Abstract：
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.
摘要：
氟中毒是全球公共卫生问题。长时间接触过量的氟化物会导致海马中的氟化物积累，导致认知功能障碍。细胞死亡是维持组织功能和形态所必需的，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，这也是氟中毒引起的认知障碍的典型特征。然而,不同程度氟暴露引起的认知功能障碍的发病机制各不相同。在这里，我们提供了不同年龄段的过度氟暴露引起的认知障碍的概述，以及各种模式生物认知障碍的潜在机制。这些损伤的潜在机制包括氧化应激，突触和神经传递功能障碍，线粒体和能量代谢的破坏，和钙通道失调.本研究旨在提供潜在的见解，为后续研究过量氟化物引起的认知功能提供参考。
