles are typical features of cell death; however, it is also a typical feature of cognitive impairment caused by fluorosis. However, the pathogenesis of cognitive impairment caused by different degrees of fluoride exposure varies. Herein, we provide an overview of cognitive impairment caused by excessive fluoride exposure in different age groups, and the underlying mechanisms for cognitive impairment in various model organisms. The mechanisms underlying these impairments include oxidative stress, synaptic and neurotransmission dysfunction, disruption of mitochondrial and energy metabolism, and calcium channel dysregulation. This study aims to provide potential insights that serve as a reference for subsequent research on the cognitive function caused by excessive fluoride.
氟中毒是一个全球性的公共卫生问题。长期暴露于过量氟化物会导致氟在海马体中积累，从而导致认知功能障碍。细胞死亡对于维持组织功能和形态是必要的，神经细胞的外部形态和许多内部细胞器的功能变化是细胞死亡的典型特征；然而，这也是氟中毒引起认知障碍的典型特征。然而，不同程度氟暴露引起的认知障碍的发病机制不同。本文综述了不同年龄组中过量氟暴露引起的认知障碍，以及各种模式生物中认知障碍的潜在机制。这些损伤的机制包括氧化应激、突触和神经传递功能障碍、线粒体和能量代谢紊乱以及钙通道调节失常。本研究旨在为后续研究过量氟引起的认知功能障碍提供潜在的见解，作为参考。
